Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 41 patients with alcoholic liver disease, antibodies to 12 common Escherichia coli O antigens (expressed as number of O antibody reactions with an agglutination titre of greater than or equal to 40) and to immunoglobulins IgG, IgA, and IgM were studied for 8 weeks. In 18 patients (8 with cirrhosis, 10 with fatty liver) who continued drinking during this period no significant changes were found. In 23 patients (11 with cirrhosis, 12 with fatty liver) who stopped or reduced drinking, a significant decrease in the levels of E. coli O antibodies and IgA was found (p less than 0.05 and p less than 0.01, respectively). In these 41 patients and in an additional 43 patients with alcoholic liver disease the amount of E. coli O antibodies was compared with type of histological lesion. The levels of E. coli O antibodies were significantly higher in cirrhosis with alcoholic hepatitis (22 cases) than in cirrhosis without alcoholic hepatitis (17 cases) (p less than 0.05). In these 17 patients antibody levels were significantly higher than in 41 patients with fatty liver without alcoholic hepatitis (p less than 0.02). In all patients a significant correlation between the number of positive reactions to E. coli O antigens and serum IgA concentration was found (p less than 0.01). No microbes were cultured from the liver biopsies, and no E. coli O antigens were demonstrated in the liver tissue by immunohistochemistry. Our results support the hypothesis that the high levels of E. coli O antibodies in alcoholic liver diseases are due to failure of the liver to extract circulating antigens and gut-derived endotoxins.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Escherichia coli antibodies in alcoholic liver disease. Correlation to alcohol consumption, alcoholic hepatitis, and serum IgA. 620 66

Drinking pattern as well as clinical, biochemical and histological findings were recorded of 282 males with alcohol-induced liver disease (fatty liver in 103, hepatitis in 61, cirrhosis in 118). The proportion of persons under 50 years of age was significantly greater with alcoholic hepatitis (70%) than cirrhosis (46%). Mean daily alcohol consumption was clearly lower among those with fatty liver than hepatitis or cirrhosis (P less than 0.02). Duration of alcohol abuse was on average shorter in patients with fatty liver and hepatitis than with cirrhosis (excessive consumption of less than 15 years was 61% and 62%, respectively, in the former, 28% in the latter (P less than 0.02). Symptoms and clinical and biochemical findings did not help in differentiating between hepatitis without cirrhotic change and cirrhosis. The most marked differences between cirrhosis and hepatitis, on one hand, and fatty liver, on the other, related to the frequency of certain signs and symptoms: upper abdominal pain, hard consistency of the liver, generalized jaundice, bleeding from esophageal varices and ascites; among biochemical findings they were: elevation of serum-bilirubin concentration above 34 mumol/l (2 mg/dl), lowering of the Quick values and of albumin concentration. Mortality rate during hospital stay was lower among patients with hepatitis but no cirrhotic change (6.6%) than among those with cirrhotic change (31.4%). While the prognosis under abstinence was relatively more favourable in patients with mild or moderately severe hepatitis, nonicteric forms require closer attention than has been given them so far.
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PMID:[Alcoholic fatty liver, alcoholic hepatitis and alcoholic cirrhosis. Drinking behavior and incidence of clinical, clinico-chemical and histological findings in 282 patients]. 623 65

The activity of prolyl hydroxylase was measured in liver tissue obtained from a small series of patients with a variety of liver disease. Enzyme levels were marginally elevated in patients with fatty liver and viral hepatitis, conditions not normally associated with progressive fibrosis. In some patients with alcoholic hepatitis and in all patients with cirrhosis and chronic active hepatitis, there was a marked increase in enzyme activity. Patients with conditions characterised by high liver prolyl hydroxylase levels showed histological evidence of extensive hepatic fibrosis and also significant increases in the serum values of glutamate dehydrogenase and gamma-glutamyl-transpeptidase. Prolyl hydroxylase activity was not detected in serum.
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PMID:Hepatic prolyl hydroxylase activity in human liver disease. 625 37

We studied Gm typing of serum samples from 838 donors; 177 had chronic hepatitis, 166 liver cirrhosis, 113 primary hepatocellular carcinoma, 21 alcoholic hepatitis, 18 fatty liver and 343 were unrelated normal blood donors. The distribution of Gm phenotypes and haplotypes in sera from patients with primary hepatocellular carcinoma differed from that in the normal controls; the Gm phenotype (1,2,21,13,15,16) and the haplotype Gm1,2,21 were significantly more common in this patient group (X2 = 18.56, corrected P less than 0.01, relative risk = 3.12; X2 = 25.52, corrected P less than 0.005, respectively). Overall, in the other liver diseases, we observed no significant Gm phenotype or haplotype association. The commitment to progression to primary liver carcinoma seems to be ascribable to a gene or polygenes close to the IgG heavy chain loci.
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PMID:Primary hepatocellular carcinoma and IgG heavy chain allotypes. 630 57

Alcoholism is a major health problem, and one of its primary manifestations is alcoholic liver disease. The mechanisms responsible for the various forms of alcoholic liver disease--fatty liver, alcoholic hepatitis, and cirrhosis--are at present poorly understood. Knowledge of these mechanisms is needed to provide a sound framework for the therapy and prevention of liver disease due to alcohol and for the identification of those individuals most susceptible to develop liver disease from alcohol abuse. These experiments were designed specifically to evaluate the postulate that ethanol-induced pericentral liver damage results from an accentuated gradient of decreasing oxygen tension leading to pericentral hypoxia. Microlight guides were used to detect NADH fluorescence, and miniature oxygen electrodes were employed to measure oxygen tensions from periportal and pericentral regions of the liver lobule from the perfused rat liver. With both techniques, ethanol treatment increased the hepatic oxygen gradient. This increase was blocked by the antithyroid drug propylthiouracil. Thus, these experiments provide evidence in support of the hypothesis that pericentral hypoxia is involved in the mechanism of ethanol-induced liver injury. Furthermore, low-flow hypoxia was shown to cause blebs in the pericentral region of the liver lobule in as little as 15 min. This surface blebbing could represent the mechanism for the well-known release of enzymes by impaired hepatic tissues.
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PMID:Alcohol-induced liver injury. The role of oxygen. 637 78

Procollagen type I carboxyterminal and type III aminoterminal peptide concentrations were measured in sera of 60 patients with alcoholic and 14 with nonalcoholic liver disease to study whether these assays are useful as clinical tests to differentiate various stages of alcoholic liver injury. Both propeptides were markedly elevated in alcoholic hepatitis and cirrhosis: procollagen type III peptide in 90% and type I peptide in 60-80% of these patients. Moderately increased values were found less frequently in patients with fatty liver. These tests did not differentiate patients with simple fatty liver from those with fatty liver and early fibrosis. There was a significant difference in serum procollagen type III peptide between fatty liver and both alcoholic hepatitis and cirrhosis (p less than 0.001), and in type I peptide between fatty liver and alcoholic hepatitis (p less than 0.005). Although serum peptide values correlated with the degree of liver fibrosis, appreciable overlap of values was found between the various groups. The peptide concentrations also seemed to be related to the degree of hepatic inflammation, and the highest values were observed in a subgroup of patients with alcoholic hepatitis in whom numerous Mallory bodies were found. The data suggest that in alcoholic liver diseases, serum collagen propeptide determination may be useful in diagnosing severe alcoholic hepatitis.
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PMID:Diagnostic value of serum procollagen peptide measurements in alcoholic liver disease. 638 61

The propensity to develop alcoholic cirrhosis is probably, at least in part, genetically determined. A striking similarity exists histologically between perhexiline and alcohol-related hepatitis and both are potentially precirrhotic lesions. Liver damage due to perhexiline is associated with impaired drug oxidation capacity which is genetically determined and tested by use of debrisoquine. Oxidation phenotyping might be used to predict susceptibility to perhexiline liver damage; it might also predict the potential to develop alcoholic cirrhosis. Oxidation phenotyping was therefore undertaken, using debrisoquine in 100 alcoholic patients, 30 of whom had only fatty liver despite prolonged alcohol abuse, while the remaining 70 had alcoholic hepatitis and/or cirrhosis. One hundred patients with nonalcoholic chronic liver disease served as controls. The number of patients with severely impaired drug oxidation capacity (poor metabolizer phenotype) was similar in the alcoholic group (8%) and the nonalcoholic control group (7%). In particular, the incidence of the poor metabolizer phenotype was similar in alcoholics with severe liver disease (10%) and in those with only fatty change (3%). There appears to be no association between the susceptibility to develop alcoholic cirrhosis and drug oxidizing capacity.
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PMID:Oxidation phenotyping in alcoholics with liver disease of varying severity. 639 Dec 52

Circulating hormone and metabolite profiles have been studied in ten patients with alcoholic cirrhosis, five patients with alcoholic hepatitis and/or fatty liver, and nine normal controls over a 12-h period of meals and activity. Blood glucose was elevated throughout the day in both cirrhotic and non-cirrhotic alcoholics (mean 12-h glucose; controls 5.38 +/- 0.16 (SEM) mmol/l; cirrhotics 6.98 +/- 0.30 mmol/l, P less than 0.001; non-cirrhotics 7.18 +/- 0.26 mmol/l, P less than 0.001). Non-cirrhotic alcoholics had an exaggerated insulin response to meals, whereas cirrhotic patients had hyperinsulinaemia throughout the day (mean 12-h insulin; controls 16.3 +/- 2.3 mU/l; cirrhotics 35.8 +/- 6.6 mU/l, P less than 0.02). Growth hormone levels were elevated only in patients with cirrhosis (mean 12-h growth hormone, 7.06 +/- 1.35 v. 0.85 +/- 0.17 micrograms/l, P less than 0.001). Serum cortisol was persistently elevated in cirrhotics but only in the evening in non-cirrhotic alcoholics. Lactate and pyruvate responses to meals were exaggerated in non-cirrhotic patients whereas in cirrhotics, levels were persistently raised. Blood glycerol was elevated in all alcoholic patients whereas ketone body levels were normal. Hypertriglyceridaemia was observed only in non-cirrhotic patients. No relationship between the endocrine and metabolic state was observed in either cirrhotic or non-cirrhotic patients.
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PMID:Hormone and metabolite profiles in alcoholic liver disease. 641 54

A prospective study has been carried out on 127 patients to test the accuracy of sonography in the diagnosis of diffuse liver diseases compared with histology based on percutaneous liver biopsy. Using sonographic criteria - size, margin, surface, elasticity, echo structure and sonic conductivity of the liver, hepatic veins and portal vein - and measuring the size of the gallbladder and the spleen, the following sonographic diagnoses were made: normal liver, fatty liver, fatty liver fibrosis, alcoholic hepatitis, chronic active hepatitis, cirrhosis. Sonographic diagnosis predicted histological diagnosis in case of normal liver in 56%, fatty liver 70%, alcoholic hepatitis 92%, chronic active hepatitis 63%, cirrhosis 79%. The specificity of sonography was 95%, the overall sensitivity was 82%: e.g. fatty liver 84%, chronic active hepatitis 93% and cirrhosis 79%. We conclude that sonography is an ideal screening method for detecting diffuse liver diseases. In cases of fatty liver and of cirrhosis it can spare the patient further invasive investigation. Furthermore, this method is suitable for evaluating the course of diffuse diseases of the liver, especially of toxic-nutritive liver damage and also of chronic active hepatitis.
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PMID:[Accuracy of sonography in the diagnosis of diffuse liver parenchymal diseases--comparison of sonography and liver histology]. 647 50

A morphological, endoscopic and bioptic (histologic and electron microscopic) study carried out in 86 patients with acute persisting hepatitis (APH) and 240 patients with noncirrhogenous alcoholic hepatitis (AH) allowed the observation of some aspects with predictive-evolutive value in liver diseases. In APH the endoscopic observation of a change of colour from bright red to variegated and the appearance on histologic examination of portal infiltrate with invasive tendency as well as of collagen spurs penetrating in the portal spaces, suggest the onset of the chronicity. In AH the changes with predictive value present in both AH and hepatic steatosis are, the alterations of the liver surface, and especially perivenular and perisynusoidal fibrosis.
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PMID:Morphological markers with predictive-evolutive value in liver diseases. 651 94


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