To the Editor: Levofloxacin, the active l-isomer of ofloxacin, is a new broad-spectrum bactericidal fluoroquinolone antibiotic that has gained wide acceptance in the treatment of a variety of infectious diseases. We also suspect that interventional pulmonologists use this antibiotic especially for postobstructive pneumonia. The drug is primarily eliminated by renal excretion without formation of pharmacologically relevant metabolites.1 Fluoroquinolones may transiently increase liver enzymes and fatal subfulminant hepatitis associated with ofloxacin has been signaled.2 Levofloxacin is generally well tolerated and has fewer reported side effects. We report a case of acute hepatitis associated with levofloxacin. An 89-year-old woman was admitted to our hospital with cough, yellow sputum, and fever of 2 days of evolution. Outstanding in her past medical history was arterial hypertension, noninsulin-dependent diabetes mellitus, and cardiac insufficiency. For more than 3 years the patient had been receiving treatment with diuretics and angiotensin-converting enzyme inhibitors (enalapril). One month earlier her liver enzymes were normal. There was no history of previous transfusion. On admission, physical examination was compatible with a lower respiratory tract infection. A chest x-ray revealed consolidation in the left lower lobe. She was empirically treated with levofloxacin 400 mg daily intravenous. The symptoms and the fever were improving by the third day of treatment. Biochemical determinations showed increase of aspartate aminotranferase: 958 IU/L (normal; 6 to 32), alanine aminotransferase: 1261 IU/L (N: 6 to 31), gamma-glutamil transpeptidase: 1126 IU/L (N: 5 to 36), and alkaline phosphatase: 77 IU/L (N: 35 to 104). Bilurubin, level of albumin, and prothrombin time were normal. Serology for hepatitis A, B, C, cytomegalovirus, Epstein-Barr, and a screening for autoantibodies were negative. Ultrasonography of the abdomen was normal. Use of levofloxacin was discontinued and 6 weeks later the liver function tests were normal. We believe this case represents an unequivocal association between levofloxacin and acute hepatitis. Liver disease was probably related to levofloxacin intake because of temporal relationship with appearance of symptoms, resolution of altered biochemical parameters after discontinuing this medication, and other causes of acute hepatitis were ruled out. The manufacturer indicates that the transaminases may be abnormal during a course of levofloxacin treatment. In a short-term clinical study comparing levofloxacin 500 mg twice daily and ceftriaxone in treatment of pneumonia, an increase in aspartate aminotranferase and alanine aminotransferase levels were observed in 3.5% and 4.8% of the 314 patients, respectively, in the levofloxacin group.3 Previously, there has been reported 5 cases of acute hepatitis associated with levofloxacin.4–8 A patient died in hepatic coma.8 Interventional pulmonologists should be aware of the possibility of acute hepatitis associated with levofloxacin when prescribing this drug. Bujanda Luis, MD, PhD Nerea Muro, MD Angel Cosme, MD, PhD Maria A. Gutiérrez-Stampa, MD, PhD Mikel Larzabal, MD Juan Ignacio Arenas, MD, PhD Department of Internal Medicine Donostia Hospital, San Sebastián, Spain