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)

IgA bound in vivo was shown by immunofluorescence on the plasma membrane of isolated hepatocytes from subjects with normal liver and patients with liver cirrhosis, chronic active hepatitis or fatty liver. IgA in sera with elevated IgA concentrations, especially from cases with alcoholic cirrhosis, was bound in vitro to isolated hepatocytes from rabbit and mouse. This was not due to the high IgA concentration per se. Moreover, polyclonal polymeric serum-type and secretory IgA, and three of ten polymeric monoclonal IgA preparations, showed similar binding properties. Conversely, purified polyclonal and monoclonal monemeric IgA did not show affinity for the hepatocytes. The binding of polymeric IgA did not seem to depend on the proportion of dimers and larger polymers, kappa- or lambda-type light chains, heavy-chain subclasses, content of J chain or affinity for secetory component. The in vivo binding of IgA by hepatocytes is probably a physiological phenomenon which in part may explain the normal clearance of polymeric IgA from serum.
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PMID:In vivo and in vitro binding of IgA to the plasma membrane of hepatocytes. 36 35

The serum immunoglobulin (Ig) G, A, and M levels were investigated with respect to their differential diagnostic significance, pathogenesis and estimation of prognosis of different forms of liver disease. The sera of 204 patients with acute hepatitis, fatty liver I and II, and cirrhosis, and of 110 healthy adutls were quantitatively determined for immunoglobulins. 1. IgG- and IgA-concentrations higher than 2000 mg% and 330 mg%, respectively, indicate chronic aggressive hepatitis or cirrhosis, and exclude all other groups. 2. A clear correlation between HBsAG (Australia Antigen) and immunoglobulin content could not be demonstrated in any group; 3. A significantly elevated level of IgA was observed in alcoholic cirrhosis when compared to non-alcoholic cirrhosis. No such differences were found inhe other groups. 4. Acute and chronic persistent hepatitis show a similar increase of immunoglobulins. Thus persistent high levels of Ig following acute hepatitis indicate the development into a chronic hepatitis. 5. A relative increase of IgA rather than IgG corresponds to the degree of inflammatory activity of a liver process.
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PMID:[Quantitative serum immunoglobulin determination: differential diagnostic significance for liver disease (author's transl)s]. 84 Jan 24

Determination of histocompatibility antigens in 63 patients with alcoholic liver disease showed that HLA-B8 was more prevalent in patients with cirrhosis than in controls, but among those with fatty liver and minimal fibrosis the prevalence of this antigen was normal. Another noticeable difference was the absence of HLAA28 in the cirrhotic group. In the total series of 219 patients the prevalence of antinuclear and smooth muscle antibodies was raised; they were especially prevalent in patients with cirrhosis. Raised serum IgA and IgG concentrations were also common (found in 50% and 37% respectively) and were again significantly associated with cirrhosis. In contrast, serum IgM levels, which were raised in 46% of cases, were not significantly related to the presence of cirrhosis but correlated significantly with the degree of portacaval shunting. These results support recent evidence suggesting that immune responses may be implicated in alcohol-induced liver damage, particularly in its progression to cirrhosis.
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PMID:Histocompatibility antigens, autoantibodies, and immunoglobulins in alcoholic liver disease. 108 18

Alcohol-feeding to rats subjected to jejunoileal bypass operation has been shown to lead to marked liver injury (fatty liver, necrosis and inflammation). This study investigated the influence of alcohol-feeding over a period of 3 months on the number of IgA-producing immunocytes and the villus surface area in various sections of the small intestine of rats subjected to a jejunoileal bypass or a sham operation. A jejunoileal bypass in animals receiving the control diet led to a decrease in the number of IgA-producing immunocytes in the duodenum and ileum, but not in the bypassed (blind) loop of the jejunum. In animals subjected to a jejunoileal bypass, alcohol-feeding led to an increase in the number of IgA-producing immunocytes in the duodenum and the bypassed jejunal loop as compared with animals with a jejunoileal bypass receiving the control diet. Among the animals with a jejunoileal bypass fed the control diet, the villus surface area within the duodenum and ileum increased as compared with the groups of sham-operated rats. The feeding of alcohol prevented this increase in the villus surface area in animals with a jejunoileal bypass. The increase in the number of IgA-producing immunocytes induced by alcohol in the animals with a jejunoileal bypass, in the duodenum and bypassed jejunum, supports the assumption of a change in antigen uptake in these parts of the small intestine, brought about by alcohol.
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PMID:Effect of alcohol-feeding on IgA-producing immunocytes in the small intestine of rats with and without jejunoileal bypass. 195 51

IgA deposition in hepatic sinusoids was demonstrated in liver biopsies from 26 patients with alcohol- or diabetes-related fatty liver and fatty liver hepatitis, and from 13 patients with normal liver or chronic active hepatitis. The pattern and extent of IgA deposition were similar in alcoholic and diabetic patients, a linear, continuous pattern being the most common. Staining for IgA cannot therefore be used to evaluate aetiology of fatty liver hepatitis in these two groups of patients.
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PMID:Does a linear pattern of sinusoidal IgA deposition distinguish between alcoholic and diabetic liver disease? 305 23

The presence of liver membrane antibody in IgG and IgA was investigated by radioimmunoassay using isolated rabbit hepatocytes as target cells. This technique was more sensitive than the immunofluorescent method. IgG liver membrane antibodies were positive in 24% of patients with alcoholic liver disease. IgA liver membrane antibodies were detected in 58% of patients with alcoholic liver disease, whereas they were detected only in 21% of those with nonalcoholic liver disease, except for cases of autoimmune chronic active hepatitis. In alcoholic liver disease, IgA liver membrane antibodies were detected at a high frequency in a group of patients with alcoholic hepatitis and active cirrhosis (94%) as compared with that of fatty liver, hepatic fibrosis, and inactive cirrhosis (42%). These results suggest that alcoholic liver disease is characterized in part by a humoral immune response of IgA liver membrane antibodies.
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PMID:Differences of liver membrane antibody frequency in alcoholic liver disease. Detection of IgG and IgA classes using radioimmunoassay. 328 54

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

The serum concentrations of prealbumin, transferrin and immunoglobulins, as well as their concentration ratios, were determined in patients with fatty liver, alcoholic cirrhosis and primary biliary cirrhosis to evaluate the usefulness of these measurements in the differentiation between these diseases, and in the evaluation of the severity of the liver injury. Alcoholic cirrhosis was characterized by high IgA/prealbumin and IgG/prealbumin ratios, whereas in fatty liver these ratios remained normal or close to normal. The IgG concentration and the ratio of IgG/prealbumin were markedly higher in advanced than in early alcoholic cirrhosis, IgG/prealbumin being the most sensitive indicator. None of the assays reflected the degree of fatty degeneration. In primary biliary cirrhosis the mean IgG concentration was 93% higher than in alcoholic cirrhosis. One of ten patients with primary biliary cirrhosis had a normal IgM level, whereas 2 of 10 patients with alcoholic cirrhosis had a value above normal (greater than 2.9 g/l). IgM alone did not differentiate between alcoholic and primary biliary cirrhosis, while the ratio of IgA/IgM seems useful: a value over 2.0 was found in all patients with alcoholic cirrhosis but in none of those with primary biliary cirrhosis.
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PMID:Serum prealbumin, transferrin and immunoglobulins in fatty liver, alcoholic cirrhosis and primary biliary cirrhosis. 685 Nov 68

The presence of high serum concentrations of immunoglobulins and hypocomplementemia is commonly observed in alcoholic patients; however, the mechanism behind their production is unknown. We studied 70 subjects (52 alcoholics and 18 healthy controls) prospectively. All the patients were active drinkers who consumed more than 100 gr of ethanol daily for at least 10 years. A biopsy of the liver was performed for all the subjects, along with immunoglobulins, C3, C4, CH100 and tests of liver function. Of the 52 alcoholics in the study, 20 showed minimal changes in hepatic steatosis (group II), 6 isolated severe alcoholic hepatitis (group III), 11 cirrhosis of the liver without alcoholic hepatitis (group IV), and 15 cirrhosis with alcoholic hepatitis (group V). There were no significant differences between the various groups according to age or quantity and duration of intake. The highest concentrations of immunoglobulins was observed in those with cirrhosis of the liver (p < 0.001) regardless of the degree of inflammation. The best correlation was found between IgA and liver histology (r = 0.64; p < 0.001). Hypocomplementemia was a factor only in those patients belonging to histological groups IV and V. Both the immunoglobulins and the complement proteins were narrowly correlated with the tests of liver function, and its alterations were more pronounced in patients with cirrhosis in Child's stage C. We conclude that the hypergammaglobulinemia and hypocomplementemia observed in the alcoholic patients are conditioned fundamentally by the degree of deterioration in liver function, indicated by cirrhosis of the liver upon presentation.
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PMID:[Serum levels of immunoglobulins and complement in alcoholic liver disease]. 811 93

The precise mechanism of the pathogenesis of alcoholic hepatitis is unknown, but immune involvement may perpetuate and exacerbate the process. Heat-shock proteins, normally protective, may be immunogenic and have been shown to induce antibody formation in some inflammatory conditions. Alcohol, cellular hypoxia and tumor necrosis factor, all involved in alcoholic hepatitis, are potent inducers of heat-shock protein. In this study, we sought 60-kD heat-shock protein in liver tissue with a murine monoclonal antibody and measured circulating antibody to 60-kD heat-shock protein on ELISA. Fourteen of 20 livers from patients with acute alcoholic hepatitis expressed 60-kD heat-shock protein in hepatocyte cytoplasm in a diffuse pattern with superimposed clusters; other cell types were occasionally positive. Twelve of these patients had high-titer IgA 60-kD heat-shock protein antibody in serum. In contrast, 60-kD heat-shock protein was identified in only 2 of the 10 patients with alcoholic cirrhosis without hepatitis (p = 0.013). These two patients had severe liver disease, and one patient in this group was seropositive for IgA 60-kD heat-shock protein antibody. Eight alcoholic patients with fatty liver alone were negative for antigen, and all but one were negative for antibody. The 10 patients without liver damage were negative for antigen and antibody. The findings that 60-kD heat-shock protein is present in liver tissue of patients with acute alcoholic liver damage and that circulating IgA 60-kD heat-shock protein antibody levels are increased may point to one pathogenetic mechanism underlying development and progression of liver damage in alcoholic hepatitis.
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PMID:Hepatic 60-kD heat-shock protein responses in alcoholic hepatitis. 851 53


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