We report a patient with primary hypothyroidism, who developed hepatocellular injury due to levothyroxine, synthetic thyroxine. A 63-year-old

3893), and even ERCP findings were significantly improved in 2 cases. Our retrospective investigation suggests that SASP is more effective to normalize hepatobiliary enzymes compared with other treatments. Interestingly, SASP was much more effective than oral 5-aminosalicylates (mesalazine, 5-ASA), which was used for IBD patients with PSC (Table 1).The mechanism of therapeutic action of SASP for PSC is not clear. One hypothesis is that SASP improves inflammation of the colonic mucosa, which then results in a decrease in translocation of bacteria and toxins into the portal tract. This hypothesis, however, is inconsistent with our observation because oral 5-ASA was ineffective. The majority of SASP passes directly into the colon and is digested by bacterial enzymes into sulfapyridine and 5-ASA. 4 5-ASA is antiinflammatory 5,6 and is the primary therapeutic compound in SASP, whereas sulfapyridine has been said to be of no value for treatment of bowel inflammation. However, sulfapyridine is effective for rheumatoid arthritis and possesses antibacterial activity, and the action of this component might be an alternative explanation of the observed efficacy. A large randomized and controlled study is warranted to clarify the efficacy of SASP in patients with PSC.

These data indicate that increased serum bile acids will not affect the pharmacokinetics of pravastatin in patients with hepatobiliary diseases. Although pravastatin inhibited biliary taurocholate excretion, it is unlikely that pravastatin significantly inhibits biliary bile acid excretion by its therapeutic doses.

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