The answer is D. Pemphigus vulgaris
Painful oral erosions preceding flaccid skin bullae, a positive Nikolsky sign, suprabasal acantholysis, and net-like intercellular IgG is pemphigus vulgaris. The antibodies target desmoglein 3 and desmoglein 1, the cadherins that hold the desmosomes between keratinocytes together. Destroy those and the keratinocytes come apart from each other — a process called acantholysis — producing a split within the epidermis, just above the basal layer. That single anatomic fact predicts every clinical feature: because the blister roof is only a few cell layers of epidermis, the bullae are flaccid, fragile, and rupture almost as soon as they form, which is why you see erosions rather than tense blisters. The basal cells stay attached to the basement membrane, giving the classic histologic description of a row of tombstones. Mucosal involvement is the discriminator to memorize. Oral erosions are the presenting sign in roughly half to 70% of patients and often precede skin disease by months, and the reason is elegant: desmoglein 3 predominates in mucosa while desmoglein 1 predominates in skin, so antibodies to Dsg3 alone produce mucosal-limited disease, and antibodies to both produce mucocutaneous disease. Any patient with chronic, painful, non-healing oral erosions deserves consideration of pemphigus. The Nikolsky sign — lateral shearing pressure on normal-appearing perilesional skin separates the epidermis — is positive here and reflects the same intraepidermal fragility. Diagnosis requires two specimens: a lesional biopsy for routine histology, showing suprabasal acantholysis, and a perilesional biopsy for direct immunofluorescence, showing intercellular IgG and C3 in a chicken-wire or fishnet pattern. Serum indirect immunofluorescence and ELISA for anti-desmoglein antibodies confirm the diagnosis and are useful for tracking activity. Treatment is systemic corticosteroids to induce remission, with rituximab now established as first-line therapy alongside steroids and steroid-sparing agents such as azathioprine or mycophenolate mofetil for maintenance. Care is as much supportive as immunologic: large denuded areas behave like burns, so attend to fluid and electrolyte balance, nutrition when oral pain limits intake, pain control, wound care, and surveillance for secondary bacterial infection — sepsis is the usual cause of death. Untreated pemphigus vulgaris was historically fatal in most patients; with modern therapy mortality is under 10%, and much of the remaining risk comes from long-term immunosuppression. Sorting the distractors: bullous pemphigoid is the one to separate carefully — it affects older patients, targets hemidesmosomal antigens BP180 and BP230 at the dermal-epidermal junction, so the split is subepidermal and the bullae are tense and itchy rather than painful, mucosal involvement is uncommon, Nikolsky is negative, and DIF shows a linear band of IgG and C3 along the basement membrane rather than an intercellular net; dermatitis herpetiformis is intensely pruritic grouped vesicles on the elbows, knees, and buttocks with granular IgA in the dermal papillae and an association with celiac disease, treated with dapsone and a gluten-free diet; Stevens-Johnson syndrome is an acute drug reaction over days with fever, targetoid lesions, and full-thickness epidermal necrosis, not a three-month indolent course; and bullous impetigo is a superficial staphylococcal infection of children in which exfoliative toxin cleaves desmoglein 1 in the granular layer, producing flaccid bullae with a collarette of scale and honey-colored crust, without oral erosions or autoantibodies.
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