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Serum alpha-fetoprotein (AFP) concentrations were serially determined during the period following cessation of alcohol on thirty-five medical and psychiatric patients with histories of long-term excess drinking. In all except two cirrhotics with posttransfusion hepatitis and hepatocellular carcinoma, all AFP determinations for more than 2 months following abstinencewere negative(<40ng/ml). The results suggest that AFP elevations after abstinence from alcohol should raise the question of associated viral hepatitis or hepatoma in alcoholics.

Hepatic ornithine decarboxylase and aniline hydroxylase activities increased as early as 6h after a single dosing of azathioprine tomale rats and reached maximum levels at the 12th h after the treatment. However, aniline hydroxylase activity dropped to levels mu lower than the cintrols 48 h following azathioprine treatment. The results are discussed with regard to the role of azqathioprine during the promotion of hepatocarcinogenesis.

<p>plasma tyramine concentrations ewre abnormally high in cirrhotic patients with hepatic encephalopathy. Oral administration of berberine hydrochloride corrected hyperyraminemia in cirrhotics and also prevented the elevation of plasma tyramine levels following the oral tyrosine load, probably because of berberine-inhibition of bacterial tyrosine decarboxylase in the intestine. This is a new approach as Anti-amine therapy for cirrhotic patients</p>

<p>The levels of HDL-cholesterol and gamma-glutamyltransferase in the sera of 17 patients with alcoholic liver injury were followed after abstinence and compared with those of 11 patients with acute non-alcoholic hepatitis. The activity of gamma-glutamyltransferase decreased in all cases irrespective of the type of liver injuries. The level of HDL-cholesterol also decreased in 11 of 17 cases with alcoholic liver injury. The other alcoholics, in whom HDL-cholesterol level increased or showed no definite change after withdrawal of alcohol, had severe and advanced liver injuries. In non-alcoholic hepatitis, the HDL-cholesterol level increased as normal liver functions were restored except for one case with cholestatic features. It was concluded that alcohol intake can increase HDL-cholesterol level even in the presence of a concomitantly induced hepatic lesion.</p>

A permeable cell system has been developed by treatment with digitonin for studying in vitro DNA replication of chromatin. DNA replication of simian virus 40 nucleoprotein complexes (SV40 chromatin) in digitonin-treated permeable cells was analyzed by electrophoresis in agarose-gel. Autoradiography of the agarose-gel revealed that [32P]dCTP was incorporated in SV40 DNA I, II and replicating intermediates. The time course of the incorporation indicated the complete replication of SV40 DNA and chromatin with a full number of nucleosomes. The digitonin-treated permeable cell system will serve as a useful system for studying in vitro DNA replication of chromatin.

In order to evaluate a clinical use of omeprazole suspension, we examined the pharmacokinetics of omeprazole after oral administration in rats. Although the administration of omeprazole suspension buffered by NaHCO3 solution did not produce a significant increase in the area under the concentration-time curve (AUC) value compared with non-buffered group, the administration of NaHCO3 buffer immediately after dosing of omeprazole suspension buffered by NaHCO3 caused a significant increase in the AUC value. These results suggest that the NaHCO3 treatment following the administration of omeprazole buffered suspension effectively decreased the degradation of the compound by gastric acid. Therefore, the successive administration of NaHCO3 solution after the omeprazole dosing seems to be a simple and useful method for the administration to patients who cannot receive tablets.

A rare gastrointestinal tract neoplasm, primary non-Hodgkin's B-cell lymphoma in a 39-year-old, asymptomatic woman is described. The tumor was originally localized in the rectum without evidence of any other lymphoma-involved organ and treated by curative surgical procedure associated with postoperative chemotherapy.

Clinical studies show that patients with liver cirrhosis associated with portal hypertension have a high incidence of duodenal ulcer and duodenitis. However, little information is available concerning pathophysiological process of such duodenal diseases in liver cirrhosis. Hemodynamics of the duodenal mucosa was studied in cirrhotics with esophageal varices (68 cases) and in noncirrhotics with non-ulcer dyspepsia (37 cases) as well. In each group, hemoglobin concentration in the peripheral venous blood was measured, and mucosal hemodynamics was examined in 4 regions of the duodenum by endoscopic reflectance spectrophotometer. No significant intergroup difference was noted in the mean age or sex ratio. Hemoglobin concentration in the peripheral venous blood was significantly lower (p less than 0.01) in the cirrhotics. There were no significant intergroup differences in duodenal mucosal blood volume. However, the cirrhotics showed significantly lower oxygen saturation of hemoglobin in all regions of the duodenum (p less than 0.01). These results show that the cirrhotics with esophageal varices had relative increase in blood volume and decrease in oxygen saturation of hemoglobin in the duodenal mucosa. Such microcirculatory disturbances seem to predispose liver cirrhosis patients to duodenal injury.

The effect of cigarette smoke on organ weights, lipid peroxidation and plasma biochemical parameters was investigated in male Wistar rats. Daily exposure (for 20 min twice a day) to cigarette smoke for 27 days caused a significant decrease in liver weight and a significant increase in lung weight. The smoke-exposure group showed increased lipid peroxidation in the liver, but not in the lung. In the smoke-exposure group, the GOT, gamma-GTP, total bilirubin and LDH values were significantly higher than those in the control group, while the plasma glucose value was significantly lower. These results suggest that cigarette smoking might induce liver injury by enhancing lipid peroxidation.

<p>To assess the role of the kidney dopamine system on the diuretic state induced by angiotensin-converting enzyme (ACE) inhibitors, we examined the changes in urinary excretion and plasma level of dopamine, and kidney dopamine receptors in spontaneously hypertensive rats (SHR) treated with cilazapril, an ACE inhibitor. We administered cilazapril 10 mg/kg orally to 13-week-old SHR daily for 21 days (CILAZA group). Systolic blood pressure was significantly decreased in the CILAZA group on Day 6 compared with that in vehicle-treated SHR (control group). The urine volume was three- to fivefold higher in the CILAZA group, and total urinary dopamine secretion was also increased compared with the control group. There was no significant difference in affinity and number of kidney dopamine receptors between the CILAZA and the control groups. In conclusion, the diuretic effect caused by cilazapril is partly mediated by inhibition of the water reabsorption via the increase of dopamine production in the kidney.</p>

Three patients with severe halothane-induced liver injury are described. All patients received halothane anesthesia twice within a short period. High fever and jaundice were noticed soon after the second operation. The prothrombin time was less than 40%, and eosinophilia was greater than 7% prior to these symptoms. Other causes of liver injury were excluded. Diagnostic criteria for halothane-induced liver injury are proposed.

A 31-year-old female with chronic myelogenous leukemia, who developed myeloblastic involvement of the central nervous system during acute myeloblastic transformation of the disease, was treated with methotrexate intrathecally. The therapy produced prompt clinical response and complete reversal of abnormal cerebrospinal fluid findings. However, the patient expired 10 months following the acute blastic crisis.

Carbon tetrachloride (CCl4)-induced hepatotoxicity was potentiated by pretreatment with beta-phenethyl alcohol, abundantly present in sake. The injury was determined by serum GPT levels and histological examination. Similar results were observed in ethanol- and phenobarbital-pretreated rats. Acetaminophen-induced hepatotoxicity was not accentuated by beta-phenethyl alcohol or ethanol pretreatment. The activities of liver microsomal enzymes, such as cytochrome P-450, cytochrome b5 reductase, aniline hydroxylase and aminopyrine demethylase, were not altered in beta-phenethyl alcohol-pretreated rats. Thus, CCl4-induced hepatotoxicity potentiation by beta-phenethyl alcohol administration is postulated to be due to a mechanism other than increased free radical generation.

The prevention of hepatic encephalopathy by the intravenous infusion of a branched chain amino acid (BCAA)-enriched solution was investigated in methionine and ammonium acetate-treated rats whose liver was already injured with carbon tetrachloride. A BCAA-enriched solution protected the rats from entering a coma. The brain BCAA contents became higher, and the brain methionine and tyrosine levels and the ratio of glutamine to glutamic acid in the brain diminished after administering the BCAA-enriched solution.

Cepharanthine, a biscoclaurine alkaloids which interact with biomembranes, has been found to inhibit platelet aggregation. The effects of this drug on morphological and physiochemical phenomena following collagen-induced platelet stimulation were investigated. In the presence of cepharanthine, stimulated platelets became spherical, but did not form pseudopoda , nor did they become aggregated. Physiochemical reactions such as accelerated oxygen consumption, release of membrane-bound Ca2+, release of Ca2+ into the extracellular medium and deporalization of the membrane potential were all inhibited by cepharanthine. Using D,L-dipalmitoyl phosphatidylcholine liposomes as the substrate, cepharanthine was shown to inhibit phospholipase A2 activity. These results suggest that the changes in the membrane following the interaction of collagen with its receptor are important for platelet activation. Cepharanthine may inhibits these membrane state changes, thus blocking all subsequent reactions.

Two cases of chronic unconjugated hyperbilirubinemia and marked retention of indocyanine green (ICG) are described. Since bilirubin uridine diphosphate (UDP)-glucuronyl transferase activities were depressed in their liver, the patients seemed to have bilirubin metabolism similar to that in Gilbert's syndrome. However, the ICG fractional disappearance rates of the cases were rather low (0.018 and 0.019) compared to the rates reported for Gilbert's syndrome. These results suggest that the patients had a new metabolic disorder which results in constitutional unconjugated hyperbilirubinemia and ICG intolerance.

A 26-year-old male with renal allograft, who received immunosuppressive treatment with azathioprine, presented marked elevations of serum biliary tract enzymes, such as gamma-glutamyl transpeptidase (5,609 units/l) and alkaline phosphatase (60.5 Bessey-Lowry units), 14 months after transplantation. Two months later the patient became icteric; he died of respiratory failure 19 months after the renal allograft. Postmortem examination revealed intrahepatic cholestasis with minimal inflammatory cell infiltration, indicating drug hepatotoxicity.

Simian virus 40 (SV40) large T antigen was partially purified from small amounts of SV40-infected and SV40-transformed cells by immunoaffinity chromatography with high recovery. T antigen, in both crude and partially purified states, was detected rapidly by a sensitive and quantitative enzyme-linked immunosorbent assay (ELISA). Stability of the partially purified T antigen was found to increase by addition of 0.01% bovine serum albumin (BSA).