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ukmla 2026

Bullous Pemphigoid

Commonest autoimmune blistering disease — TENSE blisters in elderly, subepidermal split, Nikolsky NEGATIVE, linear IgG/C3 on immunofluorescence

Review date
reviewed 2026-04-05
Reading time
4 min read
Author
Dr Kola Tytler MBBS CertHE MBA MSt MRCGP
Dermatologyrarechronic
On this page
Condition details
Dermatology
rare
4 min read
reviewed 2026-04-05
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About This Page

This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.

Key points

  • Commonest autoimmune blistering disease — typically elderly >70 years
  • TENSE blisters on normal/erythematous skin that do NOT rupture easily. Nikolsky NEGATIVE
  • Subepidermal split: IgG against BP180/BP230 at basement membrane zone
  • DIF: LINEAR IgG and C3 along basement membrane zone — diagnostic
  • Treatment: potent topical clobetasol for localised. Oral prednisolone +/- steroid-sparing for widespread

Overview

Bullous pemphigoid (BP) is caused by IgG autoantibodies against BP180 and BP230 at the dermo-epidermal junction causing subepidermal split. Tense blisters that do not rupture easily. Oral involvement uncommon (~10-30%). May have a prodromal urticarial phase. Drug-triggered BP reported with DPP-4 inhibitors (gliptins) and PD-1 inhibitors.

Epidemiology

Peak onset >70 years. ~4-7 per 100,000/year in over 70s. More common with neurological conditions (dementia, Parkinson's, CVA). Generally self-limiting over months to years.

Clinical Features

Symptoms
Prodromal pruritus, urticarial plaques before blisters appear
Large TENSE blisters on normal or erythematous skin
Intense pruritus
Signs
Tense, fluid-filled blisters 1-3 cm (serous or haemorrhagic)
Nikolsky sign NEGATIVE
Oral involvement uncommon (~10-30%)

Investigations

First-line
Skin biopsy (lesional)Subepidermal blister with eosinophilic infiltrate
Direct immunofluorescence (perilesional)LINEAR IgG and C3 along BMZ — diagnostic
Second-line
Anti-BP180/BP230 ELISACirculating antibodies — titre correlates with activity
FBCEosinophilia common

Management

BAD Guidelines on Bullous Pemphigoid
1
Localised/mild
  • Super-potent topical: clobetasol propionate 0.05% (Dermovate) BD
  • As effective as oral steroids with fewer side effects
2
Widespread/moderate-severe
  • Oral prednisolone 0.5 mg/kg/day, taper slowly
  • Steroid-sparing: doxycycline 200 mg OD (BLISTER trial — non-inferior to prednisolone in elderly)
  • Or mycophenolate, azathioprine, dapsone
3
Supportive
  • Leave tense blisters intact. Drain large ones but leave roof
  • Osteoporosis prophylaxis, glucose monitoring with steroids
  • Review medications — DPP-4 inhibitors can trigger BP

Complications

  • Secondary infection: Denuded skin vulnerable to sepsis
  • Steroid complications: In frail elderly
UKMLA Exam Tips
  • 1BP: TENSE blisters, elderly, Nikolsky NEGATIVE, LINEAR IgG/C3 on DIF
  • 2PV: FLACCID blisters, younger, Nikolsky POSITIVE, INTERCELLULAR chicken-wire IgG
  • 3BP = Below (sub-epidermal). PV = Penphigus (intra-epidermal)
  • 4Doxycycline is emerging alternative to prednisolone in elderly BP (BLISTER trial)
  • 5Drug-induced BP: DPP-4 inhibitors (gliptins)
  • 6Dermatitis herpetiformis: GRANULAR IgA — NOT linear IgG

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Verified Sources & References

BAD — Bullous Pemphigoid Guidelines
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Dermatology · Article 19 of 25