PHOTOSENSITIVITY SKIN DISORDERS IN CHILDHOOD Irene
Transcription
PHOTOSENSITIVITY SKIN DISORDERS IN CHILDHOOD Irene
PHOTOSENSITIVITY SKIN DISORDERS / PHOTODERMATOSES Irene Horkay Department of Dermatology PHOTODERMATOSES (PD-S) Number of PD-s: ever-increasing depletion of the ozone layer photosensitizing compounds, drugs, plants sunbathing/sunbeds Provoking spectrum: UV spectrum (200-400 nm) of sunlight or artificial light sources AETIOPATHOGENESIS OF PD-S UV light alone UV light + endogenous/exogenous photosensitizers Metabolic – hormonal – immunological processes Cellular and molecular targets / chromophores DNA, porphyrins, etc. DIAGNOSIS OF PD-S Typical history: sunlight exposure, familial occurrence Clinical features: morphology, localization Phototests minimal erythema/urtica dose (MED/MUD) provocation test (idiopathic PD) photopatch test (photoallergic dermatitis) Laboratory tests porphyrin analysis: urine, RBC, serum immunoserology (autoantibodies: PLE, LE) histology and immunhistology of skin lesions (PLE, HV, LE) chromosomal analysis, UDS, urine amino acid levels (geno-PD) CLASSIFICATION OF PHOTODERMATOSES (PD-S) Yashar, Lim I/ Idiopathic photodermatoses (PD-s) II/ Photosensitivity secondary to external agents III/ Cutaneous porphyrias IV/ Genophotodermatoses V/ Photoaggravated disorders I/ IDIOPATHIC PHOTODERMATOSES 1/ Polymorphic light eruption (PLE) 2/ Juvenile spring eruption of the ears 3/ Solar urticaria (SU) 4/ Hydroa vacciniforme (HV) 5/ Chronic actinic dermatitis (CAD) PATHOMECHANISM OF IDIOPATHIC PD Abnormal immune response to sunlight UV-induced antigen in the skin (unidentified) Impaired immunoregulatory mechanism Delayed (PLE, HV) or immediate type (SU) hypersensitivity reaction skin lesions Genetic basis + environmental factors 1/ POLYMORPHIC LIGHT ERUPTION (PLE) Most frequent idiopathic PD Action spectrum UVB (290-320 nm), UVA (320-400 nm) or both CLINICAL FEATURES OF PLE Pleomorphic lesions mostly on the exposed areas Erythematous papules Papulovesicles/eczematous Large plaques CLINICAL FEATURES OF PLE Diagnosis/treatment Provocation phototest 60 - 90% positivity Immunoserology: negative Therapy/prevention: regular use of topical sunscreens prophylactic narrow-band UVB phototherapy 2/ JUVENILE SPRING ERUPTION OF THE EARS Onset in childhood Papules and vesicles on the ears Dominance of boys Spontaneous healing during adolescence 3/ SOLAR URTICARIA Action spectrum: 280 - 600 nm Clinical features: itching, immediate wheal Diagnosis: MUD/ provocation test Treatment: antihistaminics, prophylactic phototherapy 4/ HYDROA VACCINIFORME Bazin Extremely rare Onset in childhood, spontaneous healing during puberty Clinical picture:papules, vesicles, vacciniforme scar Prophylaxis: sunscreens, beta-carotene 5/ CHRONIC ACTINIC DERMATITIS History: photoallergic contact dermatitis (drugs, chemicals) Action spectrum: UVA, UVB or both Onset: middle/old age, male predominance Clinical features: 1/ Persistent light reaction:perennial chronic eczema without light exposure and chemicals 2/ Actinic reticuloid: nodular eruptions beyond the exposed areas Diagnosis: photopatch test Treatment: symptomatic, preseasonal phototherapy II/ PHOTOSENSITIVITY SECONDARY TO EXTERNAL AGENTS 1/ PHOTOTOXIC DERMATITIS Action spectrum: UVA Provoking agents: psoralen containing plants tars, dyes – occupational skin disorders cosmetics drugs (tetracyclins, diuretics, amiodaron) Clinical features: erythema, edema, blisters healing: long-lasting pigmentation Therapy: symptomatic anti-H or corticosteroid loc.: antiinflamm. + steroid 2/ PHOTOALLERGIC CONTACT DERMATITIS Action spectrum: UVA Provoking agents: fragrances, sunscreens, topical medicaments (NSAID-s) Clinical features: eczematous eruptions Diagnosis: photopatch testing „crescendo” type reaction Treatment: symptomatic to avoid chemicals, drugs, sunlight III/ CUTANEOUS PORPHYRIA most common inherited cause of photosensitivity 1/ Erythropoietic porphyria erythropoietic protoporphyria (EPP) congenital erythropoietic porphyria (CEP, Günther’s disease) 2/ Hepatic porphyria porphyria cutanea tarda (PCT) hepatoerythropoietic porphyria (HEP) variegate porphyria (VP) Action spectrum: UVA 1/ CHARACTERISTICS OF ERYTHROPOIETIC PROTOPORPHYRIA (EPP) Onset of photosensitivity: early infancy Inheritance: mostly autosomal dominant Family history: frequent Enzymatic defect: ferrochelatase 100 < heterogeneous mutations in the gene Biochemistry: elevated PP in RBC lack of porphyrinuria CHARACTERISTICS OF EPP Acute symptoms: painful erythema, burning, swelling, urtica or blisters Chronic signs: scarring, waxy thickening, “orange peel” nose occasionally: fatal hepatic failure Treatment: beta-carotene prophylactic UVB phototherapy CEP (Günther’s disease) Very rare Clinical features: mutilating scarring severe extracutaneous symptoms Biochemistry: elevated porphyrin levels (RBC, urine) No case in Hungary 2/ CHARACTERISTICS OF PORPHYRIA CUTANEA TARDA (PCT) Enzymatic defect: uroporphyrinogen decarboxylase homozygous form of PCT: hepatoerythropoietic porphyria (HEP) Biochemistry: increased excretion of UP and CP elevated liver specific enzyme activities serum iron and ferritin level Family history: rare Background: hepatopathy of various origin (alcohol, HCV infection, estrogens, chemicals) CHARACTERISTICS OF PCT Clinical features: skin fragility, blisters erosions scars + milia hypertrichosis pigmentation Treatment: abstinence from alcohol combined therapy: phlebotomies + low dose of chloroquine IV/ GENOPHOTODERMATOSES Genetic defect(s) in the DNA-repair processes Xeroderma pigmentosum pigmented spots, early malignancis fatal outcome Other biochemical abnormalities Cockayne syndr. Smith-Lemli-Opitz syndrome Early development of malignancies Specific extracutaneous features V/ PHOTOAGGRAVATED DISORDERS not real PD-s with different pathogenesis Lupus erythematosus (LE) malar erythema Pemphigus group, pemphigoid Dermatomyositis Erythema multiforme Atopic dermatitiss Psoriasis, etc.