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In a consecutive series of 562 patients with pathologically documented hepatocellular carcinoma (HCC), 12 patients (2.1%) were found to have a second primary malignancy elsewhere. Of these, eight were male, four female, with ages ranging from 49 to 76 years (mean 60.7 +/- 9.3 years). The associated cancers included eight cases of gastric cancers, an esophageal cancer, a stump cancer, a case of myelocytic leukemia and a histiocytic lymphoma. Eight cases had both malignancies diagnosed at the same admission. In the other four, HCC were detected after an interval of 4, 10, 12 and 39 months. Two had received previous chemotherapy or radiotherapy. Fifty percent of the 12 patients were hepatitis B surface antigen (HBsAg) positive. Their liver function tests and alpha-fetoprotein levels were consistent with those of patients with HCC alone. The results suggest that the occurrence of HCC concomitant with or arising after another primary malignancy in Taiwan is not rare.

To examine the period between disappearance of hepatitis B e antigen (HBeAg) and appearance of anti-HBe, 48 patients with clinicopathologically verified chronic B hepatitis were followed every 1 to 3 months after HBeAg clearance. Sera were tested by radioimmunoassay for HBeAg and anti-HBe. Anti-HBe appeared in days to years, mostly (78.7%) within 1 year, after disappearance of HBeAg. Only 40.5% of patients had an "e-window" shorter than 1 month. Clinical and histological exacerbation preceding HBeAg clearance precipitated or accelerated appearance of anti-HBe. Since the patients in the "e-window" period were positive for DNA polymerase, it is suggested that the "e-window" reflects relative insensitivity of the radioimmunoassay rather than absence of HBeAg/anti-HBe. Therefore, HBeAg can reappear and clinical activity can relapse particularly during immunosuppressive therapy.

Fifteen patients with HBsAg-positive, severe chronic active hepatitis, nine DNA polymerase (DNAP)-positive and six negative were treated with intravenous adenine arabinoside (Ara-A) in a dose of 10 mg/kg/day for five consecutive days during each of two consecutive weeks. Of the DNAP-positive patients, two responded with histological and clinical remission as well as permanent loss of DNAP. However, histological and clinical remission were also observed in patients with unsatisfactory DNAP response and even in DNAP-negative patients. It is suggested that, in addition to its antiviral effect, Ara-A might have another mechanism, such as immunosuppression, that induced histological and clinical remission. Alternatively, the discrepancy of response might relate to the natural course of chronic type B hepatitis. Accordingly, controlled trial is mandatory for assessing the effect of Ara-A or any other agent in the treatment of chronic type B hepatitis.

A series of 80 patients with chronic lobular hepatitis (CLH) was reviewed clinically and histologically to demonstrate etiology, clinical presentation, course, and prognosis of this disorder. Data from our study indicate that CLH in Taiwan is a disease of viral origin, mostly hepatitis B (67.5%) and some non-A, non-B. It occurs predominantly in young males (81.3%); frequently commences as acute viral hepatitis (57.5%); and has clinical and laboratory features similar to convalescent viral hepatitis or even indistinguishable from full-blown acute viral hepatitis. Clinical and histological follow-up study indicate that CLH may extend for several years with remissions and relapses. No evidence of progression to cirrhosis was observed at least in a 4 1/2-year period of follow-up. It is concluded that CLH is a persistent but nonprogressive disease although the number of non-A, non-B CLH is too small to ascertain its nonprogressive course. The prognosis is generally good, and no specific therapy is required.

Intrahepatic hyperechoic lesions with acoustic shadows could be stones or nonspecific calcifications. To verify this, 9 patients with hepatic parenchymal calcifications were compared with 40 patients with intrahepatic stones. A set of criteria are proposed for the diagnosis of intrahepatic stones: (A) dilated intrahepatic duct; (B) pneumobilia; or (C) 2 or more of the following: (1) common hepatic duct more than 6 mm in diameter, (2) multiple lesions in one lobe, (3) left lobe involvement, and (4) elevated serum alkaline phosphatase. The sensitivity, specificity, and overall accuracy were 97.5%, 88.9%, and 95.9, respectively. The criteria help in the selection of patients for evaluation of intrahepatic stones.

Hepatocellular carcinomas (HCCs) were resected in eight patients who had preoperative transcatheter arterial embolization (TAE) and in 25 patients without preoperative TAE. Three patients in the former group had ruptured HCCs before operation. Two of the former group and three of the latter group were found to have recurrences after a follow-up of 1 1/2 years. Although preoperative TAE resulted in significantly increased tumor necrosis, it increased the risk of gangrenous change of the gallbladder, induced adhesion of the hepatoduodenal ligament, and was not effective in reducing operative blood loss or operative time if the vessel selected for TAE was inadequate. Pathologic examination revealed tumor emboli still existing in the intrahepatic veins. Daughter nodules and capsular invasion by tumor cells were not affected by TAE. Transcatheter arterial embolization seems to be effective in controlling bleeding from ruptured HCC prior to staged resection of the tumor.

A prospective study was conducted to evaluate the prognostic value of stigmata of recent hemorrhage in patients with bleeding peptic ulcer. Of 193 patients suffering from peptic ulcer bleeding identified by emergency gastrointestinoscopy, 52 patients were found to have bleeding gastric ulcer (spurt 5, active oozing 9, fresh clot 11, black clot 17, protruding vessel 4, and clear base without stigmata 6); the other 141 had bleeding duodenal ulcer (spurt 5, active oozing 26, fresh clot 43, black clot 23, protruding vessel 15, and clear base without stigmata 31). Patient with continuous bleeding or rebleeding was grouped as unstable bleeders. The rate of unstable bleeders was 39.1% (continuous bleeding 23.9% and rebleeding 15.2%) in patients with gastric ulcer, compared to 9.0% (4.5% and 4.5%) in duodenal ulcer (P less than 0.001). The unstable bleeder rate of ulcers with spurt, active oozing, clot, and protruding vessel was 80%, 44%, 35.7%, and 0%, respectively, in patients with bleeding gastric ulcer; and 33.3%, 19.2%, 6%, and 0%, respectively, in patients with bleeding duodenal ulcer. The data suggest that the stigmata of recent hemorrhage, excluding protruding vessel, has prognostic significance in bleeding gastric ulcer but less in bleeding duodenal ulcer.

To examine the early stage of the natural course of liver cirrhosis, a prospective follow-up study was conducted in a series of 76 patients with recent development of cirrhosis during the course of chronic type B hepatitis. During a mean follow-up period of 34.4 months, 45 episodes of acute exacerbation were recorded; the majority of the episodes occurred within 2 years after entry. The calculated annual incidence of acute exacerbation was significantly higher in patients seropositive for hepatitis B e antigen (HBeAg) and/or hepatitis B virus (HBV)-DNA (25.9%) than in those without these markers (11.9%). Three-fourths of the acute exacerbations were attributable to the reactivation of HBV. Spontaneous HBeAg seroconversion to anti-HBe also occurred in the early phase, but less than 30% of the events were preceded by acute exacerbation. Late hepatitis B surface antigen clearance occurred in two patients. Hepatic decompensation, esophageal variceal bleeding and hepatocellular carcinoma developed relatively late in the course of the disease with a calculated annual incidence of 2.3%, 2.3% and 2.8%, respectively. Seven patients (9.2%) died of hepatic failure or variceal bleeding, usually more than 3 years after entry. The estimated 5-year survival rate was 80%. The results suggest that the natural events of chronic HBV infection, including exacerbation, seroconversion and its sequelae could occur after the development of cirrhosis. In addition, these events might be responsible for the clinicopathological changes and the outcomes of these cirrhotic patients.