Tacrolimus is a reversible calcineurin inhibitor. It is commonly used as an immunosuppressive drug in the treatment of T cell mediated diseases such as polymyositis, graft rejection in solid organ transplant, graft-versus-host disease in hematopoietic stem cell transplant, and is postulated to have diabetogenic potential. Fluconazole, on the other hand, is frequently prescribed antifungal therapy. Fluconazole increases the serum level of tacrolimus into the supratherapeutic range, thus developing drug toxicity if the dose is unadjusted. Diabetic ketoacidosis is a rare adverse drug effect reported with the use of tacrolimus. In this report, we present a case of DKA in a 60-year-old woman with polymyositis on low dose corticosteroids and tacrolimus, precipitated by the use of fluconazole. We highlight the pathophysiologic mechanisms underlying the effect of fluconazole on tacrolimus levels causing an accelerated development of DKA along with the review of literature on this potentially life-threatening condition.
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