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ABSTRACT BOOK & FINAL PROGRAMME
KNJIGA SAŽETAKA I ZAVRŠNI PROGRAM
VI Master Class on Vitiligo
and Pigmentary Disorders
“Innovative Therapies in Dermatology” Symposium
“Dermoscopy Course”
VI. edukativni skup o vitiligu
i poremećajima pigmentacije
Simpozij “Inovativne dermatološke terapije”
“Tečaj dermatoskopije”
Split, Croatia, 30th April – 3rd May 2015, Radisson Blu Hotel
POZDRAVNA RIJEČ / WELCOME ADDRESS
SADRŽAJ / CONTENT
POZDRAVNI GOVOR / WELCOME ADDRESS
. . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
ORGANIZACIJSKI ODBOR / ORGANIZING COMMITTEE
SPONZORI / SPONSORS
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PREGLEDNI PROGRAM / PROGRAMME AT A GLANCE
TEČAJ DERMATOSKOPIJE / DERMOSCOPY COURSE
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ZNANSTVENI PROGRAM / SCIENTIFIC PROGRAMME
POSTERI / POSTERS
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DRUŠTVENI PROGRAM / SOCIAL PROGRAMME
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OPĆE INFORMACIJE / GENERAL INFORMATION
...............................................................
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KORISNE INFORMACIJE / USEFUL INFORMATION
. . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
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KNJIGA SAŽETAKA / ABSTRACT BOOK
USMENA IZLAGANJA - VITILIGO / ORAL PRESENTATIONS - VITILIGO
............................
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USMENA IZLAGANJA - INOVATIVNE TERAPIJE / ORAL PRESENTATIONS - INNOVATIVE
THERAPIES
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
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USMENA IZLAGANJA - KRATKA PRIOPĆENJA / ORAL PRESENTATIONS - FREE
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COMMUNICATIONS
. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .
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POSTERI / POSTERS
................................................................................................................
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VI Master Class on Vitiligo and Pigmentary Disorders
POZDRAVNI GOVOR / WELCOME ADDRESS
I Poštovane kolegice i kolege, dragi gosti
i prijatelji hrvatskih dermatovenerologa,
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u prigodi organiziranja Simpozija i Tečajeva s najatraktivnijim temama moderne i inovativne
dermatovenerologije, iznimna nam je čast, ali i velika radost i zadovoljstvo pozdraviti Vas u ime
Hrvatskog dermatovenerološkog društva HLZ-a, Hrvatskog saveza oboljelih od vitiliga, Svjetske
organizacije za istraživanje vitiliga (Vitiligo Research Foundation) i Svjetske zdravstvene akademije (World Health Academy).
U okružju ljepote povijesnih i kulturnih znamenitosti, u ozračju nacionalne i internacionalne
znanstvene misli koja obilježava povijest, sadašnjost i budućnost južne prijestolnice naše Hrvatske, našeg Splita, odlučni smo našoj dermatološkoj zajednici u Hrvatskoj i svijetu dati svoj
doprinos kao znanstvenici, nastavnici i liječnici koji strastveno vole svoju struku.
Ugledne institucije i predavači velike međunarodne reputacije biti će vaši domaćini u temama
o vitiligu i poremećajima pigmentacije, inovativnim dermatološkim terapijama i dermatoskopiji. Sigurni smo da je odabir tema usklađen s aktualnim zanimanjem u dermatološkoj znanosti,
ali i u svakodnevnim kliničkim izazovima koji nam se nameću u radu s našim bolesnicima.
Nadamo se vašem velikom odazivu, osobito mladih kolega, s kojima ćemo, kao i u svim našim
dosadašnjim druženjima, potvrditi veliku znanstvenu znatiželju i zajedničku odanost dermatovenerološkoj struci.
Iskreno se veselimo učenju i druženju sa Vama!
Predsjednica
organizacijskog odbora:
Prof. dr. sc.
Mirna Šitum
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Dopredsjednik
organizacijskog odbora:
Prof. dr. sc.
Andrija Stanimirović
VI Master Class on Vitiligo and Pigmentary Disorders - ‘‘Innovative Therapies in Dermatology Symposium’’
Predsjednica
znanstvenog odbora:
Prof. dr. sc.
Branka Marinović
I Respected colleagues, dear guests
and friends of Croatian dermatovenereologists,
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Having participated in the organization of the Symposium and Courses with the most attractive and innovative topics in modern dermatovenereology, it is our exceptional honor, but also
a great joy and pleasure, to greet you in the name of the Croatian Dermatovenereological Society of the Croatian Medical Association, the Croatian Vitiligo Association, the Vitiligo Research
Foundation and the World Health Academy.
Within the beautiful milieu of historical and cultural sights, in the radiance of national and international scientific ideas that mark the past, present, and future of the Southern capital of our Croatia,
our Split, we are determined to contribute to our dermatological community in Croatia and the
World, as committed scientists, teachers, and doctors, who passionately love their profession.
Prominent institutions and lectures with great international reputation will be your hosts in the
topics of vitiligo and pigmentary disorders, innovative therapies in dermatology and dermatoscopy. We are sure that the choice of topics complies with actual interests of the science of
dermatology, as well as the everyday clinical challenges that impose themselves in the work
with our patients.
We hope for your great response, especially from our young colleagues, with whom we will
confirm our great scientific curiosity and our common commitment to the dermatological
profession.
We are truely looking forward to learning and spending time with you!
President of the
Organizing Committee:
Professor
Mirna Šitum, MD, PhD
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Vice President of the
Organizing Committee:
Professor
Andrija Stanimirović, MD, PhD
President of the
Scientific Committee:
Professor
Branka Marinović, MD, PhD
VI. edukativni skup o vitiligu i poremećajima pigmentacije - ‘‘Inovativne dermatološke terapije’’
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ORGANIZACIJSKI ODBOR / ORGANIZING COMMITTEE
I Pod pokroviteljstvom / Under the auspice of
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Hrvatska akademija znanosti i umjetnosti
Croatian Academy of Sciences and Arts
I Organizatori / Organizers
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Hrvatsko dermatovenerološko društvo Hrvatskog liječničkog zbora
Hrvatski savez oboljelih od vitiliga
Svjetska organizacija za istraživanje vitiliga
Svjetska zdravstvena akademija
Croatian Dermatovenereological Society of the Croatian Medical Association
Croatian Vitiligo Association
Vitiligo Research Foundation
World Health Academy
I Predsjednica kongresa / Congress President
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Mirna Šitum
I Dopredsjednik kongresa / Congress Vice President
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I Predsjednica znanstvenog odbora / Scientific Committee President
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Branka Marinović
I Tajnici kongresa / Congress Secretaries
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Hrvoje Beclin
Maja Kovačević
I Organizacijski i znanstveni odbor / Organizing & Scientific Committee
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Andreas Katsambas
Igor Korobko
Torello Lotti
Branka Marinović
Neira Puizina-Ivić
Mihael Skerlev
Mirna Šitum
Yan Valle
I Pozivni predavači / Invited Speakers
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Giuseppe Argenziano (ITA)
Igor Bartenjev (SLO)
Ivana Binić (SRB)
Zrinka Bukvić Mokos (CRO)
Vedrana Bulat (CRO)
Andy Goren (USA)
Andreas Katsambas (GRE)
Igor Korobko (RUS)
Krešimir Kostović (CRO)
Maja Kovačević (CRO)
Piotr Kuna (POL)
Torello Lotti (ITA)
Branka Marinović (CRO)
Claudia Menicanti (ITA)
Željko Mijušković (SRB)
Joelle Nonni (FRA)
Neira Puizina-Ivić (CRO)
Nives Pustišek (CRO)
Sanja Schuller-Petrović (AUT)
Mihael Skerlev (CRO)
Andrija Stanimirović (CRO)
Jacek C. Szepietowski (POL)
Mirna Šitum (CRO)
Sanja Špoljar (CRO)
Nataša Teovska Mitrevska (MKD)
Diamant Thaci (GER)
Yan Valle (USA)
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SPONZORI / SPONSORS
I Zlatni sponzor / Gold Sponsor
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BELUPO
I Ostali sponzori / Other Sponsors
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ABBVIE
ALMAGEA
A&B
BAYER
BEIERSDORF
JANSSEN
LA ROCHE POSAY
NOVARTIS
OKTAL PHARMA
PAUL HARTMANN
PROXIMUM
REMEDIA
VICHY
VITA MED
WALDMANN
I Sponzor tečaja dermatoskopije / Dermoscopy Course Sponsor
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LA ROCHE POSAY
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PREGLEDNI PROGRAM / PROGRAMME AT A GLANCE
I THURSDAY 30th APRIL 2015 / ČETVRTAK, 30. TRAVNJA 2015.
14,00 - 19,30
Registration / Registracija
Ground floor, Reception area
/ Prizemlje kod recepcije
14,30 - 19,30
Dermoscopy Course / Tečaj dermatoskopije (Only for CDVS members
/ Samo za članove HDVD-a)
Grand Ballroom
/ Konferencijska dvorana
I FRIDAY, 1st MAY 2015 / PETAK, 1. SVIBNJA 2015.
07,30 - 18,30
Ground floor, Reception area
/ Prizemlje kod recepcije
08,30 - 11,45
Dermoscopy Course / Tečaj dermatoskopije (Only for CDVs members
/ Samo za članove HDVD-a)
Grand Ballroom
07,30 - 18,30
Slide Area / Predaja radova
Wardrobe / Garderoba
12,30
Opening Ceremony
/ Otvorenje Simpozija
Grand Ballroom
13,00 - 14,00
Welcome Drink and Snack
/ Piće dobrodošlice i mali zalogaji
In front of Grand Ballroom
/ Ispred konferencijske dvorane
14,00 - 16,00
Vitiligo - Session 1 / Vitiligo - sekcija 1 Grand Ballroom / Konferencijska dvorana
16,00 - 16,30
Coffee Break / Pauza za kavu
Sponsored by Beiersdorf
/ Sponzor Beiersdorf
In front of Grand Ballroom, Reception Area / Ispred konferencijske
dvorane, prizemlje kod recepcije
16,30 - 18,30
Innovative Therapies - Session 1
/ Inovativne terapije - sekcija 1
Grand Ballroom
19,30 - 21,00
Welcome Cocktail
/ Domjenak dobrodošlice
Pool area Hotel Radisson Blu
/ Bazen hotela Radisson Blu
I SATURDAY, 2nd MAY 2015 / SUBOTA, 2. SVIBNJA 2015.
09,00 - 19,00
Exhibiton Area / Izložbeni prostor
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Poster Area / Posteri
Grand Ballroom
08,00 - 19,00
09,00 - 10.40
Innovative Therapies - Session 2
Grand Ballroom
10,40 - 11,20
Coffee Break / Pauza za kavu
Sponsored by Novartis
/ Sponzor Novartis
11,20 - 13,30
Vitiligo - Session 2
/ Vitiligo - sekcija 2
Grand Ballroom
13,00 - 15,00
Lunch / Ručak
Hotel Restaurant “The Fig Leaf”
/ Hotelski restoran “The Fig Leaf”
15,00 - 16,40
Innovative Therapies - session 3
Grand Ballroom
16,40 - 17,00
Coffee Break
/ Pauza za kavu
17,00 - 19,15
Vitiligo - Session 3
/ Vitiligo - sekcija 3
Grand Ballroom
18,45 - 19,15
Vitiligo Round Table
/ Vitiligo okrugli stol
Grand Ballroom
I SUNDAY, 3rd MAY 2015 / NEDJELJA , 3. SVIBNJA 2015.
08,00 - 11,30
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Exhibiton Area / Izložbeni prostor
Poster Area / Posteri
Grand Ballroom
08,00 - 11,30
09,00 - 10,45
Free Communications
/ Kratka priopćenja
Grand Ballroom
10,45 - 11,00
Poster Discussion
/ Rasprava o posterima
Grand Ballroom
11,00 - 11,30
Closing Ceremony
/ Zatvaranje Simpozija
Grand Ballroom
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TEČAJ DERMATOSKOPIJE / DERMOSCOPY COURSE
Sponsored by / Organizator
La Roche Possay
(Only for CDVS members / Samo za članove HDVD-a)
Professor Giuseppe Argenziano, MD, PhD
I THURSDAY 30th APRIL 2015 / ČETVRTAK, 30. TRAVNJA 2015.
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14,30 - 15,00
Welcome Coffee
15,00 - 16,00
An Ordinary Day in the Practice
16,00 - 16,40
Screening Children
16,45 - 17,00
Discussion, Q&A
17,00 - 17,30
Coffee Break
17,30 - 18,30
Lesions in Special Locations
18,30 - 19,30
Pink Lesions
I FRIDAY, 1st MAY 2015 / PETAK, 1. SVIBNJA 2015.
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08,30 - 09,30
Difficult Benign Lesions and Rules not to Miss Melanoma
09,30 - 10,30
Special Cases with Emphasis to Patients with Single vs. Multiple Lesions
10,30 - 11,00
Dermoscopy in General Dermatology
11,00 - 11,30
Quiz Session
11,30 - 11,45
Closing Remarks
13
ZNANSTVENI PROGRAM / SCIENTIFIC PROGRAMME
I FRIDAY, 1st May 2015 / PETAK, 1. svibnja 2015.
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12,30
Opening Ceremony / Otvorenje Simpozija
14,00 - 16,00
Vitiligo (V) – Session / Sekcija 1
Chairpersons / Predsjedavajući: Igor Korobko, Torello Lotti, Branka Marinović
14,00 - 14,20
14,20 - 14,40
Pigmentary Disorders / Poremećaji pigmentacije (V-1)
Mirna Šitum
Vitiligo– What’s New and What’s True in 2015
/ Vitiligo – što je novo, što je istinito u 2015. godini? (V-2)
Torello Lotti
14,40 - 15,00
Differential Diagnosis of Vitiligo / Diferencijalna dijagnoza vitiliga (V-3)
Neira Puizina-Ivić
15,00 - 15,20
Vitiligo as a Systemic Disease / Vitiligo kao sistemska bolest (V-4)
Vedrana Bulat
15,20 - 15,40
Psychological Aspects of Vitiligo / Psihološki aspekti vitiliga (V-5)
Jacek C. Szepietowski
15,40 - 16,00
Skin Cancer and Vitiligo / Malignomi kože i vitiligo (V-6)
Andreas D. Katsambas
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16,00 - 16,30 Coffee Break / Stanka za kavu
16,30 - 18,30
Innovative Therapies / Inovativne terapije (IT) – Session / Sekcija 1
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Chairpersons / Predsjedavajući: Andy Goren, Mihael Skerlev, Nives Pustišek
16,30 - 16,50
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Management of Atopic Dermatitis
/ Liječenje atopijskog dermatitisa (IT-1)
Nives Pustišek
16,50 - 17,10
Pathogenesis and Management of Itch in Adult Atopic Dermatitis
Patients / Patogeneza i liječenje svrbeža u odraslih bolesnika s atopijskim dermatitisom (IT-2)
17,10 - 17,30
Therapeutic approach for intolerant skin-what to do?
/ Terapijski pristup intolerantnoj koži – što učiniti? (IT-3)
Branka Marinović
17,30 - 17,50
Modern Therapeutic Approach to Alopecias
/ Suvremeni terapijski pristup alopecijama (IT-4)
17,50 - 18,10
How do I treat HPV? / Kako liječiti HPV? (IT-5)
Mihael Skerlev
18,10 - 18,30
Novel Topical Cream Delivers Safe and Effective Alternative to
Traditional Psoriasis Phototherapy / Nova lokalna terapija – sigurna i
učinkovita alternativa tradicionalnoj terapiji psorijaze (IT-6)
Andy Goren
I SATURDAY, 2nd May 2015 / SUBOTA, 2. svibnja 2015.
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09,00 - 10,40
Innovative Therapies / Inovativne terapije (IT)– Session /Sekcija 2
Chairpersons / Predsjedavajući: Diamant Thaci, Neira Puizina-Ivić, Jacek C. Szepietowski
15
09,00 - 09,20
Acne in Childhood – What to Do? / Akne u dječjoj dobi – što učiniti? (IT-7)
Zrinka Bukvić Mokos
09,20 - 09,40
Treatment of acne-what’s new? / Terapija akne – što je novo? (IT-8)
Claudia Menicanti
09,40 - 10,00
Treatment of Infective Dermatoses – What’s New?
/ Terapija infektivnih dermatoza – što je novo? (IT-9)
Neira Puizina-Ivić
15
10,00 - 10,20
Therapeutic Approach to Autoimmune Bullous Diseases – State of
the Art / Terapijski pristup autoimunim buloznim dermatozama – što
je novo? (IT-10)
Branka Marinović
10:20 - 10:40
New Therapeutic Options for Psoriasis Patients
/ Nove terapijske mogućnosti u liječenju psorijaze (IT-11)
Diamant Thaci
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10,40 - 11,20
Coffee Break / Stanka za kavu
11,20 - 13,30
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Chairpersons / Predsjedavajući: Igor Bartenjev, Ivana Binić, Krešimir Kostović
16
11,20 - 11,40
Vitiligo in Everyday Life – Practical Advices
/ Vitiligo u svakodnevnoj praksi – praktični savjeti (V-7)
Igor Bartenjev
11,40 - 12,00
Quality of Life in Vitiligo Patients / Kvaliteta života bolesnika s vitiligom (V-8)
Nataša Teovska Mitrevska
12,00 - 12,20
Vitiligo and Hyperpigmentation Disorders – What’s Mutual?
/ Vitiligo i poremećaji pigmentacije – što je zajedničko? (V-9)
Ivana Binić
12,20 - 12,40
Phototherapy and Excimer Laser Treatment for Vitiligo
/ Fototerapija i Excimer laser u liječenju vitiliga (V-10)
Krešimir Kostović
12,40 - 13,00
Vitiligo-Case Reports / Vitiligo – prikazi slučajeva (V-11)
Maja Kovačević
13,00 - 13,30
Camouflage in Vitiligo Patients / Kamuflaža u bolesnika s vitiligom (V-12)
Joelle Nonni
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13,30 - 15,00
Lunch Break / Ručak
15,00 - 16,40
Innovative therapies / Inovativne terapije (IT) – Session / Sekcija 3
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
Chairpersons / Predsjedavajući: Sanja Schuller-Petrović, Željko Mijušković, Mirna Šitum
15,00 - 15,20
Dysplastic Naevi and Melanoma / Displastični nevus i melanom (IT-12)
Mirna Šitum
15,20 - 15,40
Actinic Keratoses and Epidermal Malignant Skin Tumors: Modern
Approach to Therapy / Aktiničke keratoze i epidermalni maligni
tumori kože: suvremeni terapijski pristup (IT-13)
Željko Mijušković
15,40 - 16,00
Treatment Options for Varicose Veins Syndrome / Terapijske
mogućnosti kod bolesnika sa sindomom varikoznih vena (IT-14)
Sanja Schuller-Petrović
16,00 - 16,20
Treatment Approach for Ulcus cruris
/ Ulcus cruris – suvremeni terapijski pristup (IT-15)
Sanja Špoljar
16,20 - 16,40
Pathogenesis and Management of Chronic Urticaria
/ Patogeneza i liječenje kronične urtikarije (IT-16)
Piotr Kuna
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16,40 - 17,00
Coffee Break / Stanka za kavu
17,00 - 19,15
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Chairpersons / Predsjedavajući: Andrija Stanimirović, Natasa Teovska Mitrevska, Yan Valle
17,00 - 17,20
17
Vitiligo Treatment Guidelines-Where are we now?
/ Smjernice za liječenje vitiliga – gdje smo sada? (V-13)
17
17,20 - 17,40
Vitiligo Cloud Bank: Bio-IT System for Patients, Doctors
and Investigators / Bioinformatički sustav za bolesnike, liječnike i
istraživače (V-14)
Yan Valle
17,40 - 18,00
Topical cream delivers NB-UVB from sunlight for the treatment
of vitiligo / Lokalna terapija – selektivna filtracija NB-UVB iz Sunčevog
svjetla u terapiji vitiliga (V-15)
Andy Goren
18,00 - 18,20
Immunomodulators in Vitiligo Management
/ Imunomodulatori u liječenju vitiliga (V-16)
Igor Korobko
18:20 - 18:40
18,45 - 19,15
Low dose oral cytokines therapy for vitiligo: the future is here
/ Niske doze peroralnih citokina u liječenju vitiliga – budućnost je
ovdje (V-17)
Torello Lotti
Vitiligo – Round Table / Okrugli stol
I SUNDAY, 3rd May 2015 / NEDJELJA, 3. svibnja 2015.
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Free Communications (FC) / Kratka priopćenja
Chairpersons / Predsjedavajući: Gordana Krnjević-Pezić, Jovan Miljković, Dubravka Šimić
09,00 - 09,15
18
Psychosocial factors in patient with multiple autoimmune diseases
/ Psihosocijalni čimbenici u bolesnika s različitim autoimunim
bolestima (FC-1)
Edita Simonić
19
09,15 - 09,30
Collagen induction therapy / Dermaroller
/ Indukcija kolagena medicinskim Dermarollerom (FC-2)
Željana Bolanča
09,30 - 09,45
Treatment of plane warts with systemic isotretinoin / Terapija
mladenačkih plošnih bradavica sa sistemskim izotretinoinom (FC-3)
Jovan Miljković
09,45 - 10,00
Juvenile-onset hypopigmented mycosis fungoides: a case series of 3
patients / Mycosis fungoides juvenilis hypopigmentata – prikaz tri
bolesnika (FC-4)
Sandra Jerković Gulin
10,00 - 10,15
Psoriasis patients: psychological characteristics and quality of life
impact / Bolesnici sa psorijazom: psihološke karakteristike i utjecaj
na kvalitetu života (FC-5)
Gordana Krnjević - Pezić
10,15 - 10,30
Therapeutic use of monoclonal antibodies in
psoriasis-immunological principles and immune-based adverse effects
/ Terapijska primjena monoklonskih protutijela u psorijazi (FC-6)
Vesna Lukinović Škudar
10,30 - 10,45
Dermatitis herpetiformis, gluten-sensitive enteropathy and
sacroileitis – case report / Dermatitis herpetiformis, glutenska
enteropatija i sakroileitis – prikaz slučaja (FC-7)
Dubravka Šimić
10,45 - 11,00
Poster Discussion / Rasprava o posterima
11,00 - 11,30
Closing Ceremony / Zatvaranje Simpozija
19
POSTERI / POSTERS
I Posters / Posteri (P)
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
P-1
Mycosis fungoides non-responsive to PUVA therapy – Case report
/ Prikaz bolesnika s mycosis fungoides koji nije reagirao na PUVA terapiju
Vlatka Čavka
P-2
Detection of mucasal human papillomavirus types in extra-genital Bowen’s Disease
/ Detekcija sluzničnih tipova humanog papilomavirusa u ekstragenitalnom obliku Bowenove bolesti
Vlatka Čavka
P-3
The use of preparations containing smectite, copper gluconate and zinc gluconate
in herpes zoster
/ Upotreba preparata koji sadrže smektit, bakreni glukonat i cinkov glukonat
u liječenju herpes zostera
Ljiljana Škrinjar
P-4
Anti-thyroglobulin antibody and vitiligo
/ Antitireoglobulinska antitijela i vitiligo
Emina Kasumagić Halilović
P-5
Prevalence of vitiligo in West Herzegovina
/ Prevalencija vitiliga u zapadnoj Hercegovini
Ana-Marija Sulić
P-6
Histamine Intolerance – Dermatologic Sequels
/ Intolerancija na histamin – dermatološke posljedice
Liborija Lugović-Mihić
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POZDRAVNA RIJEČ / WELCOME
DRUŠTVENI
ADDRESS
PROGRAM / SOCIAL PROGRAMME
I Petak 1. svibnja 2015. / Friday , 1st May, 2015
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19,30
21
Zajedničko druženje / Get Together Party
Bazen Hotela Radisson / Hotel Radisson Pool
21
OPĆE INFORMACIJE / GENERAL INFORMATION
I Venue and Date of the Congress / Mjesto i vrijeme održavanja kongresa
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Split, Hotel Radisson Blu, 30. travnja - 3. svibnja 2015.
Split, Hotel Radisson Blu, 30th April - 3rd May, 2015
I Professional Congress Organizer (PCO) / Tehnički organizator
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SPEKTAR PUTOVANJA
Tkalčićeva 15, Zagreb, Croatia
T: +385 1 4862 600
F: +385 1 4862 622
E: [email protected]
I Official languages / Službeni jezici
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Službeni jezici kongresa su hrvatski i engleski, simultanog prevođenja neće biti.
The official languages of the Congress are Croatian and English. No simultaneous translation will be provided.
I Certificate of Attendance / Bodovanje
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Povjerenstvo za medicinsku izobrazbu liječnika HLK kategoriziralo je i vrednovalo stručni
skup pod nazivom - VI. edukativni skup o vitiligu i poremećajima pigmentacije ‘‘Inovativne
dermatološke terapije“ i to kako slijedi:
Predavači: 14 bodova
Slušači: 9 bodova
According to Croatia Medical Chamber participants at the Congress will be rated as it
follows:
Speakers: 14 points
Delegates: 9 points
22
I Registration fee / Kotizacija
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Kategorija
Category
ON SITE
Sudionici: Liječnici – Članovi HDVD-a*
Participants: Physicians-CDVS MEMBERS
1.800,00 Kn
Sudionici: Liječnici
Participants: Physicians
2.000,00 Kn
Specijalizanti: Članovi HDVD-a*
Residents: CDVS MEMBERS
1.050,00 Kn
Specijalizanti
Residents
1.150,00 Kn
Osobe u pratnji
Accompanying Persons
500,00 Kn
Izlagači i sponzori
Exibitor and Sponsors
1.300,00 Kn
* Članovi HDVD-a dužni su uz prijavu dostaviti kopiju uplate članstva / *CDVS MEMBERS should enclose a copy of membership payment
Kotizacija uključuje: Pristup predavanjima • Konferencijske materijale • Pristup izložbi • Pauze za kavu i ručkove tijekom stanke • Knjigu “Vitiligoperspektive i smjernice” / Registration fee includes: Admission to scientific sessions • Conference materials • Admission to exhibition • Coffee
breaks and lunches • Book „Vitiligo – perspektive i smjernice“
I Registration and info desk / Vrijeme registracije
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Četvrtak / Thursday
Petak / Friday
Subota / Saturday
Nedjelja / Sunday
30.04.2015.
01.05.2015.
02.05.2015.
03.05.2015.
14,00 - 19,30
07,30 - 18,30
08,00 - 19,00
08,00 - 11,30
I Exhibiton Area / Izložbeni prostor
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Vrijeme postavljanja izložbe / Set up time
Četvrtak / Thursday
30.04.2015.
15,30 - 18,00
Vrijeme raspremanja izložbe / Dismantling time
Nedjelja / Sunday
03.05.2015.
od 11,00 / from 11,00 a.m.
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KORISNE INFORMACIJE / USEFUL INFORMATION
I O Splitu
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Split je najveći grad u Dalmaciji, drugi po veličini grad u Hrvatskoj, druga je po veličini hrvatska luka
i treća luka na Mediteranu po broju putnika. Gradsko središte čini starovjekovna Dioklecijanova palača iz 4. stoljeća (pod UNESCO-vom zaštitom od 1979. godine), što je jedinstven primjer u svijetu.
Veličinom drugi grad u Republici Hrvatskoj i najveći hrvatski grad na istočnoj obali Jadranskog mora smjestio se između rijeka Žrnovnice na istoku i Jadra na zapadu. Grad koji nudi hlad
marjanske šume na zapadnom dijelu poluotoka, 15 kilometara šetnica uz more i dalmatinsku
pjesmu na kamenim ulicama staroga grada, smješten na jednom od najsunčanijih dijelova
srednjeg Mediterana poznat je i po svojim klimatskim pogodnostima, mjerljivim i kroz 2700
sunčanih sati godišnje.
Split je važno hrvatsko, mediteransko kulturno središte, po veličini danas i drugi sveučilišni centar u Hrvatskoj, a poslije Zagreba ima i najveći broj diplomatskih, konzularnih, odnosno predstavništava međunarodnih organizacija u Hrvatskoj.
Split, kao grad na moru i jedna od najznačajnijih turističkih destinacija u Hrvatskoj. posjeduje i snažnu
brodograđevnu industriju te razvijeno građevinsko poduzetništvo, ali i prerađivačku industriju. Split
je i središte informatičke djelatnosti te sjedište jednoga od najvećih trgovinskih lanaca u Hrvatskoj.
S obzirom na broj stanovnika Split se svrstava i u među gradove s najuspješnijim sportašima
koji su osvajali olimpijska, svjetska i europska odličja u plivanju, vaterpolu, veslanju, jedrenju,
nogometu, košarci, rukometu, atletici, borilačkim sportovima…
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Split je i grad za kojega će kroničar lako zapisati kako on živi svojim usporenim ritmom, na koji
ćete se brzo priviknuti. Taj osjećaj da je ovdje svaki dan praznik, trgovi, restorani i kafići prepuni
ljudi i nezaobilazna “riva”, kojom ljeti gospodari blagi osvježavajući maestral, a zimi, kao zimski
kaput, mediteransko sunce i palača štite od hladnoće, i sve to se može izraziti jednostavnom
konstatacijom - osjećaš se kao kod kuće.
I About Split
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Split is not only an urban, cultural and traffic centre of Dalmatia with road and sea connections
to Dalmatia’s numerous summer resorts, but it is itself often a tourist and excursionists destination. A city with a 1700-year old tradition, a variety of archaeological, historical and cultural
monuments, among which the well-known Palace of Diocletian, inscribed into the UNESCO
World Heritage List, certainly occupies a special position, and the warmth and offer of a modern Mediterranean city. The first detailed tourist guide through the town and its surroundings,
published in 1894, bears witness to the long tourist tradition in Split. To be able to grasp the
historical significance of the city, one should first visit the museums of Split: the Museum of
Croatian Archaeological Monuments - a capital Croatian cultural project, established in 1893
in Knin; the Archaeological Museum from 1820, one of the oldest in Croatia; the Treasury of
the Split Cathedral, including a valuable collection of religious art; the Ethnographic Museum,
founded in 1910; the Museum of Marine History; the Museum of Natural Science. The Art Gallery, established in 1931, the Collection of the Franciscan Monastery in Poljud, the Mestrovic
Gallery, and other are also worth visiting.
Split is a major sports centre (the 1979 Mediterranean Games) with many famous and popular
sports clubs and competitors. There are also many sports facilities for recreational purposes.
The sports offer includes almost all types of water and other sports, from football, basketball
and tennis to mountain climbing and rifle-shooting, water skiing and rowing.
Worth visiting is Marjan Forest Park, the green oasis the citizens of Split have been proud of for
generations, carefully maintained and cherished. The park includes promenades, vista points,
solariums, nature paths, playgrounds and the Split zoo. A marvellous view is offered from the
top of Marjan on the old and new parts of Split. It takes only 15 minutes of pleasant walking to
reach Marjan from the historical core of Split through the old quarter Varos. The Marjan stairway, running along the crest of the hill, leads to another, higher top of Marjan, Telegrin, with a
vista point offering prospect on the Split peninsula, Kozjak, Mosor, the Kastela Gulf, Salona and
Klis, Trogir and Ciovo, and the islands of Solta, Brac, Hvar and Vis. The southern cliffs of Marjan
represent in recent times a very good training ground for mountaineers and free climbers, who
gather here every April on the occasion of the traditional Marjan Cup.
25
25
Split has a variety of restaurants and wine cellars, offering domestic specialities. There are many
beaches and public beaches in the city and its surroundings, the most popular of them being
Bacvice, a sand beach almost in the very heart of the town.
The cultural and entertainment offer of Split is extremely rich, particularly in the summer, when
the city squares, yards and other areas turn into a large open-air stage. The Split Summer, a
traditional festival in the middle of the summer season, includes dramas, operas and concerts
(from mid-July to mid-August). The Split Saturday Nights are de-voted to classical music. Split
also hosts pop-music events, the Art-Summer, folklore shows, the folk feast Day of Radunica,
and many other. Major cultural events during the year are the Days of Marulic (in April), the
Book of the Mediterranean (in October), and the traditional events include the Day of the Holy
Cross, the Flowers Show, the Ball of Split, wine show and other. The Day of St. Doimus (Duje),
who is the patron saint of the city, is commemorated on the 7th of May.
Split has several theatres, among which the Croatian National Theatre, established in 1893, deserves a special mention as a house hosting theatrical festivals, the Split Summer and the Days
of Marulic. There is also the Youth Theatre, and the Split Puppet Theatre. Split ACI Marina has
500 berths in the sea and accommodates 100 vessels on the land. Open throughout the year.
Split, a city and port in Central Dalmatia. Situated on a peninsula between the eastern part of
the Gulf of Kastela and the Split Channel. A hill, Marjan (178 m), rises in the western part of the
peninsula. The ridges Kozjak (780 m) and Mosor (1,330 m) protect the city from the north and
northeast, and separate it from the hinterland. Split has the Mediterranean climate: hot dry
summers (average air temperature in July reaches 26 °C) and mild, humid winters (average
annual rainfall is 900 mm). Split is one of the sunniest places in Europe: the average daily insolation during the year is about 7 hours (in July about 12 hours). Vegetation is of the evergreen
Mediterranean type, and subtropical flora (palm-trees, agaves, cacti) grows in the city and its
surroundings. Marjan is covered with a cultivated forest.
Development of steam-shipping, construction of railroad connections with the hinterland
before and between the World Wars, and particularly industrialization underlie the economic
prosperity and increase of the population in Split. Split is a business, administrative and cultural
centre of Dalmatia. Apart from shipbuilding industry, other manufacturers include processing of plastic masses, cement industry, food and other products. Vegetable, fruit and flowers
are grown in the surroundings. Split is an important Croatian port in terms of passenger and
goods traffic. It is the centre of the maritime connections with the ports on the coast and the
islands and terminal railway station of the rail connections with the hinterland. Ferries operate
regularly between Split and the central Dalmatian islands, as well as to Ancona in Italy. Ship
connections are established, except with the islands, with Pula, Venice, Dubrovnik and Greece.
The airport of Split is situated in Resnik (Kastela). Split has many cultural and educational institutions and schools: the University of Split (established in 1974), the theatre, museums, galleries,
26
institutes, and recently a specialized UN institution for protection of environment in the Mediterranean (Regional Activity Centre for the Priority Actions Programme).The Spit Summer, a
cultural event (open-air operas, plays and concerts), as well as music perfomances (Melodies of
the Croatian Adriatic, Split Festival of Pop Music) take place every year. Split disposes of a variety
of sports facilities, swimming pools and piers for sports boats and similar. Both stationary and
transit tourism record a permanent increase. New port, hotel and tourist facilities have been
constructed. The coves within the city offer several public beaches.
Split has four marinas: Split ACI Marina in the north-western part of the City Port; the sports
boats pier Spinut on the northern coast of Marjan; the sports boats marina Poljud in the Poljud
Port; the sports boat pier Zenta on the eastern coast of Split. The City Port of Split in the centre
of the city is used only for passenger and ferry traffic.
The city at the foot of Marjan can be reached by The Adriatic Coastal Road, winding by the
sea or by hinterland roads connected to Split. It will take you 5 hours to get to Zagreb and 4
hours to get to Dubrovnik in your car. You can also reach Split if you get on a coast ferry liner
from Rijeka or Dubrovnik, from all central Dalmatian islands. There are excellent fast and regular
ferry lines from Ancona and Pescara, Italy. From the Airport Split flights connect the city with
Zagreb several times a day, as well as with European capitals. There are also trains from Split to
the north of the country and further on to Europe. You can transport your car by train, as well.
27
27
KNJIGA SAŽETAKA / ABSTRACT BOOK
VI Master Class On Vitiligo
and Pigmentary Disorders
and »Innovative Therapy
In Dermatology« Symposium
Split, Croatia, May 1-3, 2015
VITILIGO (V) – INVITED SPEAKERS
I V 1 – PIGMENTARY DISORDERS
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Mirna Šitum, Suzana Ožanić Bulić
Department of Dermatology and Venereology, University Hospital Center “Sestre milosrdnice”,
Zagreb, Croatia; [email protected]
Pigmentary disorders are aetiologically complex part of general and corrective dermatology,
medical cosmetology, as well as dermatological oncology, requiring interdisciplinary approach
in diagnostics and treatment. Negative psychological impact of pigmentary disorders on patients’ quality of life prompts the need for successful treatment, and if necessary, aesthetic correction. This, along with positive change in physical appearance resulting in higher self-confidence and general mental health, is motivation to study this complex field of skin disorders,
mostly of unknown aetiology and modest treatment results.
Pigmentary disorders cover not only wide area of skin diseases, but also systemic disorders
causing hyper or hypopigmentation of the skin. Other important causes of skin pigmentary
disorders are environmental factors, malignancies, or even habits.
Hyperpigmentation characterized by increased melanin synthesis from unchanged number
of melanocytes are called melanotic hyperpigmentations. Less common are melanocytic hyperpigmentations resulting from increased number of melanocytes. Depending on the level
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of melanin deposition, epidermal, dermal and mixed, epidermo-dermal hyperpigmentation
can be seen. Epidermal hyperpigmentation is characterised by brown colour resulting from
increased amount of melanin in the epidermis, and is also known as melanoderma. Melanoderma has several causes; hyperproduction of melanosomes with increased transport to keratinocytes, increased size of melanosomes, or decreased keratinocyte turnover, leading to
keratinocytes overloaded with melanosomes. Dermal hyperpigmentation result from melanim
accumulation in dermis, also known as coeruloderma, after characteristic blue-gray colour. Accumulation of melanin in the epidermis and dermis gives brown-gray colour of mixed type
hyperpigmentation. Hyperpigmentation of the skin can also be classified as localized or diffuse
depending on the affected area, or linear and reticulate in relation to distribution and clinical
features of pigmentation. Most common causes of localized hyperpigmentation are melasma,
aging spots (lentigines) and postinflammatory hyperpigmentation (PIH). Diffuse hyperpigmentation can result from systemic disorders like endocrinopathies, drug administration and application of various physical and chemical substances. Linear PIH most commonly occurs on
anterior trunk and lateral limbs. Bleomicyn treatment or increased intake of uncooked or partially cooked shitake mushrooms result in flagellate hyperpigmentation. Another type of linear
hyperpigmentation along Blaschko lines represents pathways of epidermal cell migration and
proliferation during the development of the foetus, present in many inherited and some acquired skin disorders. Inherited skin disorders resulting in reticulated hyperpigmentation pattern are genodermatoses like Dyskeratosis congenita, Naegeli-Franceschetti-Jaddassohn syndrome, Dermopathia pigmentosa reticularis, X-linked reticulate pigmentation, Dowling-Degos
disease and Reticulated acropigmentation of Kitamura. Erythema ab igne represents a type of
acquired reticulate pigmentation of skin as a consequence of prolonged exposure to various
sources of heat. Majority of hyperpigmentations are localized on sun exposed, visible skin of the
face and hands, causing significant psychological distress to the patient. Hyperpigmentations
also include heterogenous group of hyperpigmented skin changes like ephelides, café-au-lait
macules, Naevus Becker, melanotic macules of mucosae, lentigo simplex, lentiginoses and senile lentigo. Despite recent advances in the treatment, hyperpigmentation remains a therapeutic challenge for physicians and patients. The other end of pigmentary disorders comprises
of hypopigmentations that result from decreased quantity of melanin in the epidermis. There
are two major types of hypopigmentations, melanocytopenic hypomelanosis, resulting from
complete or partial depletion of epidermal or follicular melanocytes due to inherited (impaired
differentiation, proliferation or migration of melanoblasts) or acquired factors. Acquired hypopigmentation is usually caused by chemicals, like phenol derivates and hydroquinone, causing
loss of pigmentation at the contact site, but also on unexposed skin. Hypopigmentation can
appear after cryotherapy, especially in dark skin types. Delayed hypopigmentation may appear
even some time after the exposure to potential agents. Chemicals cause selective destruction
and apoptosis of melanocytes sometimes permanently impairing the process of re-pigmen-
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tation. Vitiligo is another acquired type of hypopigmentation of unknown aetiology due to
the loss of functional melanocytes in epidermis and hair follicles. Melanopenic hypomelanosis
is characterized by unchanged number of epidermal and hair follicle melanocytes, but the
amount of melanin is reduced or the transport of melanin from melanocytes to keratinocytes
is impaired. Example of the latter is postinflammatory hypomelanosis, common in dark skin
types and resulting from increased mitotic rate of keratinocytes and decreased cell turn-over.
It is most common in psoriasis, atopic dermatitis, sarcoidosis, lichen sclerosus, lichen striatus,
lupus erythematosus, mycosis fungoides and pityriasis lichenoides chronica. Complete loss of
pigment is rarely seen in postinflammatory hypopigmentation and rarely occurs in atopic dermatitis and lupus erythematosus. Infective cause of pigment loss is seen with fungal infections
of the skin, e.g. Microsporosis, Pityriasis versicolor, Lepra, Treponemal infections (non-venerical
syphilis), Onchocerciasis, after Herpes zoster infection or Kala-azar disease. Halo naevus or Naevus Sutton is melanocytic naevus with acquired hypopigmentation caused by autoimmune reaction due to production of cytotoxic autoantibodies or cytotoxic T-lymphocytes characterized
by destruction of melanocytes, ultimately leading to disappearance of the naevus. Histopathology is showing junctional, intradermal or combined naevus surrounded by dense lymphocyte
and fibrohystiocyte infiltrate with complete loss of melanin in depigmented area.
In conclusion, although most pigmentary disorders are benign in nature, they present cosmetic and psychological challenges to the patient, necessitating evaluation and treatment. Proper
diagnosis will allow the physician to facilitate appropriate treatment and reassure patient.
sunčanih sati godišnje.
I V 2 – VITILIGO: WHAT’S NEW & WHAT’S TRUE IN 2015
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Torello Lotti
Institute of Dermatology, University of Rome “G. Marconi”, Rome, Italy; [email protected]
Vitiligo is an acquired disorder of pigmentation characterized by the appearance of patchy
hypo / amelanotic features in locations such as hands, genitals and face. Recent discoveries
about the pathogenesis of vitiligo have led to the development of new therapies. In particular,
developments in phototherapy, one of the cornerstones of treatment for vitiligo, has made
available new treatments such as Microphototherapy with UVB narrow band excimer laser
and monochromatic excimer light. These therapies are able to give good results both in patients with generalized vitiligo and in those with focal and segmental vitiligo. In addition to
steroids, topical medical treatment include derivatives of vitamin D, calcineurin inhibitors up
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to the promising possible use of products based on prostaglandin E or antioxidants. The actions of some topical treatments is furtherly enhanced when combined with light therapy,
thus increasing the therapeutic outcome. Ultraviolet-B (UVB) phototherapy is a well-established mode of treatment for several types of dermatological disease. For vitiligo, narrow band
UVB (NB-UVB) phototherapy is an effective therapy, demonstrating greater efficacy and safety
compared to broadband UVB or psoralen plus UVA treatments. While the treatment efficacy of
NB-UVB artificial light sources is well documented, the long term time and cost commitment
of the therapy remains a barrier to treatment adherence. Natural sunlight is an ideal source of
accessible UVB radiation; however, exposure to natural sunlight generally results in erythema
prior to the accumulation of sufficient dosage of therapeutic wavelengths of UVB. This communication describes a novel topical cream designed to selectively deliver NB-UVB therapy when
exposed to sunlight. The topical cream (Photocil) when combined with natural sunlight could
offer patients a more convenient phototherapy option for psoriasis and vitiligo, potentially increasing patient compliance.
I V 3 – DIFFERENTIAL DIAGNOSIS OF VITILIGO
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Neira Puizina-Ivić, Deny Anđelinović, Antoanela Čarija, Ranka Ivanišević, Olga Kosor,
Lina Mirić-Kovačević, Dubravka Vuković
Department of Dermatology and Venereology, University Hospital Center Split, University of
Split School of Medicine, Split, Croatia; [email protected]
Vitiligo is an acquired disorder characterized by depigmented macules and patches that result
from progressive loss of functional melanocytes. It is a multifactorial disorder related to both
genetic and nongenetic factors. In patients with complete depigmentation, the differential diagnosis includes chemical or drug-induced (e.g. imatinib, mesilat, potent corticosteroid) leukoderma, post-inflammatory depigmentation, leukoderma associated with underlaying melanoma, sleroderma, late stage of treponematosis and onchocerciasis. In young persons with single
circular lesions on the trunk, a halo nevus sould be considered. Early onset of slight hypopigmentation and depigmentation during childhood, must arouse suspicion towards diagnosis of
nevus depigmentosus or different genodermatoses, respectively. Various physical (burns, frostbites), and chemical factors (arsen, monobenzyl hydroquinone, azaleic acid, benzolyl peroxid)
can produce lesions similar to vitiligo, as well as mycosis fungoides, and hereditary disorders of
metabolism. Early lesions or those with partial loss of pigment need to be distinguished from
postinflammatory hypopigmentation, pityriasis versicolor and other cutaneous infections.
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I V 4 – VITILIGO AS A SYSTEMIC DISEASE
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Vedrana Bulat
Department of Dermatology and Venereology, University Hospital Center «Sestre milosrdnice»,
The final consequence in pathogenesis of vitiligo is the loss of functional, mature melanocytes
of the skin. Occasionally, internal organs containing melanocytes may also be affected. Recent investigations are suggesting that melanocytes are more than melanin-producing cells.
The melanocytes are likely to have a number of extra-pigmentary abilities. Melanocytes are
found at many locations throughout the body. Certain tissues (e.g. inner ear, eye, leptomeninges, heart) where melanocytes are found serve primarily for conducting the action potential.
That could also be the case with melanocytes within the epidermis. During the embryonic
development, melanocytes and neurons evolve from the same primary germ layer (ectoderm).
Melanocytes are aligned in a cyclic, regular arrangement on the basal membrane. Why are
melanocytes aligned in such an ordered manner on the basal membrane? It is possible that
melanocytes, apart from the visible pigment production, have a role in the conduction of some
kind of impulse within the epidermis. Nonsegmental vitiligo has been significantly associated
with various cutaneous and noncutaneous diseases. At first glance, vitiligo and diseases such
as atopic dermatitis, diabetes mellitus, rheumatoid arthritis, and chronic urticaria, appear to
be quite different. However, they have common genetic risk factors, which implies that they
share a similar pathogenesis, mainly autoimmune pathogenesis. There has also been found an
increased incidence of autoantibodies against melanocytes and several other types of autoantibodies. Introduction of systemic biologic treatments for nonsegmental vitiligo confirms the
hypothesis that it is a systemic disease and it should be treated with systemic agents. Despite
obvious clinical differences, vitiligo and associated cutaneous and noncutaneous diseases
share many important similarities that may help us to better understand their immunopathogeneses, and develop new treatments for our patients.
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I V 5 – PSYCHOLOGICAL ASPECTS OF VITILIGO
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Department of Dermatology, Venereology and Allergology, Wroclaw Medical University,
Wroclaw, Poland; [email protected]
Vitiligo is a chronic skin disease with loss of pigment resulting in irregular pale patches of skin.
The disease is considered in the spectrum of psychodermatological disorders with profound
psychological consequences. One may argue that psychological factors, like stressful life evens,
contribute to the etiology and the chronic course of the disease, but it is also of importance
that vitiligo influences heavily patient’s well being, especially in subjects with patches localized
on visible skin areas and in those with dark skin. In many societies the disease is poorly understood and is believed to be a sign of leprosy or sexually transmitted disease. Women suffering
from vitiligo in different parts of the world still have difficulties in getting married. Patients are
stigmatized, with significantly lowered quality of life. Both mental and physical components
are affected. Their quality of life is more decreased than patients with chronic inflammatory
diseases, such as psoriasis. Many patients feel embarrassment and shame. The depression and
anxiety are diagnosed even in up to 40% of vitiligo subjects. In summary, vitiligo has devastating effect on patient. Therefore, there is a need for effective treatment options. The benefit of
offering adjunctive psychological support should always be taken into consideration in holistic
approach to the therapy of vitiligo patients.
I V 6 – SKIN CANCER AND VITILIGO
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Andreas Katsambas
University of Athens, Greece; [email protected]
Vitiligo is a common autoimmune skin disease, affecting approximately 0.5% of the general
population. In vitiligo, cytotoxic CD8-T cells infiltrating the perilesional margin are probably
involved in the pathogenesis of the disease by destructing the melanocytes through the recognition of melanocytic differentiation antigens.There are data suggesting that strongng antityrosinase expression protects patients with vitiligo against melanoma. However, the lack of
melanine may involve greater photodamage and thus an increase risk of melanoma and nonmelanoma skin cancer. It is of interest that immunotherapy studies in a number of patients with
melanoma have resulted in the development of skin depigmentation resembling vitiligo and
that these patients have a more favorable prognosis for their tumor. Recent studies showed
that patients with vitiligo have a decreased risk of melanoma and non-melanoma skin cancer.
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I V 7 – VITILIGO IN EVERYDAY LIFE – PRACTICAL ADVICES
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Igor Bartenjev
Private practice and University of Ljubljana School of Medicine, Ljubljana, Slovenia;
[email protected]
Vitiligo is a common dermatological disorder that influence on patient’s quality of life, especially due to aesthetic impact and sensitivity to sun rays. It s a chronic skin disease characterized
by portions of the skin losing their pigment. Aside from cases of contact with certain chemicals,
the cause of vitiligo is unknown. Research suggests vitiligo may arise from autoimmune, genetic, oxidative stress, neural, or viral causes. Vitiligo is typically classified into two main categories:
segmental and non-segmental vitiligo. The only sign of vitiligo is the presence of pale patchy
areas of depigmented skin which tend to occur on the extremities. The patches are initially
small, but often grow and change shape. When skin lesions occur, they are most prominent on
the face, hands and wrists. The loss of skin pigmentation is particularly noticeable around body
orifices, such as the mouth, eyes, nostrils, genitalia and umbilicus. Although multiple theories
have been suggested as potential triggers that cause vitiligo, studies have most strongly implicated changes in the immune system as being responsible for the condition. Vitiligo has been
proposed to be a multifactorial disease with genetic susceptibility and environmental factors
both thought to play a role. Variations in genes that are part of the immune system or part of
melanocytes have both been associated with vitiligo. A genomewide association study found
approximately 36 independent susceptibility for generalized vitiligo. During the first visit of a
patient, who often do not know anything about vitiligo it is very important to give a basic information about the disease and its course. Doctors duty is to look for diseases that can be associated with vitiligo such as autoimmune and inflammatory diseases i.e. Hashimoto’s thyroiditis,
rheumatoid arthritis, type 1 diabetes, psoriasis, Addison disease, pernicious anemia, alopecia
areata, and systemic lupus erythematosus. Diagnosis is usually simple, with only clinical inspection. Rarely vitiligo can be similar to: pityriasis alba, postinflammatory hypopigmentations, pityriasis versicolor, albinism, piebaldism, idiopathic guttate hypomelanosis, progressive macular
hypomelanosis, tuberculoid leprosy. There is no cure for vitiligo but several treatment options
are available. The best evidence is for applied steroids and the combination of UV light in combination with creams. Phototherapy is required twice a week for 6–12 months or longer. In last
years due to the higher risks of skin cancer, experts suggests phototherapy only to be used if
primary treatments are ineffective. Our suggestion for first-line vitiligo treatment are topical
preparations of immune suppressing medications including glucocorticoids (such as 0.05%
clobetasol or 0.10% betamethasone) and calcineurin inhibitors (tacrolimus or pimecrolomus).
In general, non-segmental vitiligo responds to treatment better than the segmental form. Lesions located on the hands, feet, and joints are the most difficult to repigment; those on the
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face repigment most easy. In mild cases, vitiligo patches can be hidden with makeup or other
cosmetic camuflage solutions. In cases of extensive vitiligo the option to de-pigment the unaffected skin with topical drugs like monobenzone, mequinol, hydroquinone may be considered
to render the skin an even colour. The removal of all the skin pigment with monobenzone
is permanent and vigorous. Depigmentation takes about a year to complete. Some surgical
techniques are known from skin transplantation, as grafting and melanocytes transplanting to
vitiligo affected areas, but are not used widely.
I V 8 – QUALITY OF LIFE IN VITILIGO PATIENTS
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Natasa Teovska Mitrevska
ReMedika General Hospital, Dermatology Department, Skopje, Macedonia;
[email protected]
Skin disease is often obvious and very visible to others. Those who suffer from skin diseases
have to cope not only with the effects of their disease, but also with the reaction of others to
their condition. Visible disfigurement, whether present at birth or acquired later in life, can have
a profound psychological, physical, social and occupational impact. To assess the full impact
of skin disorders on a person’s quality of life, it is important to consider four different aspects:
physical, psychological, social and occupational impact. Measuring QoL is important because it
is used for making decisions especially about non clinical aspects of the disease. It is also used
for improvement of the doctor-patient relationship. It is important in discovery of functional
and psychological limitations, and in choosing the treatment in the initial phase of disease. Holistic approach is essential in dealing with dermatological disorders, because of the profound
and the far-reaching effects not only of the diseases, but also of treatments. It is necessary to
talk to patients and discuss the impact of their disease, how they cope with it and how they
feel about it. Vitiligo represents an emblematic case: often disfiguring and located in visible
areas, confused in the past (and, in many world regions, even in the present) with leprosy, often
perceived by physicians as a harmless, purely cosmetic problem, it significantly decreases the
quality of life of affected persons. After a brief overview on definition, usefulness and methods
for the assessment of quality of life, the author examines the peculiarities of its relationship with
skin diseases, particularly vitiligo. Multidisciplinary approach is essential for better quality of life
in vitiligo patients, and the team for achieving this is health professionals, groups of patients,
support communities, associations and societies.
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I V 9 – VITILIGO AND HYPERPIGMENTATION DISORDERS
- WHAT’S MUTUAL?
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Ivana Binić
Clinic for Dermatovenerology, Medical Faculty, Niš, Serbia; [email protected]
Cutaneous pigmentation is the outcome of two important events: the synthesis of melanin
by melanocytes and the transfer of melanosomes to surrounding keratinocytes. Although the
number of melanocytes in human skin of all types is essentially constant, the number, size,
and manner in which melanosomes are distributed within keratinocytes vary. Pigmentation
disorders include a large number of heterogeneous conditions that are usually characterized
by altered melanocyte density, melanin concentration, or both, and result in altered pigmentation of the skin. Melanin production results from strong cellular and molecular connections between all cell populations in the skin and the key players besides melanocytes, are fibroblasts
and keratinocytes. Minor changes in the cellular physiology of the skin can dramatically affect
pigment production in positive or negative manners. When disturbed, it may determine different types of pigmentation defects, which are classified as hypo or hyperpigmentation and
which may occur with or without an altered number of melanocytes. These two groups of disorders are different, but in the center of both is melanocyte with all associated cells, processes,
regulatory genes. Key questions that remain to be answered include what are the signal (s) that
modulate melanocyte stem cells’ awakening from and return to quiescence and to determine
what are the signals modulating melanocyte death during catagen? Also, interesting questions
may be about role of vitamin D and calcium in regulating process of pigmentation. Despite the
differences between vitiligo and hyperpigmentation disorders, a better understanding of their
etiopathogenesis and all the complex interactions between regulators of the melanogenesis
and finding their mutual characteristics will help in the future in finding better therapeutic options for both types of disorders.
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I V 10 – PHOTOTHERAPY AND EXCIMER LASER TREATMENT
FOR VITILIGO
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Krešimir Kostović
Department of Dermatology and Venereology, University Hospital Center Zagreb and
University of Zagreb School of Medicine, Zagreb, Croatia; [email protected]
Ultraviolet therapeutic options, both in the range of UVB and UVA, are first line modalities for
vitiligo affecting more than 10–20% of the skin surface. PUVA (psoralen and UVA radiation), a
standard treatment in the past, is done 2–3 times weekly. The most common complication
with PUVA is overdosage and severe burning. Narrow-band ultraviolet (NB-UVB) light has a
wavelength of 311 ± 2 nm. It has been claimed as the UV treatment of choice for vitiligo.
The efficacy of NB-UVB is comparable to that of PUVA, with the some advantages, such as the
absence of psoralen side effects and reduced cumulative radiation dose and photocarcinogenesis. Furthermore, it can be safely used in children and in pregnant women. Sessions are
repeated two or three times a week for a maximum period of 6–18 months. The best results
are achieved on the face, followed by the trunk and limbs. The poorest outcomes have been
noted for lesions on the hands and feet. The 308-nm excimer laser emits a monochromatic
light of 308 nm and produces faster repigmentation rates than any other medical method so
far reported. It permits the selective treatment of only lesional skin and ensures no unnecessary
treatment of healthy skin. Thus, the patient receives less radiation
I V 11 – VITILIGO-CASE REPORTS
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Maja Kovačević
Croatian Vitiligo Association, Zagreb, Croatia; [email protected];
[email protected]
Vitiligo is an acquired and chronic skin depigmentation disorder which affects 0.5% to 1% population worldwide. Classification of the disease is based on the distribution of lesions. Unilateral
depigmented macules following segmental (dermatomal) or focal (quasidermatomal) pattern
are considered as localized vitiligo. Generalized type of the disease includes acrofacial pattern
involving face and distal extremities, vitiligo vulgaris with widespread, usually symmetrically
distributed lesions and universal vitiligo with complete or nearly complete depigmentation
of the body. Mucosal vitiligo may be classified as localized with involvement on one mucosal
surface, or as generalized type of the disease in cases when typical depigmented macules are
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presented in more than one mucosal area. Mixed vitiligo is described as coexistence of both
segmental and nonsegmental type of disorder. Besides mentioned clinical subtypes, vitiligo
can rarely present in certain clinical variants including multichrome vitiligo, vitiligo minor, blue
vitiligo or inflammatory vitiligo. Two patients with impressive and rare clinical variants of the
disease – first with mixed form of vitiligo following Blaschko’s lines and second with inflammatory vitiligo will be presented.
I V 12 – CAMOUFLAGE FOR VITILIGO PATIENTS
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Joelle Nonni
Avène hydrotherapy centre, Avène, France; [email protected]
As we live in a society very much concerned about physical appearance, looking as good as
possible has become everyone’s objective. Consequently, unsightly skin imperfections can
have a dramatic and highly negative impact on the patient’s personal, social or working life.
The medical corrective make-up thus represents the alternative solution that helps to gain
back one’s self-confidence notably in the case of visible dermatoses. Patients suffering from
vitiligo can use medical corrective make-up on the face and body; both men and women alike.
This specific line of make-up has to be hypoallergenic, non-comedogenic, water-resistant and
with sun protection. It does not clog pores or promote acne or irritation. The technique of the
medical corrective make-up includes at least 3 steps: 1) A make-up base (day cream) adapted
to the skin type or a sun protection,2) A compact foundation which provides a perfect coverage,3) A mosaic translucent powder to fix the make-up. To increase the result and apply less
make-up, it is also possible to apply a self-tanner 2 or 3 times by week. However, to realise a
quick corrective make up with a nice result, some tips are interesting to teach patients. Medical
corrective make-up helps patients to feel once again good about themselves. Also medical
corrective make-up can give to the patients who suffer from vitiligo more confidence and
lessen feelings of self-consciousness, nervousness and anxiety. Once make-up is applied and
skin imperfections concealed, the patient’s self-confidence gradually comes back. Finally, the
patients’ quality of life is significantly improved.
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I V 13 – VITILIGO TREATMENT GUIDELINES - WHERE ARE WE NOW?
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Department of Clinical Medicine, University of Applied Health Sciences and Private
Dermatovenereology Office, Zagreb, Croatia; [email protected]
Although vitiligo is an asymptomatic disease, it can have severe consequences on patients’
quality of life and physical health. Available treatment options are aimed on stopping of the
disease spreading, induction of repigmentation and achieving of sufficient cosmetic results.
Vitiligo is neither contagious nor life threatening disease so it is often widely assumed that
problems which affect the patients just have a cosmetic nature. Due to this matter, vitiligo is
considered as an orphan disease and unfortunately, many physicians (including dermatologists) still consider vitiligo to be an incurable disease and are not familiar with available therapeutic options. Here we present five therapeutic algorithms for vitiligo treatment constituted
from different worldwide working groups and organizations in the last few years. The following therapeutic options include mainly topical corticosteroids, topical calcineurin inhibitors,
topical vitamin D3 analogues, phototherapy (PUVA and NBUVB), oral corticosteroids, antioxidants, laser and surgical therapy. A group of British authors established algorithm for the management of vitiligo in adults and children by non-specialists in 2010. One year after, group
of authors from USA suggests their algorithm for dermatologists. The European Dermatology
Forum Consensus presented algorithms for the management of patients with nonsegmental
or segmental vitiligo in 2013, the same year when Japanese authors provided their proposal
of the algorithm for the management of vitiligo in Japan. Considering available guidelines for
the management of vitiligo, both available and unavailable therapeutic options in Croatia, and
our clinical experience we have established our guidelines for the management of vitiligo in
Croatia in 2014. This proposal and selection of specific therapeutic options in several lines are
based on international up-to-date guidelines in accordance with evidence based medicine.
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I V 14 – VITILIGO CLOUD BANK: BIO-IT SYSTEM FOR PATIENTS,
DOCTORS AND INVESTIGATORS
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
Yan Valle
Vitiligo Research Foundation, New York, USA; [email protected]
Vitiligo is a heavily under investigated skin disease that affects over 70 million people worldwide. Vitiligo treatment development is an unattractive field for pharmaceutical companies
due to lack of understanding of the pathophysiology of this multifactorial disease. Available
generics have average efficacy and safety profiles, lack in ceasing the disease progression and
unsuccessful in meeting the demand.The study of vitiligo requires comparison of large numbers of affected and unaffected individuals, and comparisons within patients’ cohort to reveal
disease subtypes and responsiveness to a particular treatment. We applied a cutting edge approach to bio-informatics, bio-banking, digital healthcare technologies, and in-depth scientific
knowledge to build Vitiligo CloudBank, the first disease-specific electronic health record in vitiligo. It condenses large volumes of research-quality data, enabling investigators to cross-analyze multiple profiles, treatments and lab results. Vitiligo CloudBank allows patients to register
anonymously online, record vitiligo symptoms and monitor disease progression and treatment
outcomes over time. Doctors can securely communicate with their patients, monitor the disease progression and evaluate outcomes in order to get better treatment results. Investigators
are able to analyze aggregated data sets for clues that may lead to a better understanding of
the disease, to identify potential biomarkers and ultimately develop new treatments for vitiligo.
The CloudBank service is free for all academic vitiligo researchers and vitiligo patients.
I V 15 – TOPICAL CREAM DELIVERS NB-UVB FROM SUNLIGHT
FOR THE TREATMENT OF VITILIGO
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
Andy Goren
University of Rome “G.Marconi”, Italy; [email protected]
Ultraviolet-B (UVB) phototherapy for the treatment of vitiligo is an effective first-line choice
experiencing major decline. The cost of multiple doctor visits during the demanding treatment regimen has resulted in low compliance, limiting access to this safe and effective mode
of treatment. Here we present a novel topical cream that selectively filters solar radiation to
deliver narrow-band UVB to vitiligo lesions from solar radiation. Numerous studies have demonstrated that natural sunlight therapy at the dead sea in Israel provides therapeutic efficacy
40
for vitiligo patients on par with artificial broad-band and narrow-band UVB phototherapy; however, similar treatments at locals at or above sea level fail due to the development of erythema
prior to sufficient therapeutic dosage. We conducted a pilot study at sea level to assess the
efficacy of a novel topical cream that selectively filters non-therapeutic wavelengths of UVB
from natural sunlight and delivers treatment for acrofacial vitiligo. Our results demonstrate that
the novel topical cream can provide a convenient alternative to artificial light phototherapy.
I V 16 – IMMUNOMODULATORS IN VITILIGO MANAGEMENT
.. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
Igor Korobko
VR Foundation, New York, USA; [email protected]
Vitiligo is currently considered as a predominantly autoimmune disorder thus interventions
with immunomodulating capacity provide a rational solution to halt vitiligo progression. Indeed, conventional treatments capable to stop progression of vitiligo, narrow-band ultraviolet
B and systemic steroids, both are known to have immunosuppressive activity. While a number
of experimental treatments were tested for their capacity to cope with vitiligo spreading, their
widespread use is limited owing to frequent side effects or inconvenient and lengthy course of
treatment, besides the efficiency of available options is not absolute. Therefore there is a need
for new safe and convenient options to fight vitiligo progression, with immunomodulating
compounds, owing to their frequently good safety profile and autoimmune nature of vitiligo,
being attractive candidates. Here, available options to stop vitiligo progression are overviewed,
with the most recent developments in the field, namely the use of non-steroid immunomodulators, being discussed in details.
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I V 17 – LOW-DOSE ORAL CYTOKINES THERAPY FOR VITILIGO : THE
FUTURE IS HERE
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
Torello Lotti
Institute of Dermatology, University of Rome “G. Marconi”, Rome, Italy; [email protected]
Vitiligo is a skin disorder characterized by a progressive depigmentation which is caused by the
loss of melanocytes at the cutaneous level. The causes of melanocyte loss are still unclear, but
a relevant number of observations lead researchers to ascribe cellular immunity as having an
important role in vitiligo pathogenesis. In vitiligo, the observed imbalance in cytokine expression at cutaneous lesions level both on the border of affected area with healthy skin and in the
center of the spot, is probably due to a shift of the immune system with a prevalence of Th1/
Th17 (high IL-1 and IL-17 levels) response instead of a Tregs/Th2 one (low IL-4 level) and may
be part of etiology of this autoimmune disease. TNF-α also has a pivotal role in oxidative stressmediated cytotoxicity directed against melanocytes and keratinocytes and sustained by T-cells
and B-cells activation.
Apoptosis of keratinocytes is a key event in Vitiligo onset. Keratinocytes produce a number of
growth factors that support the viability of the melanocytes through paracrine action. Among
these factors, the basic fibroblast growth factor (bFGF or FGF2) is a potent regulator of melanocytes proliferation, differentiation and function; there is an inverse correlation between the
levels of TNF-α and bFGF in the presence of vitiligo and low levels of bFGF are responsible of
melanocytes death and, finally, of skin lesion depigmentation. TNF-α is, therefore, a key player
of cell-mediated autoimmune response and inflammation, responsible of the keratinocytes
apoptosis.
It is therefore arguable that the inflammatory phenomenon supported by this cytokine and
the breaking down of the paracrine crosstalk between keratinocytes and melanocytes are central events in inducing and sustaining vitiligo and thus represents one of the key targets within
a therapeutic strategy based on deep knowledge of the etiology of the disease.
In the last years, sustained by a critical mass of scientific evidences, a new pharmacological
concept is raising the interest of the scientific community: the low dose cytokines therapy, part
of Low Dose Medicine (LDM) paradigm.
LDM medical approach (born from the fusion of the most recent knowledge in the fields of
Molecular Biology, PNEI and nano-concentrations research is founded on the use of biological
signaling molecules that control and guide the homeostatic functions in order to restore the
physiological homeostasis) is based on the use of nano-concentrations of cytokines (in the
42
range of pg/ml), administered orally in order to achieve a systemic effect.
The availability of low-dose medicines containing nano-concentrations (in the range of pg/
ml) and Sequentially Kinetic-Activated (SKA) cytokines and growth factors represents a unique
opportunity for the study of an innovative immunological therapeutic approach for vitiligo
treatment.
The therapeutic use of SKA low dose bFGF (Guna S.p.a. – Italy) is aimed at improving the stimulation of the residual population of melanocytes (via up-regulation of trans-membrane receptors) mimicking the paracrine signaling exerted, in physiological conditions, by keratinocytes.
The effect of bFGF is improved if in association with the pool of anti-inflammatory cytokines
that acts reducing the apoptotic phenomena and the cytotoxicity mediated by TNF-α.
The anti-inflammatory SKA low dose molecules pool is composed by Anti-IL-1; IL-4 and IL-10.
Anti-IL-1 is useful in the reduction of IL-1-mediated acute inflammation, present in perilesional
region; IL-4 exerts an effective control against autoimmune triggers, reducing cell-mediated
cytotoxicity; IL-10 is the opposing cytokine of both IL-1 and TNF-α and is effective in chronic
inflammation control.
The use SKA low dose bFGF and specific SKA low dose anti-inflammatory cytokines pool represents a new therapeutic approach for vitiligo strictly based on disease etiology and aimed
both to stop the disease progression, through opposing chronic inflammation, and to induce
skin repigmentation by direct stimulation of melanocytes.
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INOVATIVE THERAPIES (IT) – INVITED SPEAKERS
I IT 1 – MANAGEMENT OF ATOPIC DERMATITIS
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
Nives Pustišek1, Mirna Šitum2, Maja Vurnek Živković3
Children’s Hospital Zagreb, University of Zagreb School of Medicine, Zagreb
2
Department of Dermatology and Venereology, University Hospital Center
“Sestre milosrdnice“, Zagreb, Croatia
3
Center for Croatian Studies, University of Zagreb, Zagreb, Croatia; [email protected]
1
Atopic dermatitis (AD) is one of the most common skin diseases which affects up to 20% of
children and 1-3% of adults in most countries of the world and is often the first step in the
development of “atopic march”. It follows a relapsing course. Although the pathogenesis of AD
is not completely understood, it is thought to result from a complex interplay between disruption of deficient skin barrier function, immune dysfunction, abnormal microbial skin colonization, environmental factors and strong psychosomatic influence. Management of AD remains
a clinical challenge where the primary goals are to improve the barrier function, to suppress inflammation and to control microbial colonization. The management should always be adapted
to the severity of the AD. Management of AD includes: basic treatment of disturbed skin barrier
function and emollient therapy (“skin care”), avoidance strategies (non-specific and specific
provocation factors), dietary intervention, topical anti-inflammatory therapy (topical glucocorticosteroids, topical calcineurin inhibitors), antimicrobial therapy, phototherapy, systemic
immunosuppressive therapy and others. The key to managing AD is education of the patient,
parents and family. It is important to give clear explanations about the disease, the disturbed
barrier function and how and why treatments are used. We will present you our knowledge
and experience in the management of AD, with an emphasis on the findings reported in the
literature over the past few years.
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I IT 2 – PATHOGENESIS AND MANAGEMENT OF ITCH IN ADULT ATOPIC
DERMATITIS PATIENTS
.. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
Department of Dermatology, Venreology and Allergology, Wroclaw Medical University,
Wroclaw, Poland; [email protected]
Itch is an important clinical problem in patients suffering from atopic dermatitis. Its pathogenesis is multifactorial with dermal, neurophathic and neurogenic components. In our recent
study we documented that at the time of examination itch was present in more than 80% of
patients. Moreover, in another recent study we showed that itch in atopic dermatitis patients
plays a crucial role in influencing patients’ psychosocial well-being. Pruritic subjects seem to be
more depressed, and the intensity of itch is related to the stress experienced by patients prior
to disease exacerbation. As the pathogenesis of itch atopic dermatitis is not completely clear,
there is no one treatment of choice available. Based on our experience the most frequently
used management regimes are topical emollients and oral antihistamines, but the long-term
effects of these agents seem to be very limited. Pruritic subjects should be informed to limit
factors exacerbating itch and suggested to avoid overheating of organism, intake of alcohol
and hot spices, irritating detergents. They should wear loose cloths of natural material, like
cotton is and they should keep their nails short cut to prevent the additional destruction of
the skin surface. Concerning the oral antihistamines, the new generation ones are of limited
effectiveness. According to the European Guidelines for Atopic Dermatitis the sedative antihistamines are useful in reducing the intensity of itch. Topical corticosteroids, and especially
calcineurin inhibitors, are effective local agents. One may also consider creams with structured
lipids with endocannobinoids or capsaicin (only very localized itch). Cyclosporin A used in the
therapy of atopic dermatitis markedly reduce itch in the vast majority of patients. In very severe
chronic cases antidepressants, such as paroxetin, were reported to be beneficial. In the holistic
approach psychotherapy should be considered, especially habit-reversal with awareness training.
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I IT 3 – THERAPEUTIC APPROACH FOR INTOLERANT SKIN - WHAT TO DO?
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
Branka Marinović
Department of Dermatology and Venereology, University Hospital Center Zagreb,
Number of patients with intolerant skin is increasing in our everyday practice. Such skin is also
described as sensitive, reactive or irritable skin. Intolerant skin is usually defined as a non-immunologic manifestation of cutaneous hyperreactivity linked to a variety of normally well-tolerated stimuli. It is also described as an inflammatory reaction without a recognition of a specific
alergen. Most commonly this disease is described as a facial condition but there are description
of patients with manifestations of different localization. There is a number of exogenous factors that can contribute to this condition. Confirming diagnosis is sometimes very difficult and
time consuming. There are no guidelines on the therapy of this condition. Therapy should be
always started with discontinuation of all cosmetic products, and when introduced again they
should be introduced one by one with some time interval in between. All potential triggers
and aggravating factors should be eliminated potentialy by changing lifestyle of the patient.
I IT 4 – MODERN THERAPEUTIC APPROACH TO ALOPECIAS
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
Department of Clinical Medicine, University of Applied Health Sciences
and Private Dermatovenereology Office, Zagreb, Croatia; [email protected]
Majority of population has experienced in certain time of their life some type of hair loss. It is
often cause of a great concern to the patient for cosmetic and psychological reasons. Here we
present available therapeutic options for alopecia androgenetica (AGA) and alopecia areata
(AA), the most common types of noncicatricial alopecias and also for folliculitis decalvans (FD),
one of the most challenging causes of cicatricial alopecia. AGA is an androgen-dependent hair
loss which affects roughly 50% of men and perhaps as many women older than 40 years. Topical minoxidil in concentration of 2% and 5% and finasteride are FDA-approved current therapies for androgenetic alopecia in men, whereas 2% minoxidil solution, oral contraceptives and
spironolacton are proposed for female patients. Other possible therapeutic options, still mostly
under clinical trial phases, include 5-α-reductase inhibitors, androgen receptor antagonists,
ATP-sensitive potassium channel openers, growth factors, antioxydants and botanical extracts.
AA is autoimmune non-scarring hair loss which affects 0,1-0,2% general population. Because
46
of its autoimmune etiopathogenesis, corticosteroids applied topically or intralesionally still remain the cornerstone of initial treatment. Other potential therapies include topical sensitizing
agents, photochemotherapy, pulse corticosteroid therapy, antibiotics and biologics. FD presents as an expanding patches of alopecia with peripheral pustules on the scalp resulting with
scar formation. Although exact etiopathogenesis is still unknown, in most cases Staphylococcus aureus can be isolated from the pustules. Treatment of this condition consists of systemic
antibiotics, topical or intralesional corticosteroids, retinoids or, newly suggested, biologics.
Nondrug alopecias therapies such as hair transplantation, low-level laser therapy (LLLT), follicular neogenesis or inductive cell therapy could be beneficial for different forms of hair loss.
I IT 5 – HOW DO I TREAT HPV?
.. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
Mihael Skerlev, Suzana Ljubojević Hadžavdić
Human papillomavirus (HPV)-associated genital pathology represents one of the major problems among STIs mostly due to the high recurrence rate, difficult eradication and oncogenic
potential. Besides, the young, sexually active population in the generative period is mostly affected. Despite some recent hopeful therapeutic developments such as immiquimod, topical
green tea derivatives (sinecatechins, polyphenon E) and nitrinzic complex, the therapy of anogenital warts (AGW) remains a medical problem. Both physician- (including cryotherapy, topical cytotoxic therapy, curettage, surgical approach and laser) and self-administered therapeutic
approaches are not fully satisfactory. So, treatment of AGW is often frustrating for physicians
and patients alike. Ultimately, within the spectrum of therapeutic options for condylomata,
no method is really superior to others; recurrences might occur in 30-70% of cases. In general,
treatment should be guided by the available resources, the experience of the provider and the
preference of the patient. Most recently, a prophylactic vaccine that targets the most relevant
HPV DNA types should substantially reduce the burden of the large spectrum of the HPVassociated clinical diseases for both men and women. Besides, a proper dermatological training is required as the clinical criterion is still very important and the HPV-induced lesions get
quite often misdiagnosed unless managed by the skilled professionals. We definitely need the
HPV vaccination programme to get rid of one of the oldest and up to now unsolved problems
of mankind. It can be thus concluded that the HPV-genital infections represent a significant
dermato-venereological issue, and the dermatovenereologists should definitely be the part of
the HPV management programme team.
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I IT 6 – NOVEL TOPICAL CREAM DELIVERS SAFE AND EFFECTIVE ALTERNATIVE TO TRADITIONAL PSORIASIS PHOTOTHERAPY
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
Andy Goren
University of Rome “G. Marconi, Italy; [email protected]
In today’s environment of shrinking reimbursement and coverage for many health care procedures, phototherapy for psoriasis has experienced a major decline. Once hailed as the cornerstone of psoriasis therapy, the increasing cost and demanding treatment regimen has resulted
in low compliance, limiting access to this safe and effective mode of treatment. We have previously reported on the development and in-vitro evaluation of a topical cream that selectively
filters solar radiation to deliver narrow-band UVB. Here, we present the results of a pilot study in
psoriasis patients. After an average of 38 sessions, all patients in the treatment arm responded
to therapy. In particular, 43% of the treatment group experienced complete clearance and the
remainder experienced at a minimum 50% lesion clearance. In contrast, none of the patients in
the placebo arm experienced more than 20% lesion clearance. Our preliminary results demonstrate that the novel topical cream could provide a safe, effective, and convenient alternative
to artificial light phototherapy.
I IT 7 – ACNE IN CHILDHOOD - WHAT TO DO?
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
Zrinka Bukvić Mokos
Department of Dermatology and Venereology, University Hospital Center Zagreb, University
of Zagreb School of Medicine University of Zagreb, Zagreb, Croatia; [email protected]
Acne is a chronic inflammatory disease that primarily affects adolescents. However, children by
the age of 12 years can also be affected by acne that is referred to as pediatric acne. On the basis
of the time of onset and clinical presentation, pediatric acne may be categorized into four clinical entities: neonatal, infantile, mid-childhood, and preadolescent acne. Neonatal acne (from
birth to 6 weeks of age) may be a term used for heterogeneous papulopustular conditions such
as neonatal cephalic pustulosis or transient neonatal pustular melanosis, as well as true acne. As
neonatal acne is typically self-limited, treatment is usually not necessary. Infantile acne (from 6
weeks to 1 year of age) is more common in boys and usually presents with comedones as well
as inflammatory lesions such as papules, pustules or occasionally nodules. Treatment modalities
include topical benzoyl peroxide, retinoids, antibiotics or combination of these; whereas more
severe cases may require employment of oral antibiotics or isotretinoin. Mid-childhood acne
48
(from 1 year to 7 years of age) is very rare and should warrant an endocrinologic workup for
causes of an underlying endocrine disorder. Preadolescent acne (from 7 years to 12 years of age
or menarche in girls) usually presents as comedonal acne located primarily on the forehead and
central face. Treatment of mid-childhood and preadolescent acne is very similar to that used
for adolescent acne with the emphasis on the limitation of use of the tetracycline family of oral
antibiotics. Furthermore, the approach to pediatric acne should be to use the mildest agents
possible with still providing therapeutic efficacy. A basic discussion of reasonable therapeutic
expectations and possible side effects is often helpful in maximizing patient compliance.
I IT 8 – TREATMENT OF ACNE – WHAT’S NEW?
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
Claudia Menicanti, Stefano Veraldi
Dermatology Unit, University of Milan, Milano, Italy; [email protected]
Current therapies of acne involve one or several pathogenic factors. Topical antimicrobial
agents and topical and oral antibiotics are used to reduce P. acnes colonization. Topical and
oral retinoids manly reduce hyper-proliferation of ductal corneocytes. Finally, estrogens and
anti-androgens can be used to reduce the effects of androgens on the sebaceous gland. The
choice of the right treatment depends on the type and the severity of the disorder but often
local treatments lead to local adverse events such irritant contact dermatitis (ICD) and they
must be employed for long periods. For all these reasons and because of the emergence of
antibiotic resistance, new nonantibiotic treatments are rising. In order to limit the side effect,
without loosing the efficacy, new retinol esters, such as hydroxypinacolone retinoate have
been synthesized. This is a new syntetic ester of 9-cis retinoid acid that, combined with papain and RNMF in gel, seems to be very effective with good tolerability and a improvement of
compliance. The use of tretinoin as short contact therapy (SCT) seems to be superimposable
to that of tretinoin used according to standard modality with a reduction of the incidence and
the severity of ICD. Other topical agents such as nicotinamide combined with potassium azeloyl diglycinate and salicylic acid and the glycolic acid combined with retinaldehyde used in
monotherapy have shown a significant clinical improvement and high adherence of patients.
As an alternative to topical conventional treatment the chemo-exfoliation with salicylic acid
(25-30%) peels has many clinical advantages being effective, economical and easy to perform
and it also improves the penetration of other active topical agents. Dapsone 5% gel is a new
option in topical therapy with more prominent effects in patients treated with oral isotretinoin.
As far as systemic treatment of acne is concerned, low dose (0,2-0,3 mg/kg/die) oral isotretinoin
may be considered as a new well tolerated therapy.
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I IT 9 – TREATMENT OF INFECTIVE DERMATOSES - WHAT’S NEW?
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
Neira Puizina-Ivić
Department of Dermatology and Venereology, University Hospital Center Split, University of
Split School of Medicine, Split, Croatia; [email protected]
In the last few decades, following development of immunology and transplantation medicine
techniques, phisician’s attention was occupiaed by increasing number of immuncompromised
patients with skin infections that are related to the underlying disease and/or its treatment.
Although susceptibility to infection is increased, due to weakened patient’s immune response
there are difficulties in early diagnosis. In fact, infections are a principal cause of morbidity and
mortality of immunocompromised patients. Therefore, a comprenhensive understanding of
the possible cause of infections and predisposing factors involved, as well as comprehensive
anti-infective strategy is imperative in patients care. Special emphasis is on folliculitis caused
by community acquired methicillin-resistant Staphylococcus aureus (CA-MRSA). Previously associated with healthcare exposure, this superbug now also accounts for a growing amount of
infections acquired among athletes, students, and the military without necessary healthcare
exposure. Fortunately, its spread can be limited with good hygiene practices. A brief overview
of current therapy of bacterial, fungal and viral infections is presented.
I IT 10 – THERAPEUTIC APPROACH TO AUTOIMMUNE BULLOUS DISEASES – STATE OF THE ART
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
Branka Marinović
Autoimmune bullous diseases are a group of intra- and subepidermal disorders with different
course and prognosis. Most of them are serious diseases which have to be treated for longer
period and controlled by experienced dermatologist. Pemphigus group of diseases is characterized by acantholysis in the epithelium of mucous membranes or / and the skin. These
diseases can have significant morbidity and morality as a result of complications of the disease
or side-effects of the therapy. Mainstay of the therapy of pemphigus are corticosteroids. Usually
together with corticosteroids, steroid-sparing agents i.e. azathioprine or mycophenate mofetil
are introduced to reduce side-effects of corticosteroids and to make remision periods longer.
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Patients who do not respond to these therapies should be treated with intravenous immunoglobulins, cyclophosphamide or rituximab.
Subepidermal blistering diseases include different diseases, most common of which is bullous
pemphigoid. This is diseases characterized by autoantibody deposition at the basement membrane zone which results with subepidermal blister. Disease most commonly affects elderly
people who have also more comorbidities which can influence decision on therapy of choice.
Bullous pemphigoid is treated with corticosteroids - systemic or topical. Refractory cases can
be additionally treated with immunomodulatory therapies to minimize side-effets of longterm
corticosteroid therapy.
As therapy in patients with autoimmune blistering diseases can last for very long time, they
should be monitored for side effects which can be very serious and also life threatening.
I IT 11 – NEW THERAPEUTIC OPTIONS FOR PSORIASIS PATIENTS
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
Diamant Thaci
Abstract not received
I IT 12 – DYSPLASTIC NAEVI AND MELANOMA
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Mirna Šitum, Željana Bolanča
Naevus dysplasticus (Clark’s nevus) is melanocytic nevus that is due to its specific histological
structure and clinical characteristics, also called atypical nevus. It mainly appears after puberty
or in adulthood in almost 5% of Caucasian. There are two basic forms; hereditary with multiple
nevi (Dysplastic naevi Syndrome, BK mole syndrome), and non hereditary form that can appear
as a single dysplastic nevi or multiple nevi. Dysplastic nevus syndrome occurs in people with
a positive family history of melanoma and in 50% of patients with sporadic melanoma. Clinically, dysplastic nevi are unevenly brownish, blackish or yellowish pigmented nevi with bizarre
shapes, asymmetric, with polycyclic edges, usually slightly elevated, and greater than 6 mm in
diameter. Histological characteristics are variable atypia of melanocytes, increased number of
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melanocytes, subepidermal fibroplasia, and a distorted rete ridge pattern with bridging between adjacent rete rides, lamellar fibroplasia and concentric lamellar fibrosis, and sometimes
proliferation of blood vessels in the presence of lymphocytic infiltrate in the dermis. Diagnosis
is based on the history, clinical and dermatoscope images and patohistological analysis upon
surgical excision of the lesion. Differential diagnosis includes malignant melanoma and pigmented basalioma and other types of nevi. The people with dysplastic nevus syndrome or with
sporadic dysplastic nevi should be followed up regularly, approximately every 3-6 month, according to the severity of clinical appearance. The follow-up should include examination of the
skin, dermatoscope examination and photographic documentation. It is important to educate
patient about importance of self-examination and protection from UV radiation. Melanoma is
a malignant tumor arising from melanocytes and due to high risk of lymphatic and hematogenous metastases; it is among the most aggressive malignant tumors of the skin and mucous
membranes. The worldwide incidence of melanoma is still increasing and it is a great medical
and public health problem. In some countries (Western European) there is prolonged survival
of the melanoma patients, which can be explained with early detection of melanoma, due
to better knowledge, education of the doctors and the patients, and better diagnostic tools.
Melanoma is the most common malignancy in Caucasian women, aged 25-29 years, and has
the highest mortality among older man. The early detection and the surgical removal increases
overall survival up to 95%, while the cure rate in advanced stages is modest. The risk factors for
the development of melanoma include positive family and / or personal history of melanoma
and non-melanoma skin cancer, dysplastic nevus, skin type (Fitzpatrick classification) and UV
radiation. Melanoma is typically red -brown to blue-back asymmetric tumor that shows visible
changes over time (months or years). The rapid onset of the lesion, or changes in the existing
nevus that follows ABCDE rule and Ugly Duck rule should be observed by the dermatologist.
The clinical features of melanoma can vary on the anatomical localization of the lesion and
the type of growth. The four main subtypes of melanoma are superficial spreading melanoma,
nodular melanoma, lentigo malignant melanoma and acral lentiginous melanoma, but there
are also rarer forms of melanoma such as mucosal melanoma, amelanotic, desmoplastic, verrucous melanoma, metastatic melanoma of unknown primary site. Melanoma can develop
lymphatic or hematogenous metastases. The earliest metastases are often found in regional
lymph nodes, and the usual site of hematogenous metastases are liver, lungs, bones and brain.
The prognosis of melanoma is almost directly related to the degree to which the tumor has
invaded the skin. The major independent risk factor is tutor thickness (Breslow depth). There
is almost a linear correlation between the measured tumor thickness and 10-year survival. The
ulceration of the tumor and an elevated LDH levels significantly worsen the prognosis. In 2001,
a new TNM -staging system was introduced by the American Joint Committee on Cancer that
includes risk factors and links them to survival. The definitive diagnosis of melanoma is based
on patohistological analysis of the excised tissue. It is recommended, whenever possible, to
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completely excise of the tumor, except in cases where it is difficult due to technical or cosmetic
reasons (eg. large lentigo maligna on the face and extremities or changes in the mucous membranes). Studies have shown that the incisional biopsy of the suspicious lesion has no effect on
the prognosis of patients with melanoma.The key to melanoma therapy is the excision of the
primary tumor. The re-excision with an appropriate margin of safety is recommended at the
earliest possible time and sentinel lymph node biopsy (SLNB) for thickness of the tumor greater
than 1 mm. According to studies, the SLNB has no impact on overall survival, but it is important
in staging of the disease and has prognostic significance. If a patient has clinically involved
lymph nodes (palpation, sonography, biopsy) then a complete regional lymph node dissection
is indicated. Treatment of patients with advanced disease is in the field of the oncologist. The
most important contribution the dermatologist can make is the follow up in order to monitor
for development of a second primary melanoma and the skin cancers. The outlook for a second primary is far better than for a metastatic tumor. The frequency of follow up depend on
tumor thickness and stage of the disease. It is important to check the operation site, in-transit
area, regional lymph nodes to identify local recurrences. Palpation alone is not sufficient, so the
ultrasonography of the lymph nodes and scars is routinely employed. The yields from routine
chest X-rays and blood work are very low. Instead, the promising method is monitoring of
serum levels of S 100 B, LDH and tyrosinase levels. In the advanced stages of disease, PET-CT
should be performed. Identifying and treating solitary metastases may both prolonged survival
and improve patients quality of life. Because of the propensity of melanoma to metastazise
many years later and because of 5-10 % chance of second tutors, follow-up for the melanoma
patients should be life-long.
I IT 13 – ACTINIC KERATOSES AND EPIDERMAL MALIGNANT SKIN TUMORS: MODERN APPROACH TO THERAPY
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Željko Mijušković
Clinic of Dermatology and Venereology, Faculty of Medicine, Military Medical Academy,
Belgrade, Serbia; [email protected]
Actinic keratoses (AK) are keratotic, precancerous cutaneous lesions occurring on chronically
light-exposed adult skin. AK are the result of chronic exposure to ultraviolet (UV) radiation and
have a low risk of progression to invasive squamous cell carcinoma (SCC). There are many options in the treatment patients with AK: cryosurgery, 5-fluorouracil cream, diclofenak gel, imiquimod cream, photodynamic therapy. Ingenol mebutate is a new option in the topical field
treatment for AK. It has a dual mechanism of action, rapid induction of necrosis that specifically
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targets dysplastic cells and neutrophil-mediated immunostimulatory effects.Basal cell carcinoma (BCC) is the most common cancer in Caucasians. The most important etiological factor
is exposure to ultraviolet radiation and sun exposures in childhood are especially critical in the
development of BCC. The treatment of BCC can be divided into surgical and nonsurgical options. Several factors may influence the decision of treatment options: patient age, histological
subtype, tumor localization and size, etc. Surgical options include: excision with predetermined
margins, Mohs micrographic surgery, curettage, electrodesiccation, CO2 laser surgery, and
cryosurgery. Surgical excision with histologic control is the standard and highly effective treatment for primary BCC. Nonsurgical options include: radiotherapy, topical 5-fluorouracil, topical
imiquimod, photodynamic therapy. Imiquimod may be an alternative to surgery for patients
with small (< 2 cm), low risk, superficial, primary BCC. 5-fluorouracil is not recommended for
the treatment of facial BCC and should only be used for small, superficial and low risk BCC. New
and promising treatment option for patients with advanced and metastatic BCC is vismodegib,
inhibitor of smoothened homologue (SMO). The NCCN guidelines have incorporated vismodegib as a treatment option for both primary and recurrent BCC.
I IT 14 – TREATMENT OPTIONS FOR VARICOSE VEINS SYNDROME
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Sanja Schuller-Petrovic
VENEX Vein Center, Vienna, Austria; [email protected]
Varicose veins are a very common venous disorder. Early diagnosis and therapy are important
for the prevention of serious complications like ulcus cruris venosum. The classical open surgery with strippng of the saphenous vein and ligation of the junction area is not anymore the
gold standard. In the last 15 years new, minimal invasive methods were established and several
studies have shown that endovenous thermal ablation (ETA) with segmental radiofrequency
catheter or laser is a highly effective and save procedure. The NICE guidlines 2013 regarding
the treatment of varicose veins recommand the ETA as the first choice for the treatment of
saphenous veins insufficiency. The treatment with ultrasound guided foam sclerotherapy is
the second choice and open surgery is only recommanded if there is no possibility to perform
ETA or foam sclerotherapy. A very new alternative is the chemical ablation with a medical cyanoacrylate glue. This method is performed without local anesthesia and without postoperative compression. First results are very promissing. The new interventional treatment options
are very save, minimal invasive, with minimal post treatment discomfort and as effective as
open surgery. Long term results with ETA have shown that there are less neovascularizations
and recurrent varicose veins than after classic open surgery.
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I IT 15 – TREATMENT APPROACH FOR ULCUS CRURIS
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Sanja Špoljar
Many factors contribute to pathogenesis of leg ulcer. The main causes are chronic venous
insufficiency, peripherial arterial occlusive disease (PAOD) and diabetes. The most common
cause of PAOD is arterosclerosis. In diabetic patients, distal symmetric neuropathy and peripherial vascular disease are probably the most impotant etiological factors in the development of
leg ulcer. Venous insufficiency is the most common etiology. The exact pathogenetic cascade
leading to ulceration is still not fully elucidated. Many patients have ulcers of combined aetiology. Other rare causes of chronic leg ulecrs are: hematologic diseases, autimmune diseases,
genetic defects, infective diseases, primary skin disease, cutaneus malignant diseases, use of
some medication and therapeutic procedures and numerous exogenous factors. Knowledge
of differencial diagnosis is essential for ensuring treatment success in patient with leg ulcer.
Ulcer have slow healing tendency caused by an underlying pathogenetic factor that needs to
be removed to induce healing. Compresion therapy has been considered the gold standard in
tretment of venous ulcer.The main priciples of tretment for arterial ulcer is surgical intervetion if
aterosclerotic occlusion affects large-size artery. The manegment of diabetic foot ulcer requires
relief of any pressure at the wound sit, surgical debridment, control of glucose level and arterial reconstruction if necessary. Despite numerous advances, chronic wounds continue to be a
tretmen challange. The beneficial effect of a moist wound enviroment and hypoxia reduction
has been well established. Negativ pressure wound therapy (NPWT) remove edema, leading
to increased localised blood flow and accelertion of granulation tissure formation. Autologus
platelet-rich plasma (PRP) seams effective for treting chronic and difficult wounds.
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I IT 16 – PATHOGENESIS AND MANAGEMENT OF CHRONIC URTICARIA
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Piotr Kuna
Medical University of Lodz, Poland
Chronic spontaneous urticaria (CSU) is defined as itchy weals, angio-oedema, or both, arising
spontaneously without external physical stimuli. Symptoms of the disease continue to develop
for more than 6 weeks. It carries a high socioeconomic burden with considerable health care
costs. Second generation H1-antihistamines are the mainstay of urticaria treatment and are
the only licensed option. However, many patients are resistant to H1-antihistamine therapy.
Omalizumab has proven to be an effective therapeutic option in patients with recalcitrant
chronic urticaria. This presentation will highlight the major therapeutic options available today
for the management of CSU knowing that good quality evidence for efficacy of many agents
is scarce except for H1-antihistamines and omalizumab. LDM medical approach (born from the
fusion of the most recent knowledge in the fields of Molecular Biology, PNEI and nano-concentrations research is founded on the use of biological signaling molecules that control and
guide the homeostatic functions in order to restore the physiological homeostasis) is based
on the use of nano-concentrations of cytokines (in the range of pg/ml), administered orally
in order to achieve a systemic effect. The availability of low-dose medicines containing nanoconcentrations (in the range of pg/ml) and Sequentially Kinetic-Activated (SKA) cytokines and
growth factors represents a unique opportunity for the study of an innovative immunological
therapeutic approach for vitiligo treatment. The therapeutic use of SKA low dose bFGF (Guna
S.p.a. – Italy) is aimed at improving the stimulation of the residual population of melanocytes
(via up-regulation of trans-membrane receptors) mimicking the paracrine signaling exerted, in
physiological conditions, by keratinocytes. The effect of bFGF is improved if in association with
the pool of anti-inflammatory cytokines that acts reducing the apoptotic phenomena and the
cytotoxicity mediated by TNF-α. The anti-inflammatory SKA low dose molecules pool is composed by Anti-IL-1; IL-4 and IL-10. Anti-IL-1 is useful in the reduction of IL-1-mediated acute inflammation, present in perilesional region; IL-4 exerts an effective control against autoimmune
triggers, reducing cell-mediated cytotoxicity; IL-10 is the opposing cytokine of both IL-1 and
TNF-α and is effective in chronic inflammation control. The use SKA low dose bFGF and specific SKA low dose anti-inflammatory cytokines pool represents a new therapeutic approach
for vitiligo strictly based on disease etiology and aimed both to stop the disease progression,
through opposing chronic inflammation, and to induce skin repigmentation by direct stimulation of melanocytes.
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FREE COMMUNICATIONS (FC)
I FC 1 – PSYCHOSOCIAL FACTORS IN PATIENT WITH MULTIPLE AUTOIMMUNE DISEASES
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Edita Simonić, Liliana Stojnić Soša, Marijana Vičić, Gordan Lakoš, Darinka Periša,
Valentina St. Georges
University Hospital Center Rijeka, Department of Dermatology and Venereology and University
of Rijeka School of Medicine, Rijeka, Croatia; [email protected]
We are presenting a female patient with multiple chronic, mostly autoimmune diseases, vitiligo, psoriasis and morphea. She has also diabetes and arterial hypertension. Our patient was
exposed to many traumatic experiences during childhood and adolescence. We explored
negative life experiences that had happened before the appearance of psoriasis and vitiligo.
Recent studies suggest that multiple traumatic life events during childhood and adolescence
in combination with genetic background could increase the vulnerability for developing some
autoimmune diseases. Therefore, for the treatment of these patients, interdisciplinary approach
is needed. That includes the participation of the dermatologist and a psychiatrist-psychotherapist.
I FC 2 – COLLAGEN INDUCTION THERAPY - DERMAROLLER
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Željana Bolanča
Zagreb; [email protected]
The Collagen Induction Therapy with Dermaroller is one the most successful minimal invasive
treatment concepts providing an improvement of the skin texture, particularly to every type of
scars.It is the treatment which aims to restore youth and smoothness to the skin by stimulating
the natural production collagen. The micro needles create small channels into the deep layers
of the skin which break up the old collagen strands, and stimulate the creation of new ones.
Collagen is an important material responsible for keeping your skin tight firm and young. Al-
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though Micro-Needling may look a little aggressive with its needles, it is actually much gentler.
This is because Micro-Needling does not harm the epidermis. As the small handheld roller with
its micro needles is gently rolled over the area being treated, it creates pin point punctures. The
pores of the top layer of the skin are parted without being damaged, leaving the epidermis, intact. The procedure usually requires the application of anesthetic cream which is effective after
30 min. The treatment usually last for about 20-30 minutes, as considering the fact that the skin
is “open” for about 10 minutes after the treatment, there are different substances that could be
applied in order to penetrate deeper in the skin. The most effective substances are hyaluronic
acid, vitamin C, ferrulic acid which helps in collagen production and the rejuvenation of the
skin. Some reddening is typical after treatment but the downtime is very quick 2-3 days the
most. The side effect of the treatment are minimal, and it is widely accepted by the patients.
I FC3 – TREATMENT OF PLANE WARTS WITH SYSTEMIC ISOTRETINOIN
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Jovan Miljković
University of Maribor School of Medicine, Maribor, Slovenia; [email protected]
Warts are benign epithelial proliferations of the skin and mucosa caused by infection with human papilloma viruses (HPV). Most people will experience infection with HPV at some time
in their life. Plane warts are mainly caused by HPV-3 and HPV-10. Diagnosis is usually based
on clinical examination. There is no single absolutely effective treatment and different types
of treatment may be combined. One must take into account the possibility of spontaneous
regression and so the therapeutic approach should not be too aggressive. Warts in adults,
in those with long duration of infection and in immunosuppressed patients are less likely to
resolve spontaneously and are more recalcitrant to treatment. Retinoids disrupt epidermal
growth and differentiation thereby reducing the bulk of the wart. There are number of case reports and a limited number of trials showing the effect of systemic retinoids in the treatment of
warts. We present two patients with plane warts on the face, in whom after 4 weeks of systemic
isotretinoin treatment we observed total clearance of warts.
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I FC 4 – JUVENILE ONSET HYPOPIGMENTED MYCOSIS FUNGOIDES:
A CASE SERIES OF 3 PATIENTS
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Sandra Jerković Gulin1, Romana Čeovic2, Karmela Husar2, Mihael Skerlev2,
Slobodna Murat-Sušić2, Mirna Bradamante2, Jaka Radoš2, Ivana Ilić3,
Andrija Stanimirović4
1
Department of Infectious Diseases, Dermatology and Venereology,
General Hospital Šibenik, Šibenik
2
Department of Dermatology and Venereology, University Hospital Center Zagreb
and University of Zagreb School of Medicine Zagreb, Zagreb
3
Department of Pathology and Cytology, University Hospital Center Zagreb
and School of Medicine Zagreb, 10000 Zagreb, Croatia
4
University of Applied Health Sciences, Zagreb, Croatia; [email protected]
Mycosis fungoides (MF) is the most common type of cutaneous T-cell lymphoma (CTCL). Primary cutaneous lymphomas (PCLs) are exceedingly rare in children and adolescents, with mycosis fungoides (MF) being the most frequent PCL diagnosed in childhood. The incidence of
MF is 6.4 per 1,000,000 per year in adults, but the occurrence in children and young adults is
rare and has not been well established yet. Hypopigmented mycosis fungoides (HMF) is an
atypical and rare subtype of MF characterized by solely hypopigmented patches or in combination with erythematous patches or plaques. There are no criteria that define a typical case
of HMF. We present three cases of juvenile-onset HMF at Department of Dermatology and
Venereology, University Hospital Center Zagreb between November 2014 and January 2015.
Patients were between 9 and 12 years old at the time of diagnosis. The diagnosis was reached
based on clinical, histopathological and immunohistochemical correlation. All patients were
investigated at the time of diagnosis with complete blood count, peripheral smear, ultrasonography of abdomen and pelvis, and chest X-ray. They were all without extracutaneous progression of disease. Narrowband UVB (311nm) phototherapy and/or potent topical steroids were
used as a first-line treatment. HMF is rare in Caucasians and with only few cases described in
children. Juvenile-onset MF is often misdiagnosed at early stages as benign condition. HMF
may simulate atopic dermatitis, pityriasis alba, pityriasis lichenoides, tinea versicolor, vitiligo,
postinflammatory hyperpigmentation or leprosy (Hansen’ disease). Although HMF has good
prognosis, it is a malignant skin lymphoma and should always be treated as such. Treatment
modalities for juvenile MF are based on general strategies for adults according to disease stage.
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I FC 5 – PSORIASIS PATIENTS: PSYCHOLOGICAL CHARACTERISTIC
AND QUALITY OF LIFE IMPACT
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Gordana Krnjević-Pezić1, Goran Maričić1, Andrija Stanimirović2,
Tija Žarković Palijan3, Dražen Kovačić3
1
Naftalan Special Hospital for Medical Rehabilitation, Ivanić Grad
2
Department of Clinical Medicine, University of Applied Health Sciences, Zagreb
3
Dr Ivan Barbot Neuropsychiatric Hospital, Popovača, Croatia; [email protected]
The purpose of this study is to determine the influence of psoriasis on quality of life and psychological characteristics of patients. Sixty-one patient (25 male and 36 female) with diagnosis
of plaque psoriasis participated in this study. During their stay at Naftalan, Special Hospital for
Medical Rehabilitation they were referred to a psychological consult. Assessment was done
through questionnaires concerning quality of life, patient’s personality, perceived social support and traumatic events. According to the results of our study, psoriasis has a substantial
impact on patient’s life. Severe traumatic event in past 6 months experienced 54.09% of patients. Personality tests revealed increased neuroticism, mainly in female patients. Also, female
patients reported about presence of indeterminate fear, shudder and tension, as well as elevated somatic anxiety and hysteria. Despite above mentioned data, patients evaluated their
quality of life higher than perceived social support – 3.75 vs. 3.61. It is well known that quality of
life is specific psychological phenomenon. Although more than 50% of our patients reported
severe traumatic event in the last six months, it did not obviously influence to much on their
quality of life. Regardless to high perceptive quality of life, psoriasis patients have increased
psychoneurotic symptoms which are particularly expressed in female patients. Therefore, apart
from medical treatment of skin lesions, psoriasis patients should have adequate psychological
treatment and support from its environment.
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I FC 6 – THERAPEUTIC USE OF MONOCLONAL ANTIBODIES
IN PSORIASIS - IMMUNOLOGICAL PRINCIPLES AND IMMUNE
- BASED ADVERSE EFFECTS
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Vesna Lukinović-Škudar1, Maja Kovačević2, Andrija Stanimirović3
Department of Physiology and Immunology, School of Medicine, University of Zagreb, Zagreb
2
Croatian Vitiligo Association, Zagreb
3
Department of Clinical Medicine, University of Applied Health Sciences, Zagreb, Croatia;
[email protected]
1
The introduction of monoclonal antibodies has provided a promising option for both shortand long-term treatment of different dermatologic diseases, and their use is continously increasing. However, because of the growing diversity and complexity of their individual action,
there is also an inevitable increasing list of immune-based and non-immune adverse effects.
The physician should be very familiar with the principles of effects of biological agents, to avoid
unnecessary risks. The basic information about immunological principles of therapeutic effects
of monoclonal antibodies will be given, with particular accent on some main groups of new
and approved biological agents in psoriasis. Immune-based adverse effects will be mentioned.
General and specific considerations about use of biologic therapy in psoriasis will be discussed,
which could help dermatologists in planning and prescribing biologic therapy. This communication reviews some basic immunological principles and immune-based adverse effects of
biological therapy in psoriasis, including considerations for their use.
I FC 7 – DERMATITIS HERPETIFORMIS, GLUTEN- SENSITIVE ENTEROPATHY AND SACROILITIS - CASE REPORT
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Dubravka Šimić, Kristina Jurišić, Anita Ostojić, Jasna Zeljko Penavić,
Suzana Jelčić Arapović, Ana-Marija Sulić
Department for Dermatology and Venereology University Hospital Mostar, Mostar, Bosnia and
Herzegovina; [email protected]
Dermatitis herpetiformis is a rare pruritic vesicular disease often related to celiac disease. It is
caused by IgA autoantibodies directed against epidermal transglutaminase. Both diseases are
the result of an abnormal immune response to gluten antigenes. There is strong HLA association, as 90% of patients are HLA-DQ2(A1*0501 and B102*), other 10% are HLA-DQ8 (A1*03,
B1*03), also other genetic factor are involved. The clinical presentation is caracterised by ex-
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tremely itchy papules and vesicles, which arise on normal or reddened skin. They tend to be
distributed symmetrically and are most often found on the scalp, shoulders, buttocks, elbows
and knees. Occasionally we can see sings and symptoms of enteropathy with malapsorption,
voluminous loose stools and weight loss. We report a case of a 27-year-old woman with pruritic vesicules on trunk and arms, with histologically confirmed diagnosis of dermatitis herpetiformis. She also had sings of bowel disease with positive specific antibodies for the confirmation of gluten-sensitive enteropathy and complained about strong pain in sacroiliac joints.
Diagnosis of sacroilitis was determined by MRI. Also HLA typisation was done. Patient was put
on gluten free diet and Dapson which she did not tolerate well. Considering that we did not
find any similar cases described in literature we find it important to emphasize this case report
as it is not so common.
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I
POSTERS (P)
I P 1 – MYCOSIS FUNGOIDES NON-RESPONSIVE TO PUVA THERAPY
- CASE REPORT
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Vlatka Čavka1, Iva Dediol1, Iva Crnarić2, Mirna Šitum1
Department of Dermatology and Venereology, University Hospital Center “Sestre milosrdnice”; Zagreb
2
Polyclinic “Sveti Rok”, Zagreb, Croatia; [email protected]
1
A 83-year-old male patient presented with disseminated pruritic papules and plaques that lasted for six months. Lesions were non-responsive to superpotent topical steroids. First histological examination of skin lesion was not specific. Second histological examination showed dense
lymphocytic infiltrate in upper dermis and immunohistochemical analysis revealed CD3 and
CD20 positivity. Third histological examination of skin lesion showed epidermotropism and
Pautrier’s micro abscesses. A diagnosis of patch stage mycosis fungoides was made. Staging
(CBC with differential, smear for Sezary cells, liver enzymes, uric acid, LDH, axilar, inguinal and
cervical lymph node ultrasound and CT scanning of thorax, abdomen and pelvis) revealed IB
stage. PUVA bath therapy (26 expositions) was conducted which led to only partial regression
but significant reduction of pruritus. Other comorbidities, including renal insufficiency with elevated creatinine levels and hyperlipidemia, disabled us to add oral retinoids to PUVA therapy.
Four weeks after completion of therapy skin status started to aggravate with appearance of
smaller tumours and recurrence of pruritus. Another skin biopsy was performed and sent to
Centre for haematologic pathology (Merkur University Hospital). Immunohistochemical analysis revealed CD3, CD4, CD2, CD5 and CD30 positivity. Part of tumor cells were CD7 positive.
Tumor cells were showing Ki67 expression and were negative for CD8. Presence of rare CD20
(B) lymphocytes were also determined. Stage IIB was diagnosed and patient was reffered to
oncologist for further treatment. Although studies have proven good response rates to PUVA
therapy in treatment of stage I mycosis fungoides (62-90% complete responses) it didn’t led to
complete clearance in our case and prompt relapse was observed. Multidisciplinary approach
is necessary for treatment and follow-up of mycosis fungoides patients.
64
I P 2 – DETECTION OF MUCOSAL HUMAN PAPILLOMAVIRUS TYPES
IN EXTRA-GENITAL BOWEN’S DISEASE
.. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
Vlatka Čavka, Ivana Ljubičić, Dora Madiraca, Mirna Šitum
The association between high-risk mucosal types of human papillomavirus (HPV) and genital
Bowen’s disease is already well established. The aim of this study was to determine presence
of high-risk mucosal human papillomavirus types in extra-genital Bowen’s disease. Nineteen
paraffin embeded tissues histologicaly verified as Bowen’s disease were analysed. All lesions
were located on the head. Detection of mucosal HPV DNA was performed using HPV screening
kit (AID, Germany) according to their protocol. High-risk HPV types (16, 18, 31, 33, 35, 39, 45, 51,
52, 53, 56, 58, 59, 66, 68, 73, 82) were detected by polymerase chain reaction and subsequent
reverse hybridisation with sequence-specific oligonucleotide probes. In all specimens analysis
was negative for high-risk HPV types. In five out of nineteen samples (26%) there were no
control DNA and we can not claim for certain that they are negative for high-risk HPV types.
Most former studies have emphasised the role of high-risk HPV types in extra-genital Bowen’s
disease, especially HPV16. Regarding our results we did not confirm connection between highrisk HPV types and extra-genital Bowen’s disease. Negative results obtained in this study could
be due to small sample and/or difficulties related to sampling and low number of copies of the
HPV genoma.
65
65
I
I P 3 – THE USE OF PREPARATIONS CONTAINING SMECTITE,
COPPER GLUCONATE AND ZINC GLUCONATE IN HERPES ZOSTER
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
Ljiljana Škrinjar1, Davorka Židak2, Zvjezdana Delibašić2
Clinic for Dermatovenerology Zagreb-Centar, Zagreb
2
Department for Infectious Diseases Dr. Fran Mihaljević, Zagreb, Croatia;
[email protected]
1
Herpes zoster is a viral disease characterized by unilateral localization, radicular pain and vesicular eruption, which is limited with the dermatome innerved by one spinal or cranial nerve.
One of the frequent complications in herpes zoster is bacterial superinfection. The aim of this
study was to present the therapeutic effect of the preparation containing smectite, copper
gluconate, zinc gluconate, arginine pidolate and Uriage Thermal water®. This product is a triple-action product (absorbent, antiseptic and soothing). Twenty patients with moderate to
severe herpes zoster were involved in the study. Ten patients with severe herpes zoster were
hospitalized, and other ten patients with moderate herpes zoster were outpatients. All patients
received Uriage Cu-Zn spray® as local therapy associated to systematic therapy (acyclovir). The
duration of the study was three weeks. Patients applied Uriage Cu-Zn® spray over the affected
area twice per day. The efficacy was evaluated by analyzing changes in typical bullosus lesions and patients and physicians global assessment. The efficacy parameters were assessed
at baseline, day 1, day 2, day 5 and day 21. Tolerability and safety was assessed by physical
examination, laboratory parameters and evalutaion of adverse events. Herpes zoster is a skin
eruption due to reactivation of the virus Varicella zoster. The eruption appears in a band-like
pattern on one side of the body. The involved area first become tender and red, and many
have a deep pain. Clusters of blisters appear and soon burst, leaving erosions and ulcers that
become crusted. Uriage Cu-Zn spray® help to dry up the blisters and ulcers and help to prevent
bacterial superinfection.
66
I P 4 – ANTI-THYROGLOBULIN ANTIBODY AND VITILIGO
.. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
Emina Kasumagić Halilović
Department of Dermatovenereology, Sarajevo University Clinical Center, Sarajevo, Bosnia and
Vitiligo is an acquired skin disorder characterized by depigmented maculae resulting from a
reduction of the number and function of melanocytes. The etiopathogenesis of the disease
is still unclear, but there is evidence that autoimmunity and endocrine disfunction may be
involved. The aim of this study was to evaluate serum levels of anti-thyroglobulin antibody
(anti-Tg) in vitiligo patients and control subjects, and also to assess the difference between the
localized and generalized forms of the disease. In this prospective study we investigated serum
level of anti-Tg in 50 patients with vitiligo and 33 healthy controls. We also examined a possible
association between serum levels of anti-Tg and disease severity. Comparison of median values
of anti-Tg has showed that serum concentrations of anti-Tg are significantly higher (p<0.05) in
serum samples of vitiligo patients in relation to control group. Statistically significant difference
was also found in values of anti-Tg between patients with generalized and patients with localized vitiligo (p<0.05). This study shows a significant association between vitiligo and thyroid
autoimmunity, and that tests to detect anti-Tg are relevant in patients with vitiligo.
67
67
I P 5 – PREVALENCE OF VITILIGO IN WEST HERZEGOVINA
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
Ana-Marija Sulić, Dubravka Šimić, Kristina Jurišić, Anita Ostojić
Department for Dermatology and Venereology University Hospital Mostar, Mostar, Bosnia and
Vitiligo is an acquired progressive pigmentary disorder characterized by depigmented maculae resulting from a reduction of the number and function of melanocytes. The prevalence of
vitiligo ranges from 0.5 to 2% with considerable variation among different racial group. The
average age of the onset is usually between 10 and 30 years of age. It is equally common in
men and women. The etiopathogenesis of the disease is still unclear, but there is evidence that
autoimmunity may be involved. The aim of this study was to determine the prevalence and
epidemiological characteristics of vitiligo. The study was conducted as a crosssectional study
of patients, treated at the Department of Dermatovenereology at University Clinical Hospital
Mostar, from January 2012 to December 2014. Data were collected using a data collection
form, included parameters of age, sex, family history, site of lesion, type of involvement and associated diseases. Results: The study included 110 patients with vitiligo, 64 female and 46 male.
The hands, neck and face were the most common involved sites. The generalized type was the
most common form of vitiligo. Associated disorder with vitiligo were documented in order for
thyroid disorders and type 2 diabetes. This study indicated that the high percentage of vitiligo
occurred in young ages therefore, it is expected that better case finding and screening methods were used to identify people with this disease so that, it can be quicker to recognize this
genetic and autoimmune disease, and finally treated with better quality.
68
I P 6 – HISTAMINE INTOLERANCE - DERMATOLOGIC SEQUELS
.. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
Liborija Lugović-Mihić1, Tomislav Duvančić1, Iva Crnarić2, Vedrana Bulat1,
Vlatka Čavka1, Mirna Šitum1
1
Zagreb
2
Polyclinic “Sveti Rok”, Zagreb, Croatia; [email protected]
Histamine intolerance (HIT) develops as a result of an impaired diamine oxidase (DAO) activity
due to gastrointestinal disease or through DAO inhibition, as well as through a genetic predisposition which was proven in a number of patients. The intake of histamine-rich foods as well
as alcohol or drugs which cause either the release of histamine or the blocking of DAO can lead
to various disorders in many organs (gastrointestinal system, skin, lungs, cardiovascular system
and the brain), depending on the expression of histamine receptors. Dermatologic sequels
can be rashes, itch, urticaria, angioedema, dermatitis, eczema and even acne, rosacea, psoriasis
and other. The recognizing of symptoms due to HIT is especially important in treating such
patients. Because of the possibility of symptoms affecting numerous organs, a detailed history
of symptoms following the intake of histamine rich foods or drugs that interfere with histamine
metabolism is essential for making a diagnosis of HIT. Considering that such symptoms can be
a result of multiple factors, the existence of HIT is usually underestimated, but considerable
expectations are being made from the future studies.
69
69
I NOTES
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ....................................................................
70
I NOTES
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ....................................................................
71
71
I NOTES
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
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. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ....................................................................
72
I NOTES
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
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. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ....................................................................
73
73
I NOTES
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
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. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
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. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ....................................................................
74
I NOTES
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
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. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
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. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .....................................................................
. .. .. .. .. .. .. .. .. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . ....................................................................
75
75
I NOTES
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76
I NOTES
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Transcription

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