Disabling bullosis diabeticorum despite optimal type 2 diabetes control

© BMJ Publishing Group Limited 2022. No commercial reuse. See rights and permissions. Published by BMJ. DESCRIPTION A woman in her 80s with type 2 diabetes diagnosed 10 years prior, hypertension, lowgrade carotid artery stenosis, stage 2 chronic kidney disease, hypothyroidism and severe obesity arrived at the consultation with a 7cmwide tenseroof bulla on the dorsum of the right foot that had developed 2 days prior and prevented her from wearing closed shoes (figure 1). The temperature was 37.1°C, the heart rate was 74 beats/min and the blood pressure was 138/96 mm Hg. There was no pruritus, no surrounding inflammation, no Nikolski’s sign, no AsboeHansen sign, a normal monofilament test result, no mucosal lesion and perceived tibial pulses. Daily treatment included acetylsalicylic acid 75 mg, hydrochlorothiazide 25 mg, irbesartan 300 mg, gliclazide 60 mg, levothyroxine sodium 50 g and metformin 850 mg, plus dulaglutide 0.75 μg as one subcutaneous injection per week. No cognitive impairment existed; there had been no trauma or recent newdrug intake; the glycated haemoglobin had been below 7.5% for more than a year; and the followup eye exam revealed no signs of diabetic retinopathy. A blood test showed haemoglobin at 11 g/ dL, leucocytes at 6.7 g/L (neutrophils: 4.49 g/L; eosinophils: 0.14 g/L), glucose at 7.48 mmol/L, glycated haemoglobin at 7.5%, creatinine at 76 μmol/L, serum albumin at 32 g/L, C reactive protein less than 10 mg/L and normal liver enzymes. The rightfoot blister ruptured spontaneously, leaving an erythematous wound that healed in 1 month with the triweekly application of hydrocellular foam dressings. A second blister formed on the right leg (figure 2) and immediately ruptured. A biopsy of the postbullous erythema revealed angiodermatitis with papillary and reticular dermal angiogenesis, neovessel endothelial turgidity and lymphocytic perivascular inflammation. Direct immunofluorescence studies were negative. Cultures were also negative. Bullosis diabeticorum (BD) was diagnosed based on these findings and the clinical history. Other blisters formed on the lower limbs in the following months, causing pain, daily discomfort and footwear issues; then they ceased. At the 1year consultation, no new blisters had developed in the past 6 months, the glycated haemoglobin level was 7.3%, which is optimal because it was below 7.5%, and there was still no diabetic retinopathy or peripheral neuropathy. BD is an infrequent, noninflammatory, diabetesrelated skin complication. The differential diagnosis includes bullous pemphigoid, friction bullae, oedemainduced bullae, bullous fixed drug reaction and epidermolysis bullosa acquisita. The annual incidence is expected to be 0.16% in patients with diabetes mellitus. Though the prognosis is favourable, BD may impair quality of life, particularly if the blister is large. 7 To avoid infectious or haemorrhagic complications and achieve a quick healing