Development of osteomalacia in a post-liver transplant patient receiving adefovir dipivoxil.

We report the case of a patient treated with living donor-related liver transplantation who suffered from osteomalacia during adefovir dipivoxil (ADV)-containing antiviral therapy for lamivudine-resistant hepatitis B virus infection. The patient had generalized bone pain, with severe hypophosphatemia after 20 mo of ADV therapy. Radiographic studies demonstrated the presence of osteomalacia. The peak plasma ADV level was 38 ng/mL after administration of ADV at 10 mg/d. It was also found that ADV affected the metabolism of tacrolimus, a calcineurin-inhibitor, and caused an increase in the plasma levels of tacrolimus. The disability was reversed with the withdrawal of ADV and with mineral supplementation. ADV can cause an elevation of plasma tacrolimus levels, which may be associated with renal dysfunction. High levels of ADV and tacrolimus can cause nephrotoxicity and osteomalacia. This case highlights the importance of considering a diagnosis of osteomalacia in liver transplantation recipients treated with both ADV and tacrolimus.

[A case of advanced hepatocellular carcinoma effectively treated with 5-fluorouracil and high-concentration cisplatin suspended in lipiodol by short-term hepatic arterial infusion chemotherapy].

A 75-year-old Japanese man was admitted to our hospital for treatment of advanced hepatocellular carcinoma (HCC) with HCV-related liver cirrhosis. He had been treated earlier with transarterial chemoembolization (TACE) in both another and our own hospital before this admission. At this time, abdominal CT revealed multiple HCCs (maximum 4.0 cm in diameter) located in hepatic S6, S5, and S8. An infused port system had been subcutaneously implanted, and he was treated with hepatic arterial infusion chemotherapy with 3 days' FPL (5-FU at a dose of 500 mg/m2 on days 1-3 and cisplatin (CDDP/IA call)-Lipiodol (LPD) suspension (10 mg/mL) at a dose of 50 mg/body on day 2) every 6-10 weeks. He was also treated with selective TACE for HCC that was supplied by extra-hepatic arterial branches. He had been treated with 3 courses of 3 days' FPL, and the selective TACE, HCCs in S6, S5 and S8 disappeared completely and multiple HCCs almost entirely vanished. During the 3-day treatment with FPL, his performance status (PS) was maintained and no severe side effects were observed. Although multiple recurrent HCC is potentially fatal and QOL is lost, hepatic arterial infusion chemotherapy with 3 days' FPL was effective and contributed to improve the patient's prognosis and QOL.

Dietary supplement implicated in fulminant hepatic failure in a well-controlled Wilson disease patient.

We encountered a patient with previously well-controlled Wilson disease who experienced fulminant hepatic failure with hemolytic anemia, possibly caused by the dietary supplement Health Proportion(®) (Jubilant Co., Ltd., Ehime, Japan). A 21-year-old woman was admitted to our hospital with marked liver dysfunction and severe hemolytic anemia. Free serum copper level was elevated at 101 µg/dl, and urinary copper excretion was extremely increased (25,600 µg/day). Plasma exchange and continuous hemodiafiltration were performed to remove serum copper and to treat the hemolytic anemia. However, liver function did not improve, and she underwent liver transplantation on 28th day after admission. Copper and iron contents in the resected liver were high at 851.9 µg and 551.7 µg/dry liver weight (g), respectively, despite the patient having regularly taken D-penicillamine since diagnosis and having a well-controlled copper level 1 year before her admission. Two months before admission, the patient had taken a dietary supplement made from soybeans for 1 month. This supplement was labeled as containing large amounts of copper and iron, and we assume that this caused fulminant hepatic failure with hemolytic crisis in this patient. It is important to be mindful of the micronutrient content of dietary supplements, especially for metabolic disorder patients.