Pemphigus Vulgaris and Bullous Pemphigoid are easy to mix up on the boards. Here's a side-by-side comparison — presentation, workup, imaging, and first-line treatment — drawn from our full outlines.
Pemphigus Vulgaris vs Bullous Pemphigoid at a glance
Pemphigus Vulgaris: Autoimmune intraepidermal blistering disease with flaccid bullae and painful mucosal erosions.
Bullous Pemphigoid: Most common autoimmune subepidermal blistering disease of the elderly; tense bullae on an urticarial base.
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Question 1DermatologyMedium
A 52-year-old woman of Ashkenazi Jewish descent presents with 3 months of painful oral erosions followed by flaccid bullae and raw, ragged-bordered erosions on her scalp, axillae, and trunk. The blisters rupture with minimal pressure, and lateral traction on adjacent normal-appearing skin produces shearing of the epidermis. A perilesional skin biopsy is sent for direct immunofluorescence. Which of the following findings best supports the suspected diagnosis?
AGranular IgA deposition within the tips of the dermal papillae
BIntercellular IgG and C3 deposition in a chicken-wire pattern
CLinear IgG and C3 deposition along the basement membrane zone
DIntercellular IgA deposition in the superficial epidermis
Reveal answer & full explanation
Correct answer: B — Intercellular IgG and C3 deposition in a chicken-wire pattern
AGranular IgA deposition within the tips of the dermal papillae
BIntercellular IgG and C3 deposition in a chicken-wire pattern✓
CLinear IgG and C3 deposition along the basement membrane zone
DIntercellular IgA deposition in the superficial epidermis
Why Intercellular IgG and C3 deposition in a chicken-wire pattern is correct
The vignette is classic pemphigus vulgaris: a middle-aged adult of Ashkenazi descent with painful oral erosions preceding flaccid cutaneous bullae and a positive Nikolsky sign (epidermal shearing on lateral pressure on perilesional skin).
PV is driven by IgG autoantibodies against desmoglein 1 and 3 within the desmosomes between keratinocytes, causing suprabasal acantholysis. Perilesional direct immunofluorescence therefore shows IgG and C3 deposited in the intercellular spaces of the epidermis, producing the characteristic net-like "chicken-wire" pattern.
This intercellular (not basement-membrane) localization is the confirmatory immunofluorescence finding; serum anti-desmoglein 1/3 ELISA further confirms the diagnosis and tracks disease activity.
Why the others are wrong
Granular IgA deposition within the tips of the dermal papillae — This is the finding of dermatitis herpetiformis, an intensely pruritic vesicular eruption linked to celiac disease, not an acantholytic mucocutaneous blistering disorder.
Linear IgG and C3 deposition along the basement membrane zone — This is the DIF pattern of bullous pemphigoid (anti-BP180/230), which causes tense subepidermal bullae on flexural skin with pruritus and usual mucosal sparing, the opposite localization from PV.
Intercellular IgA deposition in the superficial epidermis — This is the DIF pattern of IgA pemphigus (subcorneal pustular dermatosis type), which causes pruritic flaccid pustules in annular or circinate groups on the trunk and flexures with usual mucosal sparing; PV deposits IgG, not IgA, and typically begins with painful oral erosions.
Question 2DermatologyMedium
A 78-year-old man with Parkinson disease is evaluated for several weeks of intense generalized itching followed by the eruption of large, tense fluid-filled blisters on his lower abdomen, inner thighs, and forearms. The bullae arise on erythematous, urticarial-appearing plaques and remain intact when lateral pressure is applied to adjacent skin. The oral mucosa is spared. CBC shows peripheral eosinophilia. Perilesional direct immunofluorescence shows linear IgG and C3 along the basement membrane zone. Which of the following best explains the findings?
AIgG autoantibodies against desmoglein causing intraepidermal acantholysis
BIgG autoantibodies against collagen XVII causing subepidermal separation
CIgG autoantibodies against laminin-332 causing subepidermal separation
DIgG autoantibodies against type VII collagen causing sublaminar separation
Reveal answer & full explanation
Correct answer: B — IgG autoantibodies against collagen XVII causing subepidermal separation
AIgG autoantibodies against desmoglein causing intraepidermal acantholysis
BIgG autoantibodies against collagen XVII causing subepidermal separation✓
CIgG autoantibodies against laminin-332 causing subepidermal separation
DIgG autoantibodies against type VII collagen causing sublaminar separation
Why IgG autoantibodies against collagen XVII causing subepidermal separation is correct
Bullous pemphigoid is driven by IgG against BP180 (collagen XVII, NC16A domain) and BP230 within the hemidesmosome at the dermoepidermal junction.
Antibody binding triggers complement activation, mast cell degranulation, and eosinophil-derived proteases that cleave the lamina lucida, producing a subepidermal split.
Because the entire epidermis lifts off as the blister roof, the bullae are tense and intact with a negative Nikolsky sign, matching the linear IgG/C3 on DIF; the advanced age, neurologic comorbidity (Parkinson disease), pruritic urticarial prodrome, spared mucosa, and eosinophilia all point to bullous pemphigoid.
Why the others are wrong
IgG autoantibodies against desmoglein causing intraepidermal acantholysis - this is pemphigus vulgaris, which produces flaccid bullae, a positive Nikolsky sign, and near-universal painful oral erosions, none of which fit here.
IgG autoantibodies against laminin-332 causing subepidermal separation - this is anti-laminin-332 (anti-epiligrin) mucous membrane pemphigoid, which predominantly affects the oral and ocular mucosa, heals with scarring, and is associated with underlying solid-organ cancer; the spared oral mucosa and generalized pruritic urticarial plaques here fit bullous pemphigoid instead.
IgG autoantibodies against type VII collagen causing sublaminar separation - this is epidermolysis bullosa acquisita; blisters favor trauma-prone sites with scarring and milia, and salt-split skin binds the dermal (floor) side rather than the epidermal roof.
Additional high-yield points
Serum ELISA for anti-BP180 (NC16A) and anti-BP230 IgG supports the diagnosis, and anti-BP180 levels track disease activity.
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Autoimmune intraepidermal blistering disease with flaccid bullae and painful mucosal erosions.
Most common autoimmune subepidermal blistering disease of the elderly; tense bullae on an urticarial base.
Classic presentation
Painful oral erosions preceding flaccid cutaneous bullae in a middle-aged adult; positive Nikolsky.; Painful, persistent oral erosions (often the presenting symptom, precede skin disease by months); Burning, painful skin lesions rather than itch; Dysphagia, odynophagia, weight loss from oropharyngeal involvement; Hoarseness if laryngeal…
Severe pruritus and tense bullae on an urticarial base in an elderly patient.; Severe generalized pruritus, often weeks to months before blisters appear (prodromal or non-bullous phase); Tense fluid-filled blisters arising on urticarial or normal-appearing skin; Predilection for flexural areas: lower abdomen, inner thighs, axillae,…
Workup / key labs
Diagnosis requires clinical findings plus histology and immunofluorescence. Lesional biopsy: suprabasal acantholysis with 'tombstone' row of basal cells. Perilesional direct immunofluorescence (DIF): intercellular 'chicken-wire' IgG and C3 deposition. Serum anti-desmoglein antibodies confirm and track activity.; Serum indirect…
Diagnosis requires clinical features plus histopathology and immunofluorescence. Lesional biopsy: subepidermal blister with eosinophil-rich dermal infiltrate. Perilesional DIF: linear deposition of IgG and C3 along the basement membrane zone. Salt-split skin DIF: antibodies bind the epidermal (roof) side, distinguishing BP from EBA.;…
Imaging
No routine imaging required; Esophagogastroduodenoscopy if dysphagia or odynophagia suggests esophageal involvement; Chest imaging and age-appropriate cancer screening to exclude paraneoplastic pemphigus in atypical cases
No routine imaging; tailor to comorbid evaluation; Consider age-appropriate malignancy screening if atypical presentation, but routine paraneoplastic workup is not indicated
First-line treatment
Systemic corticosteroid: prednisone 1 mg/kg/day, methylprednisolone IV for severe disease; taper slowly over months; Rituximab (anti-CD20) — now first-line with steroids per 2020 international consensus and Joly et al. 2017 RITUX 3 trial; 1 g IV days 0 and 14 (rheumatoid arthritis dosing) or 375 mg/m² weekly × 4 (lymphoma dosing); Wound…
Superpotent topical corticosteroid (clobetasol propionate 0.05%) is first line at any extent: apply to lesions in localized disease and to the whole body in moderate or extensive disease (30-40 g/day when extensive, tapered over months); in Joly NEJM 2002, whole-body clobetasol matched oral prednisone in moderate BP and gave better…
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