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Aim: The beneficial effect of zinc supplementation on the efficacy of interferon as a treatment for chronic hepatitis C had been demonstrated in hepatitis virus genotype 1b of high viral load. This study focused on patients with genotype 2, which is more sensitive to interferon than genotype 1b, and used consensus interferon (CIFN) with or without zinc., Methods: We randomized 83 patients with chronic hepatitis C to CIFN at 18 MIU six times/wk for 4 wk, followed by CIFN at 18 MIU six times/wk for another 20 wk, in combination with polaprezinc 300 mg (regimen A, n=41) or as monotherapy (regimen B, n=42). Thirty-one patients in regimen A and 33 patients in regimen B completed the clinical trial; the remaining patients withdrew because of side effects or a transfer to another hospital., Results: Sustained biochemical response, defined as a normal aminotransferase level at the end of the 6-mo post-treatment observation, was 68% and 69%, and sustained virological response, defined as undetectable HCV-RNA at the end of the 6-mo post-treatment observation, was 54% and 67% for regimens A and B, respectively., Conclusion: CIFN treatment combined with zinc did not enhance the effect of CIFN as shown by biochemical, virological criteria. No side effects related to polaprezinc were noted.

Background: Autoimmune thyroid disorders are among the well-known adverse effects of interferon-alpha (IFN-alpha) therapy in patients with chronic hepatitis C. However, there are few reports regarding the long-term outcome of this complication. We aimed to evaluate the natural history of IFN-alpha-induced autoimmune thyroid disorders with long-term follow-up., Methods: Four hundred and thirty-nine patients with chronic hepatitis C were treated with IFN-alpha for 24 weeks between March 1993 and April 1998. Seventeen of 439 (3.9%) patients developed symptomatic autoimmune thyroid disorders including nine cases of hyperthyroidism and eight cases of hypothyroidism. The patients with hypothyroidism were all women. These 17 patients were followed up for 71.1 +/- 17.8 months (48-120 months) and were evaluated for long-term outcome., Results: Eight patients could discontinue the thyroid medication (2-36 months, median 10 months). Nine patients needed the thyroid medication at the follow-up period. The patients with hyperthyroidism who needed long-term thyroid medication had a significantly high titer of TSH receptor antibody on onset compared with the patients who could discontinue the thyroid medication. There were no significant differences in age, type of IFN, duration from IFN administration to onset, cessation of IFN, genotype of hepatitis C virus and thyroid hormone levels on onset between the patients who needed long-term thyroid medication and the patients who could discontinue the thyroid medication., Conclusion: All patients with IFN-alpha-induced thyroid disorders could be controlled with medication. However, the IFN-alpha-induced thyroid disorders are not always reversible. One must be careful about not only the development of autoimmune thyroid disorders during IFN-alpha therapy but also the outcome of the thyroid disease., (Copyright Blackwell Munksgaard 2005)

We describe a rare double metastasis of hepatocellular carcinoma to the supramaxillary gingiva and papillary muscle of the right ventricle. The patient was a 72-year-old woman who underwent three sessions of transcatheter arterial embolization for the primary lesions. Control of bleeding from the supramaxillary gingival metastasis was difficult by conservative treatment such as compression with gauze soaked in epinephrine. Therefore, radiotherapy was performed, but it failed to control the bleeding. The patient subsequently died due to hepatic failure. Autopsy revealed metastases of hepatocellular carcinoma to the papillary muscle of the right ventricle and paraaortic lymph node in the abdomen in addition to the supramaxillary gingival metastasis. Histopathological examination showed moderately differentiated hepatocellular carcinoma of both the primary site and metastatic sites to the gingiva and the heart and poorly differentiated in the paraaortic lymph node.

We report a 26-year-old woman who was diagnosed with Budd-Chiari syndrome following consultation for a skin nodule in the lower extremity. Histopathological examination of a biopsy specimen showed features of erythema induratum. As part of the diagnostic work-up, chest roentgenography performed to rule out possible tuberculosis showed enlarged right lower mediastinum. Computed tomography identified a dilated azygos vein and obstruction of the inferior vena cava near the liver. Liver function tests and blood cell counts were all within normal limit and no sign of portal hypertension was noted except for mild splenomegaly. Although angioplasty by balloon catheter resulted in recanalization of the obstructed inferior vena cava, obstruction of the inferior vena cava appeared again 2 months later. One-stage surgical reconstruction of the vascular abnormalities affecting inferior vena cava and hepatic vein using autologous pericardial patch was performed 11 months after angioplasty, which resulted in normalization of blood flow. Examination of a liver biopsy obtained intraoperatively revealed hepatic fibrosis compatible with early-stage Budd-Chiari syndrome. No complications were noted postoperatively and the nodular lesion in the lower extremity disappeared after surgery.

The Fas/Fas ligand interaction plays a crucial role in various liver diseases, and administration of agonistic anti-Fas antibody to mice causes massive hepatic apoptosis and fulminant hepatic failure. Several growth factors have recently been found to function in preventing apoptosis. In this study, we demonstrated that overexpression of transforming growth factor alpha (TGFalpha) has a dramatic protective effect on Fas-mediated hepatic apoptosis at the biochemical and histological levels. Moreover, 85.7% (six out of seven) of TGFalpha transgenic mice survived the lethal liver damage, whereas all wild-type mice died. Expression of Bcl-xL, an anti-apoptotic protein, was greatly increased in the transgenic mice. Taken together, our findings suggest that TGFalpha protects against Fas-mediated liver apoptosis in vivo and up-regulation of Bcl-xL may participate in protective effect of TGFalpha.