Three hepatitis B virus carriers who were HB(e)Ag negative and having normal liver function developed fulminant hepatitis with evidence of HBV replication following intensive chemotherapy for non-Hodgkin's lymphoma. Each was continuously negative for HB(e)Ag. Analysis of the precore region of HBV isolated from each demonstrated that the HBV of each had a point mutation in the precore region that inhibited the synthesis and the release of hepatitis B(e) antigen. This observation suggests that all HB carriers receiving either immunosuppressive or cytotoxic therapy should be monitored closely even if standard assays suggest that viral replication is not present. Sudden enhanced replication of a HBV mutant as a result of such therapy can be a cause of either very severe hepatitis or occasionally fulminant hepatitis.

Serial hepatic volumetry calculated from the liver area on abdominal computed tomography was performed in 19 patients with fulminant hepatic failure to determine a relationship between liver volume and prognosis. All patients received intensified artificial liver support comprised of plasma exchange and hemodiafiltration using high-performance membranes, and 10 patients survived. Liver volume was significantly larger in survivors than in nonsurvivors, both in an initial volumetry performed at the onset of coma and in subsequent volumetry performed 10-20 days after the onset of coma. The difference became more significant in the subsequent volumetry because of the recovery of liver size in some of the survivors and progressive liver shrinkage in all nonsurvivors. All patients with a liver volume greater than 656 ml at 10-20 days after the onset of coma survived, whereas all but one patient with a liver volume less than that died. Multivariate analysis revealed only liver volume in subsequent volumetry had discriminatory power upon prognosis among six prognostic factors. These observations imply that in order to obtain an accurate prediction of fulminant hepatic failure by hepatic volumetry, serial studies at least until 10-20 days after the onset of coma are necessary.

Inhibitors of 3-hydroxy,3-methylglutaryl coenzyme A (HMG-CoA) reductase have been reported to decrease the cholesterol saturation index (CSI) in duodenal bile in humans and to prevent formation of cholesterol gallstones in animal studies. We performed a prospective study to evaluate the role of HMG-CoA reductase inhibitors as gallstone-dissolving agents. Fifty patients with radiolucent gallstones in a gallbladder opacifying at drip infusion cholecystography were treated with either 10 mg/day simvastatin plus 600 mg/day ursodeoxycholic acid (group 1, n=26) or 600 mg/day ursodeoxycholic acid alone (group 2, n=24) for 12 months. The ratio of solitary to multiple gallstone cases was 21:29. Plasma lipid levels were assessed and ultrasonographic examination of the gallbladder was performed at baseline and at 3-month intervals during treatment. Duodenal bile sampling was performed in five patients in each group at baseline and after 12 months of treatment. Plasma cholesterol decreased significantly in group 1 but not in group 2. In solitary gallstone cases, no significant difference in dissolution rates was observed between groups 1 (3 of 9, 33%) and 2 (4 of 12, 33%). In contrast, the dissolution rate in multiple gallstone cases was significantly higher in group 1 (12 of 17, 71%) than in group 2 (3 of 12, 25%) (p < 0.01). Bile cholesterol saturation index was significantly decreased (p < 0.01) but did not significantly differ between the two groups. These results suggest that combination therapy with simvastatin and ursodeoxycholic acid is more effective for cholesterol gallstone dissolution than ursodeoxycholic acid monotherapy in patients with multiple gallstones.

A 72-year-old female was admitted to hospital with diarrhea containing hair. The abdominal plain film showed teeth-like structures in the right lower quadrant. Barium enema and endoscopic examination were performed, and the results indicated a possible dermoid cyst perforated into the rectosigmoid colon and small intestine. The operation revealed a dermoid cyst of the right ovary perforated into the rectosigmoid colon and small intestine. Histopathologically, a dermoid cyst and in part well-differentiated squamous cell carcinoma invading the rectosigmoid and small intestine were demonstrated.

Sera and ultrafiltrates (relative molecular mass < 10,000 Da) from patients with fulminant liver failure inhibit hepatocyte DNA synthesis in vivo. In this study the effects of ultrafiltrates from pooled sera from fulminant liver failure patients in the United Kingdom and plasma ultrafiltrates from fulminant liver failure patients in Japan have been investigated in primary cultured rat hepatocytes, with incubation for up to 72 hr. Both types of ultrafiltrate inhibited the incorporation of [3H]thymidine into acid-precipitable material and reduced the cell labeling index as determined on autoradiography in hepatocytes stimulated by epidermal growth factor and insulin compared with normal sera/plasma ultrafiltrates. The inhibitory effects observed were dose dependent, reversible when the fulminant liver failure ultrafiltrate was removed and were not associated with increased release of lactate dehydrogenase or suppression of protein synthesis as assessed on the basis of the incorporation of [3H]leucine. The effects appeared to be specific for hepatocytes; in preliminary experiments DNA synthesis was not inhibited in cultured fibroblasts (NIH 3T3 cells). These experiments are further evidence of the presence of an inhibitory factor of relative molecular mass less than 10,000 Da in the blood of patients with fulminant liver failure.

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The hemostatic effects of hemoclipping, the pure ethanol local injection method and the heat probe methods on hemorrhagic gastric ulcers associated with exposed blood vessels, were compared. The locations of the ulcers and exposed blood vessles, as well as characteristics and the severity of the hemorrhage were discussed. The hemoclipping method was used on 59 patients, the pure ethanol local injection on 32 patients, and the heat probe methods on 26 patients. The hemoclipping and pure ethanol local injection methods were effective in all of the patients in whom the exposed blood vessels were present around the margin of ulcers. The efficacy rate was 91%, 92% and 92%, respectively, when exposed blood vessels were found at the base of the ulcer. The efficacy rate was 94%, 100% and 80% for the three hemostatic methods, respectively, when an oozing hemorrhage was present. The three methods had an efficacy rate of 100% when only blood clots were present. The efficacy rate for a spurting hemorrhage was 86%, 71% and 67%, respectively, for the three methods. The hemoclipping and pure ethanol local injection were effective in 100% of slight and moderate hemorrhage cases, while the heat probe method was effective in only 89% of moderate cases. The efficacy rate was 85%, 85% and 83%, respectively, for severe cases. Overall, the efficacy rate was 93% for the hemoclipping method, 94% for the pure ethanol local injection and 92% for the heat probe method, and there was no significant difference between the three methods with regard to the overall efficacy rate.

The surface of a ceria-stabilized tetragonal zirconia polycrystal (Ce-TZP/Al 2 O 3 ) nanocomposite was sandblasted by alumina particles and veneered with feldspathic porcelain via a conventional condensation method. The part of each specimen containing the interface layer was sliced to ultrathin sections with an argon ion slicer, and these sliced sections were observed using high-resolution transmission electron microscopy (HRTEM). For both interfaces, Ce-TZP/porcelain and Al 2 O 3 /porcelain, no transition layers due to abrupt changes in atomic distributions were observed. Besides, the porcelain layers of both interfaces consisted of homogeneous amorphous phases. These results suggested that both Ce-TZP and Al 2 O 3 could be directly bonded to porcelain by Van der Waals forces arising from the close contact between them.