Bullous Diabeticorum

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A 25-year-old male patient known for poorly controlled type 1 diabetes mellitus, presented with 1-day history of acute onset asymptomatic blister on right leg. It was not preceded by trauma, an insect bite or application of any products. There was no recent introduction of new medications and he had no history of fever or constitutional symptoms. He denied any similar previous eruptions. Skin examination revealed tense bullae of approximately 8 × 15 cm on his right lateral leg with mild rim of erythema [Fig. 1]. There were no oedema, mucosal involvement or lymphadenopathy and Nikolsky sign was negative. Differential diagnoses included bullous diabeticorum, exaggerated bullous insect bite reaction, bullous fixed drug reaction and immunobullous disorders. His glycated haemoglobin ranged between 14–15%. Skin biopsy revealed cell poor subcorneal blister with no inflammatory or acantholytic cells [Fig. 2]. Immunofluorescence for IgA, IgG, IgM and C3 were negative from perilesional skin. Fluid swab culture grew light growth of staphylococcus argenteus. Subsequently, he was diagnosed with bullous diabeticorum and managed with optimal wound care and prophylactic systemic antibiotic to prevent bacterial superinfection given large area of involvement. He healed completely in 10 weeks with post inflammatory hyperpigmentation.

1. Comment

Bullous diabeticourm is a rare cutaneous complication of diabetes mellitus. It is characterised by the abrupt spontaneous onset of asymptomatic non inflammatory bullous eruption.^1^ It preferentially occurs on distal acral areas, lower extremities followed by upper extremities and rarely the trunk.^2^ Its aetiology is not fully known but multifactorial theories and hypotheses have been proposed. Microangiopathy, sympathetic autonomic denervation, increased venous pressure, diabetic neuropathy, ultraviolet exposure and trauma are some suggested mechanisms for the formation of diabetic bullae.^12345^ There is risk of recurrence at the same or different sites.^5^ It could be complicated by secondary bacterial infection and rarely osteomyelitis.^15^

Differential diagnoses include autoimmune blistering disorders (e.g., bullous pemphigoid, porphyria cutanea tarda, pseudoporphyria) and friction or oedema blister.^5^ Diagnosis is mainly clinical; however, other autoimmune blistering disorders could be excluded with direct immunofluorescence. Culture from the fluid is advised if secondary bacterial infection is suspected.^25^ Diabetic bulla affects mainly diabetic patients with long standing disease with complications. Although it is often linked to poor glycaemic control, the association between its occurrence and glycaemic control seems inconsistent.^2^ In the United States, its incidence is 0.5% of diabetic population and males are twice as affected as females.^3^

Supportive therapy is the mainstay of treatment as it is a self-limiting condition. Aspiration of the fluid to prevent accidental deroofing and wound care are suggested in large bullae. Resolution generally occurs with 2–6 weeks.^12^ In the current case, diagnosis was supported with history and clinical morphology. Pathology ruled out other differential diagnoses and his swab culture grew light growth of Staphylococcus argenteus, which was thought to be due to contamination rather than infection as no clinical or pathological features were suggestive of infection.

Authors' Contribution

Maisam Al Salmani: Investigation, Visualization, Writing - Original Draft. Ayida Al Khalili: Project administration, Supervision, Writing - Review & Editing. Maya Al Bahri: Investigation, Resources, Writing - Review & Editing.

Ethics Statement

Patient consent was obtained for publication purposes.