was admitted to hospital. Physical examination findings were normal except for jaundice. Serum chemistry showed total bilirubin of 28.45 mg/dl (normal = 0.3–1.3); conju- gated bilirubin, 20.6 mg/dl (normal = 0 – 0.4); ALP, 249 U/L (normal = 35–120); AST, 37 U/L (normal = 5– 40), and ALT, 58 U/L (normal = 5– 40). Abdominal ultrasonog- raphy, CT scan, and cholangiography magnetic resonance were normal and ruled out obstruction of the bile ducts. Serology excluded viral causes. Screening for autoantibod- ies and metabolic diseases was negative. A liver biopsy specimen showed predominantly casts in canaliculi and mild portal inflammatory infiltrates with lymphocytes and eosinophils. Results of liver tests became normal during the subsequent 2 months. Trovafloxacin, another new quinolone, has been with- drawn from the market in Europe and limited to life-threat- ening conditions in the United States because of hepatic toxicity (3– 6). This is, to our knowledge, the first published report of liver injury due to moxifloxacin. Other causes of liver injury were ruled out. The histological picture was consistent with drug-induced hepatic injury. It is noteworthy that there was a delay of 3 wk between the end of the treatment and the onset of jaundice that may hinder the diagnosis. Santiago Soto, M.D. Leopoldo Lo ´pez-Rose ´s, M.D. Susana A ´ vila, M.D. A ´ ngel Lancho, M.D. Abel Gonza ´lez, M.D. Eva Santos, M.D. Begon ˜a Urraca, M.D. Digestive Diseases Unit Hospital Xeral de Lugo Lugo, Spain REFERENCES 1. Culley CM, Lacy MK, Klutman N, et al. Moxifloxacin: Clinical efficacy and safety. Am J Health Syst Pharm 2001;58:379 – 88. 2. Landen H, Moller M, Tillotson GS, et al. Clinical experience in Germany of treating community acquired respiratory infections with the new 8-methoxyfluoroquinolone, moxyfloxacin. J Int Med Res 2001;29:51– 60. 3. Bertino J Jr, Fish D. The safety profile of the fluoroquinolones. Clin Ther 2000;22:798 – 817. 4. Chen HJL, Bloch KJ, MacLean JA. Acute eosinophilic hepatitis from trovafloxacin. N Engl J Med 2000;342:359 – 60. 5. Ball P. Future of the quinolones. Semin Respir Infect 2001;16: 215–24. 6. Zhanel GG, Ennis K, Vercaigne L, et al. A critical review of the fluoroquinolones: Focus on respiratory infections. Drugs 2002; 62:13–59. Reprint requests and correspondence: Santiago Soto Iglesias, M.D., “Unidad de Endoscopias,” Hospital Xeral de Lugo, Ru ´a Severo Ochoa s.n., 27004 Lugo (Galicia), Spain. Received Feb. 4, 2002; accepted Feb. 18, 2002. Chronic Hepatitis C, Ibuprofen, and Liver Damage TO THE EDITOR: Riley and Smith reported in 1998 (1) three patients with chronic hepatitis C who developed marked elevations in liver transaminases after taking ibu- profen. No other cases have been reported thereafter, and the plausibility of such an association has recently been ques- tioned (2, 3). We describe an additional patient with chronic hepatitis C who experienced an increase in liver tests in the range of acute hepatitis during a course of ibuprofen. A 57-yr-old active homosexual man was diagnosed as having chronic hepatitis C (HCV antibody positive by the second generation ELISA assay) in 1996 during a routine evaluation to discard HIV infection. Confirmatory analysis included HCV RNA by reverse transcription polymerase chain reaction (1,390,000 copies/ml). Baseline liver chem- istry was abnormal for an AST of 99 IU/L and for an ALT of 130 IU/L. A liver biopsy showed chronic active hepatitis with bridging fibrosis. He was intolerant to interferon alfa-2b (3 MU three times weekly) started in early 1997, and routine liver tests performed every 6 months thereafter showed values similar to baseline. In late 2000 he was prescribed ibuprofen (600 mg b.i.d.) for painful abdominal hernia. Liver transaminases 30 days after initiation of ibu- profen were as follows: AST, 355 IU/L; ALT, 1,093 IU/L; and -glutamyltranspeptidase 355 IU/L. He drank alcohol occasionally in the past, but denied current intake as well as the use of any other medication or herbal remedies. Screen- ings for viral hepatitis A and B, cytomegalovirus, herpes- virus, and Epstein-Barr virus were negative, as was repeated testing for HIV infection. Ibuprofen was stopped and 3 months later the AST level was 52 IU/L; ALT, 119 IU/L; and -glutamyltranspeptidase, 41 IU/L. No new elevations in liver enzymes have been noted in the follow-up. The patient discussed here had a flare of ALT markedly exceeding those usually seen in the natural outcome of chronic hepatitis C. In fact, this prompted us to search for a superimposed factor. A drug-induced etiology should al- ways be kept in mind, especially when other common causes of acute hepatitis have been ruled out. This patient had been taking ibuprofen several days before symptoms appeared. Assessment of this case by the Council for Inter- national Organizations of Medical Sciences (CIOMS) scale yields a score of 9 points for ibuprofen, which falls into the category of highly probable (4). As in the cases previously reported (1), the pattern of hepatic injury was hepatocellu- lar. In addition, the absence of the hallmarks of hypersen- sitivity (fever, rash, and eosinophilia) does not support an immunological idiosyncrasy. Ibuprofen is thought to be far less hepatotoxic than other nonsteroidal anti-inflammatory drugs (NSAIDs), with an estimated incidence of acute liver injury of 1.6/100,000 users (5). No other instances of ibuprofen-associated hepa- totoxicity in patients with chronic liver disease unrelated to 1854 Letters to the Editor AJG – Vol. 97, No. 7, 2002