Spontaneous tendon rupture after ofloxacin treatment in renal transplant recipients on high-dose corticosteroids

Abstract

<h2>Abstract</h2> Acute tendon rupture without any history of trauma, a rare complication occurring mainly in metabolic diseases, is increasingly reported after treatment with fluoroquinolones. We report here on the occurrence of Achilles tendinitis and Achilles tendon rupture after ofloxacin treatment for uncomplicated urinary tract infection in four patients receiving high-dose corticosteroid treatment after renal organ transplantation and compare them with a control group without this complication. Patients experiencing tendon rupture had been on regular dialysis treatment for 54.5 ± 39.5 months before receiving cadaveric kidney transplants. All had secondary hyperparathyroidism, with parathyroid hormone levels ranging from 247 to 707 ng/L, had low or normal serum phosphate levels (1.21 to 2.69 mg/dL), and had moderately elevated alkaline phosphatase levels (75 to 285 U/L). Tendon ruptures occurred at a median of 49 days after organ transplantation and 15.3 ± 9.6 days after initiation of quinolone treatment. Mean time of treatment was 5 days. All patients received triple-regimen immunosuppression consisting of methylprednisolone, cyclosporin A, and mycophenolate mofetil. Transplant function was stable, and none had experienced transplant rejection. Mean ingestion of prednisolone ranged from 6 to 16 mg/d, and mycophenolate mofetil from 1 to 2 g/d; cyclosporin A serum levels were 208 ± 76 μg/L. After kidney transplantation, spontaneous large tendon rupture after quinolone treatment is deleterious during the early posttransplantion phase. Secondary risk factors are high-dose corticosteroid treatment and history of secondary hyperparathyroidism. Quinolones should be restricted for treatment of severe urinary tract infection only, which failed to respond to other antibiotic regimens in the early posttransplantation period after kidney transplantation under high-dose corticosteroid treatment.