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	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

We read with interest the recent case report of acute fulminant hepatitis ascribed to the use of rabeprazole.¹ This case exemplifies the difficulty in establishing the role of a drug in hepatic reaction when the patient is being treated with several other drugs simultaneously. Assessment of this case by the CIOMS (Council for International Organizations of Medical Sciences) scale yields a score of 8 points for terbinafine, which falls into the category of "probable," while causality assessments for rabeprazole and citalopram yield scores of 5 points each, falling into the category of "possible." Of note, for drugs with unrecognized hepatotoxic potential (such as rabeprazole), diagnostic scales tend to underestimate causality.²

However, the arguments posed by Johnstone et al¹ that rabeprazole was the cause of the episode of acute hepatitis are not convincing. To rule out terbinafine, Johnstone et al¹ focus on the characteristic signature of clinical and histopatologic features of . . . [Full Text of this Article]

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