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

Long-term administration of ethanol into animals within 1-6 months resulted in distinct alterations of blood serum fatty acid composition as well as in elevation of the saturation rate simultaneously with a decrease of fatty acid polyunsaturation. Calculated coefficients, which included ratios between fatty acid with various rates of unsaturation, were highly informative. Alterations of fatty acid composition in blood serum, registered during observations, reflected the state of fatty acid metabolism in tissues. Analysis of fatty acid spectrum in blood serum enabled to evaluate the severity of impairments in liver tissue and pancreas under conditions of alcohol intoxication: increase in the rate of phospholipid catabolism, in content of cholesterol, triglycerides and total lipids was observed both in blood serum and liver tissue. These impairments of lipid metabolism may produce alcohol hepatitis, which is the basis for liver tissue alcohol cirrhosis.
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PMID:[Features of lipid metabolism impairment in chronic alcoholic intoxication]. 144 Dec 98

Alcoholic liver disease is associated with abnormalities in circulating levels of thyroid, adrenal and gonadal steroid hormones. The relative importance of ethanol consumption and severity of liver disease in the aetiology of these changes and their relationship to clinical abnormalities are unclear. We studied 31 subjects with alcohol-induced liver disease divided into three groups according to the severity of histological features: fatty change, hepatitis and cirrhosis. Circulating concentrations of thyroid, adrenal and gonadal steroid hormones, together with their major binding proteins, were measured in all subjects, and changes related to histology and tests of liver function, as well as clinical endocrine status. A reduction in circulating free tri-iodothyronine (fT3) was seen in subjects with alcoholic hepatitis and cirrhosis, in association with normal or reduced levels of thyrotrophin (TSH). The absence of abnormalities in subjects with fatty change despite similar ethanol intake to the other groups, and correlations between fT3 and liver function tests, suggest that changes in fT3 reflect the severity of underlying liver disease. Similarly, marked increases in circulating cortisol in the hepatitis and cirrhosis groups, and correlations between cortisol and liver function, suggest that changes largely reflect hepatic disease. The absence of clinical features of hypothyroidism or Cushing's syndrome in these groups, despite abnormalities of fT3 and cortisol, suggest an altered tissue sensitivity to hormone effects. In contrast, increases in circulating oestradiol and reductions in testosterone were found in all three groups in males. These findings suggest that both direct effects of ethanol and hepatic dysfunction determine changes in gonadal steroids in males.
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PMID:Severity of alcoholic liver disease and markers of thyroid and steroid status. 146 52

The serum activity of alcohol dehydrogenase was determined in healthy controls and in patients with liver diseases. The mean activity in hepatoma (6.4 +/- 1.0U/L) was significantly higher (P less than 0.05) than the mean values in liver cirrhosis (2.7 +/- 0.5U/L); hepatitis (4.3 +/- 1.0U/L), obstructive jaundice (2.9 +/- 0.5U/L) and healthy controls (0.7 +/- 0.1U/L). Alcohol dehydrogenase purified by CM-cellulose chromatography from the sera of patients with hepatoma had a higher affinity for butanol long chain saturated and unsaturated alcohols than the purified enzyme from healthy controls. Similarly, hepatoma alcohol dehydrogenase oxidized ethanol very poorly (KM = 154 microM) when compared with that from healthy controls (KM = 40.2 microM). Hepatoma alcohol dehydrogenase was inhibited by pyrazole while those of other liver diseases and the healthy controls were not. These properties of serum alcohol dehydrogenase may prove useful in the early diagnosis of hepatoma since biochemical changes occur before morphological changes in the development of cancer.
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PMID:Properties of serum alcohol dehydrogenase in Nigerians with primary hepatoma. 166 17

Human intravenous immunoglobulins prepared by the cold ethanol fractionation technique of Cohn are considered safe with respect to infectivity. However, there have been several instances of transmission of both hepatitis B and non-A,non-B hepatitis viruses after administration of intravenous immunoglobulins. To determine the prevalence of hepatitis C virus antibody in intravenous immunoglobulins and protein preparations, 30 commercially available products were tested. Using the Abbott enzyme immunoassay for hepatitis C virus antibody, 27 of 30 (90%) immunoglobulins tested positive. The Ortho immunoassay showed that 28 of 30 (93%) were positive, with one discordant result between the Ortho and Abbott assays. An antigen-blocking or neutralization test (Abbott) confirmed the results of the Ortho assay. Bovine, sheep, goat, and horse sera also were tested before and after isolation of animal immunoglobulins. All results on the animal sera were negative, indicating that the fractionation process did not produce false-positive results. The high prevalence rate of hepatitis C virus antibody in intravenous immunoglobulins has important implications for follow-up of recipients, selection of serum donors, and implementation of anti-hepatitis C virus testing.
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PMID:Prevalence of non-A,non-B hepatitis/hepatitis C virus antibody in human immunoglobulins. 849 58

An evaluation of indices of poor zinc status was undertaken in five male subjects in whom dietary zinc intake was reduced from 85 mumol d-1 in an initial phase of the study to 14 mumol d-1. One of the subjects developed features consistent with zinc deficiency after receiving the low zinc diet for 12 days. These features included retroauricular acneform macullo-papular lesions on the face, neck, and shoulders and reductions in plasma zinc, red blood cell zinc, neutrophil zinc and plasma alkaline phosphatase activity. Alcohol induced hepatitis, which was suspected in this subject, may have caused a predisposition to altered zinc metabolism and possible zinc deficiency which was exacerbated by subsequent zinc deprivation. The report supports the value of neutrophil zinc concentration as an indicator of poor zinc status.
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PMID:Symptomatic zinc deficiency in experimental zinc deprivation. 174 May 25

It has been pointed out that one of the pathogenetic causes of alcoholic liver injury is the hepatocytic accumulation of exportable proteins due to a decrease in hepatic microtubules caused by acetaldehyde. To confirm and extend this secretory protein accumulation in the hepatocytes, the effects of alcohol treatment on the intracellular transport of secretory protein in the hepatocyte was studied using radioisotope-labeled leucine and fucose. Acute ethanol administration to rats did not show any effects on intrahepatocytic transport and secretion of transferrin. In alcohol pyrazole hepatitis rats, the secretion of transferrin labeled with both radioactive leucine and fucose into the serum was significantly delayed. Delaying in the secretion of fucose-labeled transferrin was more prominent than in leucine-labeled transferrin. This secretory inhibition was accompanied by a corresponding increase in the hepatic retention of both leucine- and fucose-labeled transferrin. At the time of the maximum inhibition of secretion, radioisotope labeled transferrin mainly retained in the Golgi apparatus. These results indicated that movement of secretory proteins along the secretory pathway impaired in alcoholic liver injury and that accumulation of the secretory proteins might play an important role in the development of alcoholic liver injury.
Alcohol
PMID:Effects of ethanol on the secretion of hepatic secretory protein in rat alcoholic liver injury. 178 19

The authors examined the aminoterminal type III procollagen peptide level of serums and killer-cell activity peripheric blood lymphocytes with 75 patients suffering from ethanol originated liver diseases as well as control samples from 40 healthy volunteers. Determination of type III procollagen peptide (Fab) took place by the RIA method. The cytotoxic activity of killer-cells was tested against human red blood cells. Both in fatty liver and chronic alcoholic hepatitis the level of type III procollagen peptide increased, while in liver cirrhosis the same level reached a value three times of the normal. At the same time in cirrhosis hepatitis an increased killer-cell activity could be observed. Type III procollagen peptide values were also analysed in view of the cytotoxic capacity of killer-cells. At first ill, then healthy control individuals were divided into three groups according killer-cell activity values. Results have shown that in the group with a high level killer-cell activity average type III procollagen peptide values were significantly greater as compared to those of the medium or low level activity groups. These results might indicate a relation between a conditional antibody-dependent cellular cytotoxicity reaction and increasing collagen synthesis.
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PMID:[Serum aminoterminal type III procollagen peptide level and killer cell activity in patients with alcoholic liver diseases]. 195 78

Rhynchotechum vestitum Hook, F. et Thoms. mainly distributed in the southern part of Yunnan Province of China, has been used as a folk remedy for the treatment of hepatitis. No information has been found in the literature about its chemical investigation. In this paper, five compounds isolated from the ethanol extract of the stem and root of the plant are reported. Four of them were identified as beta-sitosterol (I), lupeol (II), rubiadin 1-methylether (III) and rubiadin (IV). The fifth, an orange needle crystal (C17H14O6, mp 236, 5-238 degrees C) is a new anthraquinone compound named rhynchotechol. Its structure has been proved to be 1,6-dihydroxy-7,8-dimethoxy-2-methyl-9,10-anthraquinone by spectral analyses and chemical methods.
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PMID:[Studies on the chemical constituents of Rhynchotechum vestitum Hook. F. et Thoms]. 209 79

24 patients with alcoholic intake were classified according to the amount of alcohol ingestion; clinical symptoms and signs, liver function tests (bilirubin, aminotransferases and prothrombin time) were analyzed. In all patients a percutaneous liver biopsy was performed and tissue stained by hematoxylin-eosin, wilder reticulin and Mallory trichromic. 9 Histologic criteria were analyzed. 4 groups according to the histology were identified. Group 1 (5 patients) hepatic fibrosis and/or fatty liver. Group 2 (5 patients) alcoholic hepatitis. Group 3 (10 patients) cirrhosis. Group 4 (4 patients) normal. 20% of patients with fatty liver, 80% of alcoholic hepatitis and 100% of cirrhotics referred ingestion or more than 160 g of ethanol and important correlation between liver histological damage and alcohol ingestion. Telangiectasia was the most common clinical finding and present in all hepatitis, 70% of cirrhotics and only 20% of fatty livers. Hemosiderosis was found in 60% of cirrhotics and in alcoholic hepatitis. Only 40% of patients with fatty liver and inflammatory cells while this was evident in all patients with alcoholic hepatitis and those with cirrhosis. Mallory bodies were identified in only 20% of cirrhotics and in none of the alcoholic hepatitis. The results suggest that there are significant differences from a histological and clinical point of view that distinguish alcoholic liver disease as seen in Venezuela from that reported in other countries.
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PMID:[Alcoholic liver disease in Venezuela. Clinical hepato-functional and histopathologic course]. 215 50

Hepatocellular carcinoma (HCC), the most frequent malignant tumour of the liver, is the commonest cancer occurring in males in the world. The annual incidence of the disease worldwide is estimated to be one million cases. There are variations in its geographical distribution. It tops the list of malignancies amongst males in sub-saharan Africa; it is the second most common cancer in Southeast Asia, including Hong Kong, and ranks third amongst males in China. It is relatively rare in America, Europe North Africa, and the Middle East. During the last 15 years, epidemiologic and laboratory investigations have established a strong and specific association between chronic hepatitis B virus (HBV) infection and HCC. Hepatic cirrhosis is another major aetiologic factor incriminated. In areas with a low incidence of HCC, cirrhosis due to alcohol may be a relatively more important predisposing factor. Chronic non-A, non-B hepatitis (NANBH) infection has now been incriminated as a cause of HCC, especially in Japan. Other environmental factors, particularly chemical carcinogens such as Aflatoxin, smoking, genetic predisposition and sex hormones may also act to promote hepatocarcinogenesis. The exact mechanisms of neoplastic transformation, however, are still far from understood. The following factors are discussed in detail: 1. HBV infection 2. Cirrhosis 3. NANBH infection 4. Aflatoxin B1 5. Cigarette smoking 6. Alcohol A number of less important associated diseases are also listed in Table I. At the end of this paper, a tentative scheme for hepatocarcinogenesis has been proposed and the methods for prevention is discussed in light of the risk factors considered.
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PMID:Hepatocarcinogenesis. 216 75


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