Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Absolute numbers of T and B lymphocytes as well as active E rosette-forming cells were measured in twenty-seven patients with chronic active hepatitis (CAH), and in thirty control patients. In patients with CAH without cirrhosis, active E rosette-forming cells (a subpopulation of T lymphocytes considered to be actively involved in cell-mediated immune reactions) as well as lymphocytes with surface markers for IgA, IgM and IgG were increased. In patients with CAH and cirrhosis, total T lymphocytes were decreased. These results emphasize the significance of lymphocytes in CAH, and suggest the importance of monitoring T- and B-cell populations in patients with this disease.
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PMID:T and B lymphocytes in patients with chronic active hepatitis (CAH). 30 78

Increased antibody production and hypergammaglobulinaemia in cirrhosis are probably to a large extent due to decreased hepatic extraction of antigens. The deceased extraction is presumably related to changed microcirculation caused by damaged anatomical structure of the liver. It is therefore to be expected that immunoglobulin and antibody levels in serum in cirrhotic patients are related to the degree of certain morphological changes of the liver. This hypothesis has been tested. In 50 patients with cirrhosis, 28 alcoholics and 22 non-alcoholics, the degree of architectural destruction, the degree of fibrosis, the degree of fatty infiltration, and the degree of "activity" were compared with immunoglobulins G, A, and M and E. coli O antibody levels. The comparison was carried out within each of the aetiological groups. Identical relationships were found in both groups. Patients with completely destroyed lobular architecture had higher levels of E. coli O antibodies than patients with partly destroyed architecture. Patients with severe fibrosis had higher IgA and E. coli O antibody levels than patients with moderate or slight fibrosis. Patients with moderate and severe steatosis and patients with no or slight steatosis had the same immunoglobulin and E. coli O antibody levels. Patients with active cirrhosis had higher IgG levels than patients with inactive cirrhosis. When architectural destruction and fibrosis were combined significantly higher IgG, IgA, IgM, and E. coli antibodies were found in the group with the most severe changes. These findings support the hypothesis that immunoglobulin and antibody levels are related to the degree of morphological changes in the liver--namely, destruction of lobular architecture, fibrosis, and "activity".
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PMID:Correlation between hepatic morphology and immunoglobulins and antibodies to Escherichia coli in cirrhosis. 32 Jan 10

Rapid progression of acute type B hepatitis to chronic active liver disease and cirrhosis in a young male with hypogammaglobulinemia is described. Absent circulating IgA, significantly low IgG, and normal IgM levels were detected during the acute phase of illness. Enumeration of peripheral lymphocytes revealed a decreased number of T cells and normal numbers of B cells. In vitro pokeweed stimulation of Ig synthesis correlated with the in vivo circulating levels of the three immunoglobulins. Cell-mediated immune responses were normal except for lymphocyte stimulation to hepatitis B surface antigen. It was concluded that the defective synthesis of IgG and IgA antibodies to hepatitis B surface antigen contributed to the accelerated progression to chronic active type B hepatitis in this person.
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PMID:Rapid progression of chronic active type B hepatitis in a patient with hypogammaglobulinemia. 33 24

The effect of a portocaval shunt with and without portal arterialization of the liver on serum immunoglobulin concentrations and on the incidence of antibodies to 8 different serotypes of Escherichia coli was studied in 29 patients with cirrhosis of the liver. Compared with healthy controls, the serum concentrations of IgG, IgA and IgM were significantly elevated in cirrhotic patients. No difference in immunoglobulin concentrations could be observed between shunted and arterialized cirrhotics. The incidence of E. coli antibodies was significantly higher in patients with cirrhosis of the liver, showing a further increase in patients with portocaval shunt operations. Portal arterialization of the liver after portocaval shunting did prevent this additional increase, presumably by restoring the antigen clearing capacity of the cirrhotic liver, thus avoiding an additional stimulation of the antigen response after the portocaval shunt. The quantitative contribution of E. coli antibodies to the hyperimmunoglobulinemia of patients with cirrhosis of the liver seems to be of little significance. The results of this study underline the significance of the portal hepatic blood flow for the function of the reticulo-endothelial system of the liver.
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PMID:[Effect of portocaval shunt and arterialization of the liver on antibodies to Escherichia coli in patients with cirrhosis of the liver (author's transl)]. 36 Jun 47

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

Sera of twenty-five patients with alcoholic liver disease and forty normal control sera were screened for circulating immune complexes by means of the anti-antibody neutralization test and by Raji-cell membrane immunofluorescence assay. IgG-containing immune complexes were detected in thirteen out of twenty-five patients with alcoholic liver diseases and in one out of forty normal individuals; in addition, IgA-containing complexes were demonstrated in seven out of thirteen sera positive for IgG complexes. The presence of immune complexes was restricted to alcoholic hepatitis and active cirrhosis, thus indicating a relationship with disease severity.
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PMID:Detection of circulating immune complexes in alcoholic liver disease. 37 31

Secretory IgA (sIgA) were searched in 60 sera of healthy blood donors and in 1 590 sera of subjects having various diseases. 20 percent of these subjects showed an increased amount of sIgA in their sera. The only subjects presenting a constant increase (sometimes more than 20 fold the normal amount) were people with liver diseases. Quantitation of sIgA, in relation with the determination of the IgA/transferrin ratio (IgA/T) in sera, showed an important difference between Laennec's cirrhosis on one hand and virus hepatitis or post-hepatitic cirrhosis on the other. In Laennec's cirrhosis a moderate increase in sIgA went with a strong elevation of the IgA/T ratio, the latter being proportional to the degree of evolution of the disease. In virus hepatitis, the sIgA amount was largely increased while the IgA/T ratio remained at a normal value.
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PMID:[Use of serum s-IgA detection in liver pathology (author's transl)]. 39 19

The authors propose electro-immunodiffusion on cellulose acetate instead of agar gel. This simple, rapid and economical method was applied to the estimation of serum immunoglobulins A and transferrin. The following results were obtained for the IgA/transferrin ratio in 108 cases: Normal: 0.87 +/- 0.29; alcoholics without proved cirrhosis: 1.61 +/- 0.95; alcoholic cirrhosis: 3.36 +/- 2.30. The interest of this determination in detection is increased by this simple test.
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PMID:[Trial of immunodiffusion on cellulose acetate. Application to the estimation of immunoglobulins A and serum transferrin. Results in alcoholism and cirrhosis (author's transl)]. 41 95

Serum immunoglobulins were determined in 39 healthy subjects and 55 patients with a variety of acute and chronic liver diseases. Elevation of IgG and IgA was frequently observed in healthy subjects and patients with acute viral hepatitis, liver cancer and miscellaneous liver disorders. IgG and IgM were elevated in cirrhosis of the liver.
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PMID:Immunoglobulins in liver disease. 41 44

We evaluated 20 patients with primary biliary cirrhosis and seven controls with extrahepatic biliary obstruction for presence of circulating immune complexes, having found serologic evidence of alternate complement-pathway activation in eight of the 20. Immune complexes were isolated by cryoprecipitation from serum and measured directly by the sensitive Raji-cell radioimmunoassay. Cryoproteins, found in high concentrations in 90 per cent of the patients with cirrhosis but undetectable in the controls, were composed of IgM (60 per cent), IgG-IgM (25 per cent) and IgA-IgM (5 per cent) and were capable of activating the complement system in vitro. Immune complexes detected by the Raji assay were found in 95 per cent of the patients with cirrhosis and circulated in exceedingly high concentrations (474 microgram per milliliter; range, 16.2 to 2192) but were absent in the controls. Furthermore, the alternate complement pathway was activated in eight cirrhotic patients. These complement-fixing immune complexes differ from immune complexes isolated from other types of liver diseases and may be important in the pathogenesis of primary biliary cirrhosis.
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PMID:Circulating immune complexes and complement activation in primary biliary cirrhosis. 61 65


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