Spongiotic and psoriasiform reaction pattern

Transcription

Spongiotic and psoriasiform reaction pattern
Spongiotic and psoriasiform reaction
pattern
Boštjan Luzar
Institute of Pathology
Medical Faculty, Ljubljana, Slovenia
Spongiotic and psoriasiform
reaction pattern
• Dynamic prosess
• Different changes as the lesions evolve
• Distinguishing clinical subtypes on histological
features frequently NOT possible
• Patterns can overlap
– Some entities can have a variety of patterns
(spongiotic and psoriasiform)
• Epidermis and dermis
Spongiotic reaction pattern
Spongiotic reaction pattern
- Definition • Intraepidermal and
intercellular edema
(spongiosis)
 Widened
intercellular
spaces
 Elongation of
intercellelar
bridges
E
A
R
L
Y
Spongiotic reaction pattern
• Spongiosis
 Microscopic foci
 Vesicles
 Bullae
 DE juction
separation
 Crusting
• Exocytosis
 Lymphocytes
 Neutrophils
 Eosinophils
L
A
T
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Pathogenesis of spongiosis
• Increased permeability of superficial vascular
plexus
– Immunological reactions
– Direct damage
– Unknown causes
• Increased hydrostatic pressure
• Osmotic gradient towards the epidermis
Three phases of spongiotic dermatitis
• Acute
• Subacute
• Chronic
! There is a continuum of changes and
histological features frequently overlap
Acute spongiotic dermatitis
- Changes in the epidermis • Stratum corneum retains normal basketweave pattern
• Palor of keratinocytes
• No acanthosis
• Spongiosis
– Microvesicles
Acute spongiotic dermatitis
Acute spongiotic dermatitis
- Changes in the dermis • Edema of the papillary dermis
• Dermal perivascular inflammatory cell
infiltrate is variable
 Lymphocytes
 Eosinophils
 Neutrophils
Subacute spongiotic dermatitis
• Reactive changes of the epidermis
 Acanthosis (overlap with psoriasiform
pattern)
 Parakeratosis
• Granular layer may be diminished
• Less spongiosis
• Less dermal edema
• Variable inflammation in the dermis, often
with eosinophils
Chronic spongiotic dermatitis
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Hyperkeratosis
Parakeratosis (with/without)
Acanthosis
No/little spongiosis
Granular layer thickened, irregular
Dermal inflammation mild
Dermal fibrosis can be present
Chronic spongiotic dermatitis
Conditions featuring spongiosis
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Eczema dermatitis family
Stasis dermatitis
Pityriasis rosea
Infections
Insect bite reaction
Polymorphous eruption of pregnancy
Erythema multiforme
Papular acrodermatitis of childhood
....
Eczematous dermatitis = Eczema
• Clinical term
• Group of disorders
• Similar clinical features
 Moist
 Papules and plaques
 Vesicles
 Crust scale
 Erythematous base
• Similar histological features
 Spongiosis
• Frequently have different etiologies
Eczema
- Background • Insufficiently distinct to reliably separate them on
histological grounds alone, clinical data vital
Spongiotic dermatitis, consistent with eczema
• Clinicians can subclassify on the basis of clinical
presentation, history and possibly additional tests
(e.g. allergic or irritant contact dermatitis, ...)
Eczematous dermatitis
- Variants • Endogeneous
– Atopic
– Seborrheic
– Discoid
(nummular)
– Hand eczema
– Autosensitization
(id) reaction
• Exogeneous
– Contact
– Infective
– Asteatotic
Hand eczema
(dyshidrotic eczema, pompholyx,
palmoplantar eczema)
Hand eczema (palmoplantar eczema)
• Recurrent pruritic vesicular
eruption
- Palms (70%)
- Soles (10%)
- Palms and soles (20%)
- Digits (volar part, sides)
• Vesicles appear as small
pale papules
• Scaling, cracking
• F>M
Hand eczema (palmoplantar eczema)
- Pathogenesis • Idiopatic
– Patients frequently have atopy
– Majority of cases
• Allergic contact dermatitis
– Drugs, shover gels, food, ...
– Significant proportions
• Id-reactions
Hand eczema (palmoplantar eczema)
• Important to exclude dermatophyte infection
(PAS stain)
– ! The presence of neutrophils in the stratum
corneum
Contact dermatitis
Contact dermatitis
• Allergic
 Type IV hypersensitivity
 Exposure to specific antigen
 Poison ivy, latex, nickel, rubber, ...
• Irritant
 Direct damage of the epidermis
 80% of the occupational skin diseases
 Detergents, solvents, acids, alkalis, ...
Contact dermatitis
- Clinical presentation • Erythematous plaues, papules and sometimes
vesicles
• Distribution and shape of the lesion can
suggest etiology
Allergic contact dermatitis
Langerhans cell microabscesses
Eosinophilic granulocytes
can be
scarce or absent
in contact dermatitis.
Irritant contact dermatitis
- Histological features
• Changes depend on the concentration of the
offending agent
• Pallor and ballooning of keratinocytes in the
upper dermis
• Necroses of keratinocytes in variable numbers
• Exocytosis of neutrophils in the area(s) of
ballooning and necrosis of keratinocytes
Discoid dermatitis
(nummular eczema)
Discoid dermatitis (nummular eczema)
- Clinical features • Single/multiple pruritic lesions
• Usually starts as tiny papules or
papulovesicles
– Confluence of lesions
– Grouping in the shape of coins
• Surface wheeping and/or crusted
• Margins usually flat
Discoid dermatitis (nummular eczema)
- Clinical features • Sites of predilection
– Lower legs
– Forearms (extensor)
– Dorsum of hands
• Two peak ages of onset
– Young women
– Middle aged adults
• Chronic course with
remissions and relapses
Nummular dermatitis
- Pathogenesis • Poorly understood
• Related to atopy
• As a consequence of allergy to
– Nickel
– Cobalt
– Chromate
• Can follow exposure to irritants
– Soap, acid, alkalis
Nummular dermatitis
- Histology • Acute/subacute/chronic spongiotic dermatitis
• Progressive psoriasiform hyperplasia of the
epidermis, not as uniform as in allergic contact
dermatitis
• Scale crust frequent
• Dermal infiltrate contains lymphocytes,
occasional neutrophils, eosinophils and
plasma cells
‘Specific’ forms of spongiotic dermatitis
• Stasis dermatitis
• Pityriasis rosea
• Vesicular dermatophytosis
! ALWAYS CORRELATE WITH CLINICAL HISTORY
Stasis (varicose) dermatitis
Middle aged and older patients
Impaired venous return from lower limbs
Medial aspects of lower leg / ankle
Clinical presentation
- Oedema with shiny or erythematous
appearance
- Dry, scaly, crusted erythematous or
brawnish discolorations
• Often around stasis ulcer(s)
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Stasis (varicose) dermatitis
• Spongiosis and acanthosis
• Lobular vascular proliferation
– Can be prominent with formation of papules
• Hemosiderin
– Abundant, throughout the dermis
• Fibrosis
– prominent in long-standing lesions
• Inflammation (L, MF, PL)
• Erythrocyte extravasation
Pityriasis rosea
Pityriasis rosea
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Acute self limited disease
F>M
15-55 years (about 75% of patients)
Seasonal variations
Recurrent disease in < 5%
Pityriasis rosea
• Single red scaly
plaque = herald
patch
• Usually on the trunk
• Increases in size
over 48 hours (2-10
cm)
• Systemic symptoms
can also be present
Pityriasis rosea
• Secondary
incubation period
of 7-14 days
• Generalized
eruption of
erythematous
scaly lesions
• Chest, abdomen,
thighs, arms, back
• Cause unknown
Pityriasis rosea
- Histology Subacute/chronic spongiotic dermatitis
Focal hyperkeratosis
(multi)focal parakeratosis
Slight irregular acanthosis
Vesiculation rare
Superficial perivascular mononuclear
inflammatory cell infiltrate
• Extravasation of erythrocytes
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!
Neutrophils in the cornified layer are not a
feature of pityriasis rosea
*
Consider guttate psoriasis
*
Exclude infection
Spongiotic dermatitis
- Secondary changes• Frequently becomes infected
• Dramatic change in histopathology
 Marked acute inflammation
 Development of pustules
• Subcorneal
• Intraepidermal
• Subepidermal
• Additional stain(s) necessary
Psoriasiform reaction pattern
Psoriasiform reaction pattern
• Epidermal
hyperplasia
(acanthosis)
• Uniform and
markedly enlarged
rete ridges
Psoriasiform reaction pattern
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Psoriasis
Reiter’s syndrome
Pityriasis rubra pilaris
Pityriasis rosea
Lichen simplex chronicus
Psoriasiform drug eruptions
Subacute/chronic spongiotic dermatitis
Necrolytic migratory erythema
....
Psoriasis vulgaris
is
the prototype of
psoriasiform dermatitis
Psoriasis vulgaris
• Classic features
 Sharply demarcated erythematous plaques
 Silvery scaly surface
• Sites of predilection
– Scalp
– Extensor surfaces
– Lower back
– Periumbilical
– Nails (pitting, distal onycholysis, ...)
• Granular layer
absent
Psoriasis vulgaris
- Histology •
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Uniform acanthosis
Parakeratosis (prominent, confluent)
Diminished/absent granular layer
Collections of neutrophils in the epidermis
Thinning of suprapapillary plates
Papillary dermal vessels
 Dilated, congested
 Turtous
Eosinophils
are typically
ABSENT
in psoriasis
If present, consider psoriasis-like
eczematous process, drug eruption, ...
*
Classic psoriasis not difficult to
recognize
*
Rarely biopsied
*
Variants of psoriasis can be challenging
Evolving psoriasis
- Histology • Epidermal changes
– Mild initial spongiosis
– Mild acanthosis
– Focal parakeratosis
– Mild lymphocyte exocytosis
• Dermal changes
– Dilatation and congestion of superficial
vascular plexus
– Mild perivascular lymphocytic infiltrate
Evolving psoriasis
Gutate psoriasis
• Rapid onset of
numerous small
plaques and papules
(0.5-1.5 cm)
• Upper trunk, proximal
extremities
• Young patients
• Often history of
antecedent pharyngitis
(streptococcal)
Guttate psoriasis - histology
Histological features overlap with those of
evolving disease
Guttate psoriasis
• Acanthosis much less marked
• Parakeratosis
 Focal
 Neutrophils
• Focal loss/diminution of granular cell layer
• Mild spongiosis
• Superficial dermal inflammation
– Neutrophilic granulocytes, lymphocytes
– No eosinophils!
Guttate psoriasis
Pustular psoriasis - generalized
• Fever of several days
duration
• Sudden appearance of
sterile pustules (2-3
mm)
• Erythematous skin –
progression to
erythroderma
• Recurrent episodes of
fever and pustules
Pustular psoriasis - generalized
• Predisposing conditions
– Infections (bacterial, viral)
– Withdrawal of systemic steroid therapy
– Drugs
– Pregnancy
– Hypocalaemia
– Sunlight / phototherapy
– Emotional stress
– ...
Pustular psoriasis
A characteristic
histological feature is
formation of
macropustule(s)
Pustular psoriasis
• Large collections of neutrophils within
epidermis and/or stratum corneum
• Granular layer
 Normal
 Partially diminised
• No significant acanthosis due to the rapid
development
Pustular psoriasis – dif. dg.
• Infection (fungi)
 Additional stains (PAS, ...)
• Generalized exentematous pustulosis
 History of new medications
 Eosinophis!!!
Pityriasis rubra pilaris
Pityriasis rubra pilaris
• Rare disease
• Small follicular papules
(trunk)
– Central keratin plug
• Erythema
– Perifollicular
erythema
– Confluent
– Large expanding
plaques
Pityriasis rubra pilaris
• Islands of spared
skin
• Erythema has
orange-yellow tint
• Palmoplantar
keratoderma
Pityriasis rubra pilaris –
non follicular lesions
• Checkerboard parakeratosis (alternating ortho
and parakeratosis in horizontal/vertical
fashion)
• Focal/confluent hypergranulosis
• Marked uniform acanthosis
• Broad rete ridges
• Thick suprapapillary plates
• Narrow dermal papillae
Pityriasis rubra pilaris
‘Shoulder parakeratosis’
Pityriasis rubra
pilaris
• Follicular plugging
Pityriasis rubra pilaris
Can be confused
with
psoriasis
on histology.
Pityriasis rubra pilaris
1.
2.
3.
Lacks neutrophils in stratum corneum
or epidermis
No suprapapillar plate thinning
Granular layer not diminished
Pityriasis rubra pilaris - beware
1.
2.
Biopsies from early lesions can be
inconclusive
Biopsies from follicular papules nonspecific
Lichen simplex chronicus and prurigo nodularis
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Related entities
Result of persistent rubbing or scratching
Pruritic scaly plaques
Pruritic nodules
Ulceration secondary to excoriation
Lichen simplex chronicus and prurigo nodularis
Only
on areas
that patient
can
reach
Lichen simplex chronicus and prurigo nodularis
Nape of the neck
Shin
Forearms
Dorsal feet
Perianal / genital areas
Lichen simplex chronicus
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Prominent hyperkeratosis
Psoriasiform hyperplasia
Focal parakeratosis
Hypergranulosis
Lichen simplex chronicus
Fibrosis of papillary dermis characterised by
vertically oriented
thick collagen fibres
(vertical streaking)
Lichen simplex chronicus
Prurigo nodularis
• Pseudoepitheliomatous
hyperplasia
• Extension into hair
follicle
Spongiotic and psoriasiform reaction pattern
- Conclusions • Dynamic prosess
• Different changes as the lesions evolve
• Distinguishing clinical subtypes on histological
features frequently NOT possible
• Patterns can overlap
• Clinico-pathological correlation crucial

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