Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Several groups including ours at Hyland have studied the incidence of HTLV-III/LAV seroconversion and non-A, non-B hepatitis (NANBH) in recipients of products made from unscreened plasma. Of 18 previously untreated patients who received heat-treated factor VIII concentrate (HEMOFIL T), none seroconverted for HTLV-III/LAV. However, 11 of 13 similarly treated patients showed aminotransferase elevations indicative of NANBH. None of 21 patients receiving anti-inhibitor coagulant complex (Autoplex) seroconverted for HTLV-III/LAV, while 28 of 50 patients receiving other forms of treatment did seroconvert. Of 30 recipients of AUTOPLEX, 9 had elevated aminotransferase levels. Since all patients had hepatitis B markers when the study began, a diagnosis of NANBH cannot be made. Of 16 patients who received large doses of immune globulin for intravenous administration (IGIV, GAMMAGARD), none seroconverted for HTLV-III/LAV. Retrospective and prospective studies of 157 recipients of GAMMAGARD did not reveal a single case of NANBH attributable to receipt of this product. In contrast, NANBH has occurred following administration of HEMOFIL T, indicating that heating in the dried state does not eliminate the NANBH agent(s). In spite of lingering concerns about NANBH infectivity, the available data strongly suggest that heat treatment and/or cold ethanol fractionation render these plasma products safe from HTLV-III infectivity.
 ...
PMID:The incidence of HTLV-III/LAV seroconversion and non-A, non-B hepatitis in recipients of plasma products. 244 Jul 45

Although hepatitis B virus (HBV) has been closely associated with the development of hepatocellular carcinoma (HCC), no serologic markers of HBV can be found in up to 11% of HCC patients in developing countries and up to 68% of HCC patients in industrialized countries. Despite the absence of HBV serologic markers in these HCC patients, HBV DNA sequences have been found to be integrated into HCC DNA in 13-100% of these patients, indicating a possible role of HBV in the etiology of their HCC. Although six patients with chronic non-A, non-B hepatitis virus infection who were followed have been documented to develop HCC, it is not known whether the non-A, non-B hepatitis viruses cause or contribute to the development of HCC in some HCC patients without HBV serologic markers. Ethanol, cigarette smoking, oral contraceptives, and aflatoxin also have been suggested as possible etiologies and should be studied further. Suggested etiologies that are not supported by the published data include alpha-1-antitrypsin deficiency and schistosomiasis.
 ...
PMID:Hepatocellular carcinoma: possible etiologies in patients without serologic evidence of hepatitis B virus infection. 253 73

Alcohol inhibits phospholipase (PL) activity in a number of animal models. We have therefore measured prostaglandin E2 (PGE2) and leukotriene B4 (LTB4), liberated by stimulated peripheral blood mononuclear cells (PBMC) and neutrophils respectively in chronic alcoholics and in control subjects. Peripheral blood mononuclear cells from alcoholics produced less PGE2 (p less than 0.01) and neutrophils produced less LTB4 (p less than 0.025). Reduced PGE2 production by PBMC of alcoholics was corrected by the addition of exogenous arachidonic acid (p less than 0.005) whilst neutrophil LTB4 production remained lower in the alcoholics (p less than 0.01). Percutaneous liver biopsies were undertaken in the 20 alcoholics having abnormal liver function tests. Prostaglandin E2 biosynthesis was lower in PBMC from patients with alcoholic hepatitis than with alcoholic cirrhosis (p less than 0.05). Analysis of PBMC fatty acid composition demonstrated that endogenous arachidonate and linoleate contents were not significantly different in alcoholics and controls. Cells from controls and alcoholics were incubated with 0, 50 and 150 mmol/l ethanol for two hours but there was no alteration in PGE2 or LTB4 biosynthesis. In summary, we found reduced eicosanoid production by peripheral leucocytes in alcoholics, supporting the hypothesis that chronic alcohol consumption either inhibits membrane bound phospholipase activity or enhances, alternatively, catabolism of eicosanoids. This phenomenon is more marked in alcoholic patients with hepatitis than in those with cirrhosis alone.
 ...
PMID:Prostaglandin E2 and leukotriene B4 synthesis by peripheral leucocytes in alcoholics. 255 53

Pharmacokinetics of ornidazole, a nitroimidazole derivative, was investigated after intravenous injection in 3 groups of 10 patients with different hepatic diseases: hepatitis, noncholestatic cirrhosis and extrahepatic cholestasis. Plasma concentrations of ornidazole and its two major hydroxylated metabolites, M1 [alpha-(chloromethyl)-2-hydroxymethyl-5-nitroimidazole-1-ethanol] and M4 [3-(2-methyl-5-nitroimidazole 1-yl)-1,2-propane diol] were measured by HPLC assay. As a consequence of a decreased clearance (26% to 48%), the half-life and MRT are increased in all patients by 19% to 38% when compared with healthy volunteers. No clear difference could be established between the different groups. The volume of distribution remains the same in all patients and controls except those suffering from cancer. As previously shown in patients with severe liver cirrhosis, both metabolites accumulate in plasma as a result of decreased elimination; formation is no longer the rate-limiting step of their kinetics. This metabolite accumulation is in part due to decreased biliary excretion and to hepatocellular failure.
 ...
PMID:Pharmacokinetics of ornidazole in patients with acute viral hepatitis, alcoholic cirrhosis, and extrahepatic cholestasis. 270 94

We studied the relationship between the ratio of serum aspartate aminotransferase (ASAT) to alanine aminotransferase (ALAT) and histologic changes in human and experimental alcoholic liver disease. The patient population included 52 hospitalized patients enrolled in a Veterans Administration Cooperative study. The experimental animal group consisted of male Wistar rats fed an ethanol-liquid diet. Of the 52 patients with alcoholic hepatitis, 33 had evidence of cirrhosis. The mean +/- SD for the ASAT/ALAT ratio in the group with alcoholic hepatitis and no cirrhosis was 1.47 +/- 0.84, the mean +/- SD in the group with hepatitis and cirrhosis was significantly higher (2.68 +/- 1.32, p less than 0.01). There was no difference in the ratio between the rats with and without liver fibrosis. The cause for the increased ASAT/ALAT ratio in serum in the presence of cirrhosis is unknown and may reflect more severe liver damage.
 ...
PMID:Serum aspartate aminotransferase to alanine aminotransferase ratio in human and experimental alcoholic liver disease: relationship to histologic changes. 270 13

Human retroviruses causing AIDS (HIV) may occur in human plasma. Since HIV contaminated plasma cannot be completely excluded by testing for anti-HIV, AIDS safety of human plasma products can only be achieved by introducing HIV inactivating and/or eliminating methods into the manufacturing procedure. Here we review a number of methods used when manufacturing plasma derivatives at Behringwerke. These methods were previously developed either to produce a protein of required purity or to manufacture hepatitis safe products. Methods used to produce purer proteins are ethanol fractionation, pepsin treatment, affinity chromatography or various protein precipitation procedures. The method developed at Behringwerke for inactivating infectious viruses in plasma protein preparations not destroying the biological activities of the human protein is pasteurization, i.e. 10 h heat treatment of the aqueous protein solution at 60 degrees C. To investigate the HIV inactivating efficiency of the methods mentioned above, aliquots of an infectious HIV type 1 concentrate were added to a protein preparation, the resulting HIV spiked preparation treated according to the method to be studied and the amount of infectious HIV in this preparation determined before and after treatment. By all methods reported on here the HIV type 1 isolate was completely inactivated resulting in high inactivation factors. In addition, the heat stability of HIV type 2 was tested in aqueous solution at 60 degrees C proving that both HIV-1 and HIV-2 isolates are of comparably low heat stability under these conditions. From the results discussed here it can be concluded that all commercial human protein products of Behringwerke derived from either human plasma or placenta do not contain any infectious retrovirus causing AIDS and thus have a high margin of safety regarding the transmission of AIDS.
 ...
PMID:Inactivation of AIDS-causing retroviruses by the manufacturing procedures for human plasma proteins. 304 47

Malotilate (diisopropyl 1,3-dithio-2-yldenemalonate), a hepatotrophic drug, was administered to rats with alcohol-pyrazole hepatitis, which is considered to be a suitable experimental model for alcoholic liver injury, in order to elucidate the effects of malotilate on alcoholic liver injury. The number of ballooned hepatocytes and necrotic hepatocytes were smaller in the alcohol-pyrazole hepatitis rats treated with malotilate for 12 weeks (Al-Py Mal group) than for those without malotilate treatment (Al-Py group). Immunohistochemically, the retention of transferrin, one of the secretory proteins from the liver, in the ballooned hepatocytes was inhibited by malotilate. Biochemically, transferrin content in the Golgi fraction of the hepatocytes was significantly lower in the Al-Py Mal group than in the Al-Py group. Hepatic acetaldehyde levels in the Al-Py Mal group were significantly lower than those in the Al-Py group, even though ethanol metabolic rates were not different between the two groups. These results indicated that malotilate prevented the development of hepatocytic injury in alcohol-pyrazole hepatitis by decreasing hepatic acetaldehyde levels and preventing the retention of transferrin in the hepatocytes.
Alcohol Clin Exp Res 1988 Oct
PMID:Effects of malotilate on alcoholic liver injury in rats. 306 13

Human immunoglobulin for intravenous (IV) use has an established safety record with regard to transmission of hepatitis B virus. The bulk of available evidence also suggests that the human immunodeficiency virus (HIV) is not transmitted by IV immunoglobulin. There has been one report, however, of isolation of HIV from two patients with hypogammaglobulinaemia who had been treated with several immunoglobulin products. Certain IV immunoglobulin products have transmitted non-A, non-B (NANB) hepatitis but careful clinical assessment of recipients of other products suggests that non-infective preparations can be made. Interpretation of available data most likely to be correct is that contamination with NANB is reduced but not eliminated by cold-ethanol fractionation and that the use of further virucidal procedures in the finishing of immunoglobulin products will confer a higher degree of safety.
 ...
PMID:The viral safety of intravenous immunoglobulin. 311 93

About 90 per cent of morbidly obese patients show histological abnormalities of the liver. One third of patients have fatty change involving more than 50 per cent of hepatocytes. Fatty liver disease can be divided into four histological groups: Fatty liver, fatty hepatitis, fatty liver with portal fibrosis, and cirrhosis. Most patients show only fatty change. Alcohol, drugs, diabetes, poor nutrition, and weight-reducing surgery contribute to progressive liver damage, but morbid obesity alone may lead to severe disease showing all the features of alcoholic hepatitis and may end in cirrhosis and liver failure. The accumulation of fat alone is unlikely to be the stimulus to inflammation and fibrosis. Only one fifth of patients have complaints that arise from the liver. The development of severe fatty liver disease may also be asymptomatic and rarely shows the florid picture associated with alcoholic hepatitis. There is poor correlation of liver function test results with morphology in obesity. ALT levels exceeding twice the normal limit have some predictive value for histological grades of severity, but they are present in few patients. Pericentral and pericellular fibrosis in prebypass liver biopsies may be an important prognostic lesion for the development of fatty hepatitis and cirrhosis. In contrast with the frequent progression to massive fatty change, inflammation and fibrosis after bypass surgery, weight loss by low-calorie dieting, or starvation is accompanied by improvement in fatty change and return of liver function tests to normal.
 ...
PMID:Fatty liver disease in morbid obesity. 331 4

We recently presented preliminary data indicating the presence of antibodies against acetaldehyde adducts in sera of over 70% of alcoholic patients. To assess the respective roles of liver disease and alcohol consumption as well as the specificity of this immune response, 141 patients in various stages of alcoholic and nonalcoholic liver diseases were tested by a hemagglutination assay. Sixty-three (73%) of 86 alcoholics had antibody titers above control levels (p less than 0.0001). Alcohol consumption of these individuals was significantly higher (p less than 0.001) than that of those alcoholics with normal titers. Twenty-two patients (39%) with nonalcoholic liver diseases also had elevated levels of antibodies against acetaldehyde adducts (p less than 0.0005); of these, 8 had primary biliary cirrhosis (7 in Stages III and IV), 9 had chronic active hepatitis (6 with cirrhosis) and 5 had acute (virus- or drug-induced) hepatitis. Antibody titers did not correlate with levels of transaminase or alkaline phosphatase activity, nor with bilirubin, and albumin. However, in 52 alcoholics and in nonalcoholic patients with biopsy-confirmed liver disease, the highest titers were seen in the more advanced stages of liver damage. Thus, in addition to alcohol consumption, severity of liver disease may play a role in the appearance of circulating antibodies against acetaldehyde adducts.
 ...
PMID:The role of alcoholism and liver disease in the appearance of serum antibodies against acetaldehyde adducts. 337 72


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>