A 41-year-old man with family history of diabetes mellitus was referred from a primary health centre with a 20-year history of insulin-dependent diabetes mellitus, a 4-year history of hypertension controlled with captopril and a 6-month history of small nodular lesions on both elbows. The patient was on simvastatin 20 mg/day for dyslipidaemia. The lesions progressively increased in size. The dermatologist decided to start treatment with intralesional corticosteroids as a treatment for keloids (fig 1) and took a biopsy. Examination of the patient revealed an adult male with multiple nodular lesions on his arms, elbows and back with long hypertrophied irregular, branching keloid-like lesions on his elbows and multiple nodular lesions on his back (fig 2). Blood pressure was 150/90 mm Hg in a sitting position. Full blood counts were normal. Fasting blood glucose was 11.7 mmol/l (normal 3.6–5.8 mmol/l), triglycerides 146 mmol/l (normal 0.6–1.7 mmol/l), serum total cholesterol 17.7 mmol/l (normal <5.2 mmol/ l), low density lipoprotein 11.1 mmol/l (normal <4 mmol/l) and high density lipoprotein 0.65 mmol/l (normal >0.8 mmol/l for males). Serum uric acid level and liver enzymes were normal. The patient had no evidence of neuropathy but had early retinopathy and microalbuminuria of 0.45 g/24 h. The patient was started on enlapril 10 mg/day, gemfibrozil 1.2 g/day, simvastatin 80 mg/day and the insulin dosage was adjusted to 60 units/day (Mixtard 30/70). Two weeks later the patient’s fasting lipid profile revealed triglycerides 4.0 mmol/l, cholesterol 4.2 mmol/l, low density lipoprotein 5.3 mmol/l and high density lipoprotein 0.8 mmol/l. Fasting blood sugar was 6.7 mmol/l, but liver and muscle enzymes were almost twofold increased (normal range for aspartate aminotransferase 10–45 U/l, alanine aminotransferase 10–50 U/l, lactate dehydrogenase 200–260 U/l, creatine phosphokinase 55–170 U/l). Blood pressure was 120/80 mm Hg. The skin lesions were diagnosed as eruptive xanthomas with spontaneous Koebner phenomenon and biopsy of one of the lesions was consistent with keloid and areas of lipid laden cells (fig 3). The patient is being regularly followed up. Liver enzymes and muscle enzymes returned to normal levels within 1 month and now 6 months after aggressive treatment for dyslipidaemia, the lesions seem to have regressed in size. We report this interesting second case of type 1 diabetes mellitus, hypertension, hypertriglyceridaemia type V and eruptive xanthomas with spontaneous Koebner phenomenon.

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Figure 1

Eruptive xanthomas as popular lesions with early koebnerisation and keloid formation.

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Figure 2

Eruptive xanthomas on the back of the patient.

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Figure 3

Biopsy of lesion showing scarring of keloid and lipid laden macrophages (H&E).

Eruptive xanthomas have been well reported in patients with diabetes mellitus and hypertriglyceridaemia.1 The Koebner phenomenon, which is well described for diseases such as psoriasis,2 has been reported in a single case report of eruptive xanthomas in hypertriglyceridaemia,3 but the management is that of diabetes mellitus and dyslipidaemia.