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The Annals of Pharmacotherapy: Vol. 37, No. 12, pp. 1821-1824. DOI 10.1345/aph.1D188
© 2003 Harvey Whitney Books Company.
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Colchicine-Induced Myopathy in a Teenager with Familial Mediterranean Fever

Mehmet Sayarlioglu, MD

Assistant Professor, Chief of Rheumatology, Department of Internal Medicine, Division of Rheumatology, Medical Faculty, Yuzuncu Yil University, Van, Turkey.

Hayriye Sayarlioglu, MD

Assistant Professor, Department of Internal Medicine, Division of Nephrology, Medical Faculty, Yuzuncu Yil University

Suleyman Ozen, MD

Assistant Professor, Department of Pathology, Medical Faculty, Yuzuncu Yil University

Reha Erkoc, MD

Associate Professor, Chief of Nephrology, Department of Internal Medicine, Division of Nephrology, Medical Faculty, Yuzuncu Yil University

Ahmet Gul, MD

Associate Professor, Department of Internal Medicine, Division of Rheumatology, Istanbul Medical Faculty, Istanbul University, Istanbul, Turkey

Reprints: Mehmet Sayarlioglu MD, Yuzuncu Yil Universitesi, Tip Fakultesi, Arastirma Hastanesi, Ic Hastaliklari AD, Romatoloji BD, 65200 Van, Turkey, FAX 90 432 2155051, sayarli{at}hotmail.com

OBJECTIVE: To report a case of colchicine-induced myopathy in a teenager with familial Mediterranean fever (FMF).

CASE SUMMARY: A 15-year-old boy of Turkish origin, diagnosed as having FMF at the age of 14 years, was treated with colchicine 1.5 mg/d. He had experienced only 2 mild peritonitis attacks with fever within 1 year. The patient used the recommended dose regularly, and he described progressive proximal muscle weakness and generalized myalgias, which started 1 month before presentation. Physical examination showed proximal muscle weakness in his arms and legs. Laboratory tests revealed elevated serum creatine kinase, aspartate aminotransferase, alanine aminotransferase, and lactate dehydrogenase. All other laboratory values were within normal range. Electromyographic investigation revealed a myopathic pattern in proximal muscles without any neuropathic changes. A biopsy of the deltoid muscle showed vacuolar degeneration of striated muscle fibers with no inflammatory findings.

DISCUSSION: Colchicine, the most important drug in treatment of FMF, can cause myopathy in patients with impaired renal and hepatic function. In our patient, an objective causality scale showed that therapeutic doses of colchicine for FMF were the definite cause of myopathy, even though his renal and hepatic function were normal. The treatment of FMF attacks in patients who cannot use colchicine is an important problem. There are insufficient data about the use of immunosuppressive agents in the treatment of FMF attacks; however, we now successfully control the attacks with colchicine 0.5 mg/d and azathioprine 2 mg/kg/d.

CONCLUSIONS: Colchicine-induced myopathy should be excluded in patients with FMF who present with generalized muscle weakness. Clinicians should be aware that myopathy can occur in patients with FMF who have normal renal and hepatic function.

Key Words: colchicine, familial Mediterranean fever, myopathy

Published Online, October 29, 2003. www.theannals.com, DOI 10.1345/aph.1D188


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