docSpongiotic and psoriasiform reaction pattern
download 
Report 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 E R 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 • • • • • • • 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 • • • • • • • • • 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) • • • • 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 • • • • • 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 • • • • • • ! 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 • • • • • • • • • 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 • • • • • • 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 • • • • • 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 • • • • 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
