Gatifloxacin-induced rhabdomyolysis

P George¹, J Das¹, B Pawar², D Badyal³,  
¹ Department of Internal Medicine, Christian Medical College and Hospital, Ludhiana - 141 008, India
² Department of Nephrology, Christian Medical College and Hospital, Ludhiana - 141 008, India
³ Department of Pharmacology, Christian Medical College and Hospital, Ludhiana - 141 008, India

Correspondence Address:
P George
Department of Internal Medicine, Christian Medical College and Hospital, Ludhiana - 141 008
India

Full Text

Flouroquinolone antibiotics cause musculoskeletal adverse effects like myalgia, arthralgia, tendon disorders and rhabdomyolysis. [1] Ofloxacin and levofloxacin rarely cause rhabdomyolysis, [2] but gatifloxacin has not yet been reported to cause rhabdomyolysis.

A 50-year-old male was admitted with intermittent fever and lower urinary tract symptoms for two days. No oliguria or dark urine was noticed. No alcohol abuse, illicit drugs, unprescribed medication use, unaccustomed exercise or trauma was present. A routine health evaluation two months prior was normal. Clinical examination at admission was unremarkable.

Renal failure (blood urea 52 mg/dl, serum creatinine 3.2 mg/dl, serum potassium 5.8 meq/dL, metabolic acidosis) with leucopenia (total leucocyte count 3200/mm 3 ) was observed. Bacteriuria was present on urine microscopy (urine white blood cells 60/HPF). Leptospira antibodies were negative. Ultrasonography of the kidneys was normal. He was treated with intravenous gatifloxacin 200 mg once daily.

The renal failure worsened over the next three days (blood urea 100 mg/dl, serum creatinine 5.5 mg/dl, worsening metabolic acidosis) and he complained of severe muscular pain and weakness. Grade 4 muscle power with generalized muscle tenderness and an inability to sit up, stand or walk unsupported was noticed. The serum muscle enzymes were elevated [creatinine phosphokinase (CPK) 5915 U/L, lactate dehydrogenase (LDH) 1466 U/L, serum glutamic oxaloacetic transaminase (SGOT) 364 U/L.] Urine and serum myoglobin were not significantly raised. Hypocalcemia (serum calcium 6.6 mg/dl), hypophosphatemia (2 mg/ dL), hyperuricemia (serum uric acid 10.4 mg/dL) and thrombocytopenia (platelet count 96000/cu mm) developed. Creatinine phosphokinase peaked at 7314 U/L. Electromyography did not show evidence of myopathy.

Gatifloxacin-induced rhabdomyolysis was considered and intravenous cefoperazone/sulbactam 1 g twice daily was used instead, along with rehydration and furosemide-alkaline diuresis. Twenty-four hours after stopping gatifloxacin, his renal functions improved and a downward trend of muscle enzymes was noticed. Five days later his renal function normalized and the muscle enzymes declined significantly (CPK 304 U/L, LDH 751 U/L, SGOT 145 U/L) with resolution of all muscle symptoms. He was discharged with a word of caution on future use of quinolones. He did not come for review subsequently.

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