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The purpose of this study was to compare the hemodynamics of the liver vasculature as determined by Doppler sonography for patients with Osler-Weber-Rendu disease and for healthy subjects.Real-time color Doppler sonography and pulsed Doppler sonography were used to study 10 patients with Osler-Weber-Rendu disease and 25 healthy subjects. Vessel diameter and flow velocity in the hepatic artery and its branches as well as in the portal vein and its segmental branches were determined. Flow patterns in the hepatic veins were analyzed. The clinical manifestations of the disease were correlated with the Doppler sonographic findings.The hepatic artery and its branches were dilated and tortuous, and flow velocity was greater in patients than in healthy subjects; hepatic artery velocities (mean +/- SD) were 153 +/- 65.2 cm/sec versus 64.9 +/- 11.4 cm/sec (p.005). The resistive index measured in the hepatic artery did not differ significantly between the two groups (p was not significant). No intrahepatic arteriovenous shunt sites were detected by color Doppler sonography. However, arterioportal shunts were observed in two patients, one of whom also had a portovenous shunt. A portovenous shunt and multiple shunts between hepatic veins were found in another patient. Portal venous flow was similar in both groups. No relationship between Doppler sonographic changes and clinical manifestations was found.The multiple microscopic arteriovenous shunts found in Osler-Weber-Rendu disease were not detected in our patients but resulted in dilatation and increased flow velocity in the hepatic artery. Flow velocity in the portal vein appeared to be undisturbed. Large intrahepatic shunts were easily outlined by Doppler sonography.

A controlled trial was conducted to compare the efficacy of interferon (IFN) between two groups of patients with type C liver. Thirty-five patients were randomly assigned to group A (17 patients) or group B (18 patients). The former received 3 megaunits (MU) of human lymphoblastoid IFN six days per week for two weeks, followed by three days per week for 50 weeks; the latter group received 6 MU six days per week for two weeks followed by three days per week for 24 weeks. The percentages of biological sustained responders (B-SR) and virological sustained responders (V-SR) were 29.4 and 23.5%, respectively, in group B, and 17.6% for both in group A. The therapeutic effects were not different between two groups. HCV genotype 2 accounted for significantly higher percentage of B-SR and V-SR (both 57.1%, respectively). These findings indicate that IFN is effective in type C cirrhosis with genotype 2.

Class II antigens are strongly expressed on the inflamed colonic epithelium in inflammatory bowel disease. However, the mechanism of this epithelial class II antigen induction is not fully understood. Increased activities of interferon (IFN)gamma, tumor necrosis factor (TNF)alpha, and interleukin (IL)2 have been shown in the inflamed mucosa of inflammatory bowel disease. Therefore, we studied whether these cytokines could induce class II antigens on the human colonic epithelium. By an organ culture technique, 284 normal colonic biopsy specimens obtained from 49 individuals were cultured in media containing different concentrations of cytokines with/without anti-IFNgamma R antibody. Colonic epithelial class II antigens were identified by the indirect immunoperoxidase staining method with anti-human leukocyte antigen (HLA)-DR, DP, and DQ monoclonal antibodies. IFNgamma, TNFalpha, and IL2 induced epithelial class II antigens in 16 of 16 cases (100%), 2 of 16 cases (12.5%), and 6 of 17 cases (35%), respectively. Epithelial class II antigen expression in response to TNFalpha was induced via IFNgamma but not via IL2. This is the first demonstration that: (i) the induction of class II antigens on the colonic epithelium in response to TNFalpha is mediated via IFNgamma, and (ii) that IL2 induces class II antigens.

The morbidity rate for retinopathy of unknown origin was significantly higher (P0.001) in the chronic hepatitis C group, 27 (31.8%) of 85 cases, than in the control group, 6 (6.0%) of 100 cases. Among hepatitis C virus (HCV)-associated retinopathy patients, 6 cases (22.2%) were aware of ocular subjective symptoms, retinopathy recurred in 8 (29.6%) cases, binocular retinopathy occurred in 14 (51.9%) cases, and retinopathy related to liver dysfunction, in 13 (81.3%) of 16 tested cases. HCV-associated retinopathy involved hemorrhage at the posterior pole retina in 21 (77.8%), cotton-wool patches in 9 (33.3%), and hemorrhage at the peripheral retina in 7 (25.9%) cases. Sequelae occurred in only one case. Retinopathy worsened or recurred in all 7 cases treated with interferon. The risk factors for HCV-associated retinopathy were mild thrombocytopenia (P0.001), long-term hepatitis illness (P0.005), advanced age (P0.02), concurrence with liver cirrhosis (P0.02), history of systemic hypertension (P0.05), and female gender (P0.05).

The clinical significance of serum sialyl SSEA-1 antigen was evaluated using the sera of 1261 patients with malignant tumors and 717 patients with non-malignant diseases measured with Otsuka Assay Laboratories' RIA Kits. The results indicate that the antigen was frequently elevated in the sera from the patients with various adenocarcinomas, including lung (45%), pancreas (64%) and ovary (57%). The false positive incidence of antigens in the sera from the patients with non-malignant disorders was as low as 4.9%. No correlation was observed with other tumor markers examined in this study, and the diagnostic efficiency increased significantly by the combined determination of sialyl SSEA-1 antigen level with other markers. The serial determination of the serum sialyl SSEA-1 antigen level has a clinical utility also in monitoring the patients with adenocarcinoma receiving surgical operation and/or chemotherapy as indicated by the results of the longitudinal observation of the patients.

Antitumor effect of MMC + UFT(A) and MMC + tegafur(B) therapies for advanced gastric carcinoma was compared from February 1985 to March 1988. UFT and tegafur were orally given at dose of 400 mg/m2 daily, and MMC was intravenously administered at dose of 6-8 mg/m2 every two weeks. The following results were obtained. 1. Twenty-nine cases entered in this study were divided into A or B therapies at random. All cases entered were eligible. Fourteen of 29 cases were randomized into A therapy and 15 cases into B therapy. One case treated with B was evaluated as incomplete. 2. There were no differences in the characteristics of patients between A and B therapies. 3. Among 29 eligible cases, a partial response was obtained in 3 out of 14 cases (21.4%) treated with A and in 3 out of 15 cases (20.0%) treated with B. Among 28 cases evaluated completely, a partial response was obtained in 3 out of 14 cases (21.4%) treated with each A and B. 4. Response rate with every ps or for every lesion did not differ between A and B therapies. 5. Median survival day treated with A and B therapies was 223 and 181 days, respectively. The survival curve did not differ significantly between the two therapies. 6. The frequency of adverse reactions within eight weeks after beginning the therapy was 64.2 and 73.3% with A and B therapies, respectively. From the results mentioned, it was concluded that the antitumor effect of UFT was not superior to that of tegafur for advanced gastric carcinoma.