Serum Immunoglobulins and Organ Non-Specific Antibodies in Diseases of the Liver

Abstract

Serum immunoglobulins and C3 levels, auto-antibodies to smooth muscle (SMA), mitochondria (MA), and nuclei (ANA), rheumatoid factors (RF), HB-antigen and HB-antibody were studied in 9 groups of liver disease. Hypergammaglobulinaemia was a prominent feature in most groups, IgG being particularly raised in active chronic hepatitis, IgM in primary biliary cirrhosis, and IgA in alcoholic liver disease, respectively. IgE was often increased in alcoholic liver disease and was frequently low in hepatic tumours, whereas IgD showed no typical pattern in any liver disorder. SMA was most frequently found in active chronic hepatitis (68%), and MA in primary biliary cirrhosis (58%), while ANA was detected in 50% of the patients with active chronic hepatitis. However, a pronounced over-lap of tissue antibodies was observed among the various groups of liver disease, particularly in active chronic hepatitis and primary biliary cirrhosis. The concurrent presence of SMA and ANA was most frequent in active chronic hepatitis. It was not excluded that antibody titres might have provided better diagnostic discrimination, since titration of antibodies was not performed. Low C3 levels in active chronic hepatitis were correlated with low levels of other liver-synthetized proteins, and no evidence was found of increased consumption by immunologic reactions.

Expression of Fc Fragment Receptors of Immunoglobulin G (Fc?Rs) in Rat Hepatic Stellate Cells

“…Based on these data, we propose that IgG plays a role in the activation of HSCs and in hepatic fibrogenesis. This hypothesis is supported by clinical observations that there is an increased level of immunoglobulin in patients with liver fibrosis and cirrhosis (17)(18)(19).…”

Rejection and Steroid Dependence: Unique Risk Factors in the Development of Pediatric Posttransplant De Novo Autoimmune Hepatitis

“…In some series patients with liver disease have been described as having higher IgG levels secondary to portosystemic shunting (29,30). Alternatively, others have described up to 26% of post-LT recipients as being hypogammaglobulinemic (31).…”

Soluble interleukin-2 receptor and soluble CD8 in liver cirrhosis and obstructive jaundice

“…Both liver cirrhosis and obstructive jaundice are known to result in some kind of immune defect: liver cirrhosis results in polyclonal hypergammaglobulinaemia with enhanced concentrations of IgG, IgM, IgA (Feizi, 1968;Wilson et al, 1969;Iturriaga et al, 1977;Husby et al, 1977) and IgE (van Epps et al, 1976), but cellular immunity is defective; peripheral blood T cells (Bereny et al, 1974;Thomas et al, 1976), delayed-type hypersensitivity (MacSween & Thomas, 1973;Berenyi et al, 1974;Thomas, 1977), lymphocyte proliferation (MacSween & Thomas, 1973;Berenyi et al, 1974) and natural killer cell function (Nakamura (? ;Charpentiere/fl/., 1984) are all diminished in liver cirrhosis.…”