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Clinical Specialist Liver Unit Department of Gastroenterology School of Medicine Virgen de la Victoria University Hospital Málaga, Spain
Clinical Specialist Associate Professor of Clinical Pharmacology School of Medicine Virgen de la Victoria University Hospital
Head of Liver Unit Associate Professor of Medicine Department of Gastroenterology School of Medicine Virgen de la Victoria University Hospital Campus de Teatinos s/n. 29071-Málaga Spain andrade{at}uma.es FAX 34-952-131511
Clinical Specialist Department of Gastroenterology Hospital Valme Sevilla, Spain
Clinical Specialist Clinical Pharmacology Unit Hospital Torrecárdenas Almeria, Spain
Published Online, October 1, 2003. www.theannals.com, DOI 10.1345/aph.1C268
Case 1. A 33-year-old man was prescribed lansoprazole 30 mg/d for peptic esophagitis. He reported alcohol intake (50 g/d) but denied the use of any other medication or illicit drugs. His baseline liver function test values were normal. He was asymptomatic, and physical examination was unremarkable. Serum chemistry was suggestive of acute liver injury (Table 1); serology ruled out viral causes. Screening for autoantibodies was negative, and findings on abdominal ultrasonography were normal. Lansoprazole was withdrawn; hepatic parameters performed within 3 months were normal. Seven months later, the patient was inadvertently rechallenged, and alanine aminotransferase (ALT) values increased 2.5 times over the normal upper limit. Normalization was achieved after 3 months.
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Case 2. A 44-year-old man was treated with lansoprazole 30 mg/d and domperidone for peptic esophagitis and duodenitis. Twenty days later, he presented with a 1-week history of asthenia, weight loss, and pruritus. Two years earlier, when a cholecystectomy was performed, he had ALT levels of 47 units/L. He had no toxic habits and was taking no other drugs or herbal remedies. Laboratory results indicated cholestatic injury without evidence of viral causes (Table 1). Screening for autoantibodies was negative, and an abdominal ultrasonography showed no expanded bile ducts. Lansoprazole was withdrawn (but not domperidone) and laboratory findings returned to baseline at 26 days.
Discussion. Two cases of significant liver damage due to lansoprazole have been published, one of them in the context of a hypersensitivity syndrome.2,3 The role of lansoprazole is supported because other causes of liver damage were ruled out, there was a temporal relationship between drug administration and subsequent development of liver disease, and liver function tests improved after withdrawal of the drug. Also, the serum biochemistry pattern was not consistent with alcoholic hepatitis. Furthermore, recurrence of the illness upon inadvertent drug rechallenge in Case 1 implies the drugdisease association. According to the Naranjo probability scale, the relationship between lansoprazole and the adverse reaction in these cases was rated possible and probable, respectively.4
The mechanism of lansoprazole-induced impairment in liver profile remains unknown, but the lack of a dose-dependent effect and delayed onset of hepatic dysfunction are in keeping with metabolic idiosyncrasy, although the eosinophilia presented in the second case suggests that an immune mechanism might be operating in some cases.3
To date, a few cases of acute hepatocellular damage related to omeprazole, a widely used drug, have been published.5 Therefore, it is difficult to state that hepatotoxicity related to PPIs is a class effect due to the basic benzimidazole structure shared by these drugs. Since occurrence of cross-hepatotoxicity between PPIs has not been described, use of other agents in the same class would be considered only in absence of other options and under careful monitoring.
Footnotes
This report was in part supported by a research grant from Agencia Española del Medicamento.
References
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