Page 622 - Concise Pathology for Exam Preparation ( PDFDrive )

22 The Skin 607

Morphology:
• Histological hallmark in all forms of pemphigus is acantholysis (separation of indi-
vidual keratinocytes due to lysis of intercellular adhesion sites); detached acantho-
lytic cells become rounded.
• In pemphigus vulgaris, acantholysis involves the layer of cells just above the basal
layer giving rise to a suprabasal blister.
• In pemphigus foliaceus, acantholysis involves the superficial epidermis at the level
of stratum granulosum.
• Variable superficial dermal infiltration by lymphocytes, histiocytes and eosino-
phils accompanies the acantholysis.
2. Bullous pemphigoid
• Affects elderly people, presents with bullous lesions on normal or erythematous skin
and mucosa; the bullae are tense and filled with clear fluid.
• Usual sites are inner aspect of thighs, flexor surface of forearms, axillae, groin and
lower abdomen.
Pathogenesis:
• It is an autoimmune disorder in which the characteristic finding is linear deposits of
IgG antibodies and complement in the basement membrane zone.
• Area affected is the basal cell-basement membrane attachment (haemidesmosomes),
where the bullous pemphigoid antigen (BPAG) is located. This protein is normally
involved in dermoepidermal bonding.
• IgG autoantibodies to haemidesmosome components fixes complement with subse-
quent tissue injury.
Morphology:
• Characterized by a subepidermal nonacantholytic blister.
• Lesions show perivascular inflammation (lymphocytes, eosinophils and occasional
neutrophil), superficial dermal oedema and associated basal cell liquefaction, which
eventually gives rise to the blister.
3. Dermatitis herpetiformis
• Affects predominantly males in the 3rd and 4th decades.
• May be associated with gluten-sensitive enteropathy (celiac disease).
• Urticarial plaques and vesicles are seen in a bilaterally symmetrical distribution on
the extensor surface of elbows, knees, upper back and buttocks.
Pathogenesis:
• Presence of IgA antibodies to dietary gluten.
• Antibodies cross react with reticulin (a component of fibrils that anchor the epidermal
basement membrane to the superficial dermis).
• Resulting injury produces a subepidermal blister.
Morphology:
• Formation of microabscesses (fibrin and neutrophils at the tips of dermal papillae).
• Basal cells show vacuolization and focal dermoepidermal separation, eventually leading
to formation of a subepidermal bulla.
• Direct immunofluorescence shows discontinuous, granular deposits of IgA localized
in the tips of dermal papillae.

Q. Write briefly on seborrheic keratosis.

Ans. It is a common epidermal tumour that occurs most frequently in middle-aged and
older individuals, usually on the trunk, extremities, head and neck.
Pathogenesis:
• Presence of activating mutations in the fibroblast growth factor (FGF) receptor 3.
• Onset of lesions may be part of a paraneoplastic syndrome (sign of Leser–Trélat).
• Patients may have internal malignancies, which produce growth factors that stimulate
epidermal proliferation.
Morphology:
• It is a raised, pigmented lesion with a verruca-like surface, which histologically exhibits
hyperkeratosis, papillomatosis, entrapment of keratin in the epidermis (horn cysts) and
proliferation of basaloid (basal cell-like) cells showing increased pigmentation.

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