Cirrhosis and hypergammaglobulinemia

Stobo, John D.

doi:10.1007/bf01317204

Cited by 25 publications

(6 citation statements)

References 24 publications

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“…(c) Also, it is not possible to rule out chronic and, before abstinence, direct or indirect toxic effects of alcohol on the lymphocytes. The pattern of hyperimmunoglobulinemia observed in AC patients is different from that found in other chronic hepatopathies (33) such as PBC (34). In this study, we found that the alteration in the B-cell regulation pathway of PBC patients is different from that described for AC patients: BCDF I& and BCDF IgM secretion by T lymphocytes from PBC patients are increased, but BCDF IgA production is normal.…”

Section: Discussioncontrasting

confidence: 81%

Increased spontaneous and lymphokine-conditioned IgA and IgG synthesis by B cells from alcoholic cirrhotic patients

et al. 1992

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Immunoglobulin secretion by B lymphocytes is a complex process in which lymphokines secreted by T lymphocytes play an important regulatory role. Increased serum levels of IgA and IgG have been characteristically detected in patients with alcoholic cirrhosis. We have studied the functional alterations of T and B lymphocytes implicated in the physiopathology of this common immunoglobulin abnormality. After activation with phytohemagglutinin, purified T cells from alcoholic cirrhotic patients showed significantly enhanced secretion of B-cell differentiation factors for IgG and IgA with respect to those secreted by T cells from healthy controls (p less than 0.05). Simultaneously, normal secretion of B-cell differentiation factor for IgM was demonstrated in T lymphocytes from these patients. The pattern of secretion of the lymphokines involved in the regulation of the B-cell differentiation pathway found in alcoholic cirrhotic patients was different from that of the primary biliary cirrhotic patients studied. Purified B cells from patients with alcoholic cirrhosis secreted significantly higher amounts of IgA and IgG than did those found in healthy controls, both spontaneously (p less than 0.05) and after sequential activation with immunoglobulin ligands (Staphylococcus aureus Cowan I) and a standard B-cell differentiation factor preparation (p less than 0.05). By contrast, the IgM secretion and regulatory pathway were normal in alcoholic cirrhotic patients. These results support a physiopathological explanation for the characteristic hyperimmunoglobulinemia found in patients with alcoholic cirrhosis.

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Section: Discussioncontrasting

confidence: 81%

Increased spontaneous and lymphokine-conditioned IgA and IgG synthesis by B cells from alcoholic cirrhotic patients

et al. 1992

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“…For example, hypoalbuminemia and hypergammaglobulinemia are accepted biochemical features of liver cirrhosis [10, 11]. Patients with liver cirrhosis also typically have thrombocytopenia due to the accumulation and destruction of platelets in the spleen and due to the reduced synthesis of thrombopoietin [12-14].…”

Section: Discussionmentioning

confidence: 99%

Association of different types of liver disease with demographic and clinical factors

Cheng

Lin

Liu

et al. 2016

BioMed

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Background and Aim:A metric that predicts the presence of cancer-related liver disease would allow early implementation of treatment. We compared the demographic and clinical characteristics of patients with no evidence of liver disease, with a cancer-associated liver disease, and with a liver disease not associated with cancer.Methods:Retrospective, hospital-based, cross-sectional study which reviewed the medical records of subjects who underwent health examinations at a Taiwanese hospital from 2000 to 2004 and who had normal levels of amino transaminases. Demographic and clinical data were analyzed by univariate and multivariate statistics.Results:A total of 2344 subjects had no evidence of liver disease (non-LD), and 1918 subjects had at least one liver disease (LD). The LD group was further divided into those with a cancer-associated liver disease (LD-1, n = 1632) and those with a liver disease not associated with cancer (LD-2, n = 286). Age, BMI, percentage of males, globulin:albumin ratio (G/A), percentage of patients with gallstones, AST, and ALT were significantly higher in the LD group. Univariate analysis showed that the G/A was significantly higher in the LD-2 group than the LD-1 group; multivariate analysis indicated that the G/A was not independently associated with liver disease, but that subjects who were older and had higher BMI were significantly more likely to have a cancer-associated liver disease. Conclusions: For patients with liver disease, a multivariate model can be used to distinguish those with a cancer-associated liver disease from those with a liver disease not associated with cancer.

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“…However, the exact mechanism underlying the high level of antibody formation is not fully understood, but two general theories have been postulated. One is that the diseased liver fails to sequester or inactivate antigens and endotoxins absorbed from the gut because they bypass the liver via the collateral circulation, and consequently antigens and endotoxins become available to antibodies [ 12 , 13 ]. Another theory is that in the state of generalized immunologic reactivity, the level of immunoglobulin is elevated due to the non-specific activation of many different clones of antibody producing-cells that secrete immunoglobulins [ 14 , 15 ].…”

Section: Introductionmentioning

confidence: 99%

The Injured Liver Induces Hyperimmunoglobulinemia by Failing to Dispose of Antigens and Endotoxins in the Portal System

et al. 2015

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Hyperimmunoglobulinemia is frequently observed in patients with chronic liver diseases. However, the exact mechanism underlying the high level of antibody formation is not fully understood. In our study, we provide evidence for the functional role of the liver and the stimulation of plasma cell proliferation in hyperimmunoglobulinemia. We collected sera from patients with chronic liver diseases, and the level of serum immunoglobulins in patients was examined; this was also investigated in animal models of liver cirrhosis and hepatocellular carcinoma. An end-to-side microsurgical portacaval shunt was used to mimic liver dysfunction in rats. We used portal vein serum and inferior vena cava serum to immunize healthy rats and mice in order to confirm the function of the healthy liver in disposing of antigens and endotoxins from the gut. For the analysis of the state of plasma cell activation, plasma cells from mice were stained with PE-conjugated anti-CD138 and FITC-conjugated anti-BrdU for flow cytometry analysis. Hyperimmunoglobulinemia was observed both in patients with chronic liver diseases and in related animal models, and high plasma LPS levels were also observed. There was a significant increase in the activation and proliferation of plasma cell in mice immunized with antigens or LPS-positive serum compared with controls that were immunized with antigens and LPS-negative serum. We confirmed that the healthy liver plays an important role in disposing of antigens and endotoxins derived from the gut. Hyperimmunoglobulinemia in chronic liver diseases mainly arises due to the collateral circulation secondary to portal hypertension, gut antigens and endotoxins that bypass the liver and reach the antibody-producing cells.

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Cirrhosis and hypergammaglobulinemia

Cited by 25 publications

References 24 publications

Increased spontaneous and lymphokine-conditioned IgA and IgG synthesis by B cells from alcoholic cirrhotic patients

Increased spontaneous and lymphokine-conditioned IgA and IgG synthesis by B cells from alcoholic cirrhotic patients

Association of different types of liver disease with demographic and clinical factors

The Injured Liver Induces Hyperimmunoglobulinemia by Failing to Dispose of Antigens and Endotoxins in the Portal System

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