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Acne keloidalis nuchae in renal transplant patients receiving tacrolimus and sirolimus

Acne keloidalis nuchae (AKN) is a chronic inflammatory scarring condition usually found on the nape of the neck or occipital scalp of dark-skinned young men. We report two cases of drug-related AKN following organ transplantation. The first patient, a 52-year-old, blue-eyed Caucasian man, had received a renal transplant 8 years previously, after developing renal failure due to occupational mercury poisoning. His immunosuppressive regimen consisted of sirolimus 4 mg/day, mycophenolate mofetil 1500 mg/day and prednisone 5 mg/day. He was also taking atenolol and hydralazine. One year after the transplantation he noticed the onset of occipital pustules that evolved into pruritic papules. On examination, firm, grouped, hypertrophic follicular papules were found in the occipital region (Fig. 1). Skin biopsy results were consistent with the clinical diagnosis of AKN. Treatment was started with topical mupirocin and intralesional dexamethasone with a notable reduction in the size of lesions. The second patient, a 27-year-old woman of mixed race, had undergone a renal transplant 2 years previously due to diabetic nephropathy. Her treatment included tacrolimus 6 mg/day, mycophenolate sodium 1440 mg/day, prednisone 5 mg/day and insulin. Six months after the transplantation, she noticed pruritic areas on her scalp. On examination, reddish-brown hypertrophic hairless papules were found in the occipital region. Intralesional dexamethasone resulted in a marked amelioration of the lesions, except for an area of scarring alopecia. There has been an increasing number of reports of drug-related AKN in organ transplant recipients taking the calcineurin-inhibitor cyclosporin, though none were of dark-skinned ethnicity. In 2000, Azurdia and colleagues first reported cyclosporin-related AKN following organ transplantation in three Caucasian men. Interestingly, Carnero and colleagues noted that the severity of the lesions fluctuated with changes in the dosage of cyclosporin in one patient. The pathogenesis of AKN remains poorly understood. Cyclosporin-related AKN probably has multiple trigger factors, such as bacterial infections, immunosuppression, pseudofolliculitis and cyclosporin-induced hypertrichosis. The immunosuppressive regimen of our patients did not include cyclosporin. One patient was treated with tacrolimus, also a calcineurin inhibitor. The other patient received sirolimus, an immunosuppressant with a mechanism of action independent of calcineurin. Although both cyclosporin and tacrolimus (but not sirolimus) have been shown to induce anagen and inhibit spontaneous catagen development in mice, switching from cyclosporin to tacrolimus or sirolimus in organ-transplant recipients has been reported to result in the resolution of hypertrichosis. Such diverging data, along with the paucity of reported cases, hampers analysis of the possible implications of hair growth control by immunosuppressants in the pathogenesis of AKN. Both patients were also taking the antimetabolite mycophenolate, but none of the putative trigger factors of drug-related AKN considered so far is among its common adverse effects. To our knowledge, this is the first report of AKN following transplantation in patients receiving tacrolimus and sirolimus, and the first report involving a female patient. It is difficult to evaluate the precise role of cyclosporin and other immunosuppressants in the pathogenesis of AKN, as these patients are commonly treated with a number of drugs. Recent case reports of drug-related AKN in immunosuppressed transplant patients emphasise the need to monitor these patients closely in order to clarify its pathogenesis.