MBBS viva · dermatology
Dermatitis herpetiformis — clinical viva
A 12-minute viva on DH recognition, biopsy handling, TG3, coeliac assessment, gluten-free diet, and dapsone safety.
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Q1: Recognition and mechanism (2 minutes)
What is dermatitis herpetiformis? [1][6]
DH is the gluten-driven cutaneous manifestation of coeliac autoimmunity. IgA complexes containing epidermal transglutaminase 3 (TG3) deposit in papillary dermis, recruit neutrophils, and produce a subepidermal blister. [1][6]
How does the patient present? [1][2]
Severe itch with symmetrical grouped papules, small vesicles, crusts, and excoriations on elbows, knees, buttocks, sacrum, scalp, neck, or upper back. Scratching may remove every intact vesicle. Gastrointestinal symptoms are often absent. [1][2]
TG2 is the principal coeliac/gut autoantigen and the target of routine anti-TG2 serology. TG3 is the principal DH skin autoantigen. The precise evolution from gut autoimmunity to papillary IgA–TG3 deposition remains incompletely defined; do not present simple TG2-to-TG3 cross-reaction as settled fact. [1][2]
Q2: Differential diagnosis (2 minutes)
Name the closest mimics and one discriminator for each. [2][6]
- Linear IgA bullous dermatosis: annular “string of pearls”; DIF shows linear IgA at the basement membrane zone.
- Bullous pemphigoid: older patient with larger tense bullae; DIF shows linear IgG/C3.
- Scabies: burrows, finger-web/genital distribution, itchy contacts, or a positive scraping.
- Atopic/contact dermatitis: eczematous flexural or exposure-shaped eruption without granular papillary IgA.
- Prurigo nodularis: firm scratch nodules without primary grouped vesicles. [2][6]
Q3: Biopsy and serology (3 minutes)
What is the gold-standard test, and exactly how do you take it? [2][3][6]
Take normal-appearing perilesional skin adjacent to an active lesion for DIF. Send it in the laboratory-approved immunofluorescence medium and keep it out of formalin. The diagnostic pattern is granular IgA in papillary dermis and/or along the dermoepidermal junction. Lesional/inflamed sampling has more false negatives. [2][3][6]
What does routine histology show? [2]
A separate fresh lesional biopsy in formalin may show neutrophilic microabscesses at dermal papillary tips and a neutrophil-rich subepidermal blister. It is supportive but can be nonspecific. [2]
Which blood tests help? [2][4]
Use IgA anti-TG2 with total IgA while the patient is eating gluten; follow an IgG pathway if IgA deficient. Anti-TG3 is more specific for DH than anti-TG2 and may support diagnosis when available, but it is not diagnostic alone; assays, availability, and cut-offs vary. EMA is reserved for selected unclear cases rather than required routinely. HLA-DQ2/DQ8 is useful mainly to exclude disease in selected uncertainty; a positive result is not diagnostic. [2][4]
Must every patient have duodenal biopsy? [1][2]
No. Correctly DIF-confirmed DH does not require duodenal biopsy simply to prove coeliac disease. Consider endoscopy when the skin diagnosis is uncertain, symptoms are severe or incongruent, tests conflict, or refractory coeliac disease/malignancy is suspected. [1][2]
Q4: Treatment and dapsone safety (3 minutes)
Give the treatment in one sentence. [1][2][3]
Use a strict lifelong, dietitian-led gluten-free diet as disease-modifying therapy; add short-term dapsone when rapid control is needed. The diet may take months to years to control skin disease, while dapsone works within hours to days but does not treat enteropathy. [1][2][3]
Give a safe adult dapsone regimen. [1][2]
After baseline assessment, start 25–50 mg orally once daily and increase gradually toward 100 mg daily only if needed, using the lowest effective dose. Mean withdrawal after effective GFD is about two years, with wide variation; do not promise stopping at 6–12 months. [1][2]
What do you check before and after starting? [2]
Check CBC with differential, G6PD activity, liver function, and renal function before treatment. One published protocol checks CBC weekly in month 1, every two weeks for the next eight weeks, then every 3–4 months; it checks liver tests every two weeks in month 1 and then every 3–4 months with renal function. Local protocols vary. Reticulocytes and methaemoglobin are checked when haemolysis or methaemoglobinaemia is suspected, not automatically as serial tests in every stable patient. [2]
Does normal G6PD testing eliminate haemolysis risk? [2]
No. G6PD deficiency markedly increases risk, but dose-related haemolysis and methaemoglobinaemia can occur with normal G6PD activity. Warn about fever/sore throat, jaundice, cyanosis, dyspnoea, rash with systemic illness, and unusual fatigue. [2]
Q5: Follow-up, complications, and traps (2 minutes)
What do you follow? [5]
Review rash control, dietary adherence, drug toxicity, coeliac serology when useful, and previously abnormal nutritional tests. Assess fracture risk and request DXA selectively; current adult guidance does not mandate baseline DXA in every low-risk patient. Repeat duodenal biopsy is symptom/risk-driven rather than routine. [5]
What about lymphoma surveillance? [2][5]
The absolute risk is low and long-term GFD lowers it. Do not schedule routine lymphoma imaging in asymptomatic uncomplicated disease. Investigate alarm symptoms such as persistent abdominal pain, weight loss, fever/night sweats, obstruction, or lymphadenopathy. [2][5]
What makes apparent DH “refractory”? [1][2][3]
First revisit the original DIF, the clinical diagnosis, and ongoing gluten exposure. Only after these are secure should a specialist consider alternative sulfonamides or the weak case-report evidence for other immunomodulators. Iodide and indomethacin may exacerbate established DH, but there is no accepted non-coeliac “drug-induced DH” subtype. [1][2][3]
Examiner's closing question: what single error most often loses the diagnosis?ShowHide
Taking the DIF specimen from an eroded blister or placing it in formalin. The correct answer is normal-appearing perilesional skin in the laboratory's immunofluorescence transport system.
References6ShowHide
- [1]Reunala T, Hervonen K, Salmi T. Dermatitis Herpetiformis: An Update on Diagnosis and Management Am J Clin Dermatol, 2021.PMID 33432477
- [2]Nguyen CN, Kim SJ. Dermatitis Herpetiformis: An Update on Diagnosis, Disease Monitoring, and Management Medicina (Kaunas), 2021.PMID 34441049
- [3]Görög A, Antiga E, Caproni M, et al. S2k guidelines (consensus statement) for diagnosis and therapy of dermatitis herpetiformis initiated by the European Academy of Dermatology and Venereology (EADV) J Eur Acad Dermatol Venereol, 2021.PMID 34004067
- [4]Al-Toma A, Zingone F, Branchi F, et al. European Society for the Study of Coeliac Disease 2025 Updated Guidelines on the Diagnosis and Management of Coeliac Disease in Adults. Part 1: Diagnostic Approach United European Gastroenterol J, 2025.PMID 40999951
- [5]Al-Toma A, Branchi F, Zingone F, et al. European Society for the Study of Coeliac Disease (ESsCD) 2025 Updated Guidelines on the Diagnosis and Management of Coeliac Disease in Adults. Part 2: Management, Follow-Up, and Complex Disease Courses United European Gastroenterol J, 2026.PMID 41831197
- [6]van Beek N, Holtsche MM, Atefi I, et al. State-of-the-art diagnosis of autoimmune blistering diseases Front Immunol, 2024.PMID 38903493