261 Colchicine Induced Myopathy in a Tacrolimus-Treated Renal Transplant Recipient

Abstract

COLCHICINE INDUCED MYOPATHY IN A TACROLIMUSTREATED RENAL TRANSPLANT RECIPIENT Samitha Reddy, Zeenat Bhat, Mona Doshi and Elizebeth Wilpula. Detroit Medical Center, Detroit, Michigan. Colchicine induced myopathy is well described in literature. Several cases of colchicine toxicity have been reported in cyclosporine-treated patients due to a drug-drug interaction. However, to our knowledge, none have been reported in patients on tacrolimus. A 62-year-old African American male underwent a deceased donor renal transplant 4 years ago and had been doing well on tacrolimus-based immunosuppression. He presented to the clinic with an episode of gout and was started on colchicine 0.6 mg to be taken twice daily. After a few days, he was noted to have a four fold increase in AST (52 to 209 units/L) and an elevated CPK (9084 units/L). A stable therapeutic concentration of tacrolimus (6.1ng/mL), stable creatinine (1.2 mg/dL) and WBC were documented. His other medications were mycophenolate mofetil, omeprazole, allopurinol, losartan, atenolol, nifedepine, and vardenafil. He was not drinking grapefruit juice, or taking over-the-counter or herbal supplements. Colchicine toxicity was suspected and the drug was discontinued with prompt decrease of CPK to 5204 units/L in 3 days. Muscle and liver enzymes returned to normal in 2 months. Cyclosporine is a P-glycoprotein and CYP3A4/5 inhibitor causing increased colchicine absorption and decreased elimination. We hypothesize that tacrolimus, a weak inhibitor of P-gp and CYP3A4/5 increased the susceptibility of our patient to colchicine toxicity.