Synopsis
Recognise the pruritic pre-bullous and tense-blister phases, obtain correctly paired biopsy specimens, stabilise frail patients, and select topical or systemic treatment with infection and steroid safeguards.
- Bullous pemphigoid usually affects older adults and may begin with weeks or months of intense itch, urticarial plaques or excoriated eczema before any blister is visible.
- Established blisters are tense because the split is subepidermal; they arise on normal or inflamed skin and are less easily ruptured than pemphigus bullae.
- Mucosal disease can occur but is less dominant than in pemphigus vulgaris; extensive oral, ocular or genital involvement should widen the differential and increase referral urgency.
- Biopsy a fresh blister edge for routine histology and take a separate normal-appearing perilesional specimen for direct immunofluorescence in the receiving laboratory's transport medium.
- Linear IgG and C3 along the basement membrane on direct immunofluorescence supports pemphigoid; serum BP180 or BP230 antibodies add evidence and may help follow difficult disease.
- Review DPP-4 inhibitors, checkpoint inhibitors, diuretics and other temporal medicines, but do not stop essential treatment without coordinating the prescribing clinician and diabetes or oncology consequences.
- Superpotent topical corticosteroid is the preferred disease-directed treatment when nursing support and treated area make whole-body application feasible; quantity and taper need specialist supervision.
- Doxycycline 100 mg twice daily can be a safer initial systemic strategy for selected patients in whom long-term corticosteroid toxicity is a major concern, although blister control may be slower or less complete.
- Oral prednisolone is used for rapidly progressive or extensive disease when topical treatment is impractical, with an explicit response-led taper and early plan to minimise cumulative exposure.
Key red flags
Fever, hypotension, confusion, rapidly spreading erythema, purulence, severe skin pain, extensive denudation, eye symptoms, dysphagia, inability to maintain intake or a recently started high-risk medicine requires urgent assessment for infection or another severe blistering disorder.
Increasing pain, purulence, odour, spreading warmth, fever or confusion around erosions suggests bacterial complication and requires urgent reassessment.
Investigation priorities
Demonstrate the anatomical split and inflammatory pattern while preserving blister roof and adjacent skin.
Management branches
Tense blisters or otherwise unexplained severe pruritic plaques suggest autoimmune subepidermal disease.
- Examine the entire skin and mouth, eyes and genital symptoms, photograph representative fresh lesions with consent and review medicines, neurological disease and infection risk.
- Take a blister-edge specimen into formalin for routine histology and a separate normal-appearing perilesional specimen into the laboratory-specified immunofluorescence medium.
- Request BP180 and BP230 serology and specialist salt-split testing when needed, then reconcile every result with lesion age, biopsy site and treatment exposure before assigning the diagnosis.
Pemphigoid is confirmed or strongly supported and topical application can be performed safely over all active skin.
- Dermatology defines the clobetasol quantity from disease extent, age and frailty and teaches thin application to active and recently active areas rather than individual intact blisters alone.
- Arrange carers, district nurses or admission when self-application is impossible, and protect erosions with non-adherent dressings and infection-aware washing.
- Once new blister formation stops, taper application and cumulative quantity gradually against objective activity while checking skin atrophy and systemic steroid absorption.