The distribution of lesions in pemphigus vulgaris is explained by the desmoglein compensation theory. A patient whose serum contains autoantibodies against desmoglein-3 alone will characteristically show:

• A Mucocutaneous disease involving both skin and oral mucosa
• B Mucosal-dominant disease, because desmoglein-1 compensates for desmoglein-3 loss in the skin ✓
• C Skin-only disease, because desmoglein-3 is absent from mucosa
• D Subcorneal blistering resembling pemphigus foliaceus

Explanation

Desmoglein-3 is the dominant desmosomal cadherin in mucosa while both desmoglein-1 and desmoglein-3 are expressed in skin. Antibodies against desmoglein-3 alone disrupt mucosa, but in the skin desmoglein-1 maintains adhesion, so no cutaneous blisters form. When antibodies against desmoglein-1 are also present, skin adhesion fails and mucocutaneous disease results.

Reference: Robbins and Cotran Pathologic Basis of Disease, 10th ed.

High-yield for: NEET PGINI-CETNExTFMGEUSMLEPLABMRCP

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