Nilgün Güvener

A possible case of gynecomastia with fluoxetine.

ocardial band, troponin-T, viral markers, and serologic screening were normal. The patient was treated with an infusion of NaCl 0.9%. Colchicine and fluvastatin were stopped. Intraarticular steroid was administered for acute gouty arthritis. As the patient’s urine output increased, serum creatinine and CK decreased steadily. He was discharged 19 days after admission, feeling well, with CK 70 U/L and creatinine 1.4 mg/dL. Fluvastatin was reinitiated after the CK level was normalized. Renal function of the patient was normal 2 months later. Discussion. Two different mechanisms may be responsible for the pathogenesis in our patient. Drug interactions that potentiate adverse effects may occur when colchicine is coadministered with a statin since both drugs are metabolized by cytochrome P450 isoenzymes and myotoxic effects are well known.2,3 Colchicine and fluvastatin, however, are cleared through 2 different CYP450 isoenzymes. The second possible mechanism is synergistic myotoxicity.4 Statin therapy is associated with myonecrosis, membranous myeloid bodies, and vacuolization. Finally, statins can disrupt cytoskeletal integrity. In addition to this, colchicine induces myopathy via disruption of tubular function with subsequent vacuolization. Concerning the potential cytoskeletal toxicity of colchicine and statins, it would appear that their combined use produced a synergistic drug-induced myopathy via both pharmacokinetic and related pharmacodynamic mechanisms. According to the Naranjo probability scale, our case suggests that rhabdomyolysis was probably related to colchicine.5 Patients on colchicine therapy should be informed about the possible muscular and gastrointestinal adverse effects and advised to stop this drug immediately if any symptoms occur. In addition, if colchicine is used together with fluvastatin in renally impaired patients, one should be cautious about myotoxicity.