[Humoral and cellular adaptation mechanisms in development of intoxication syndrome in patients with acute viral hepatitis].
OBJECTIVE
To study endotoxin-binding function of blood in patients with acute viral hepatitis (AVH) in the course of the disease.


METHODS
A total of 335 patients with AVH were examined. The titers of IgG antiendotoxin antibodies to glycolipid of Re-chemotype were estimated in enzyme immunoassay (Diaendotox-2 kit), endotoxin-binding activity (EBA) of high density lipoproteins (HDLP) in EIA with the kit Liprobind (Microecos). The number of polymorphonuclear leukocytes (PL) binding lipopolysaccharides were counted by M. Yu. Yakovlev et al. method. For detection of PL binding endotoxin of gram-negative bacteria, kits Endim (Microecos) were used, beta2-microglobulin was estimated by a radioimmunoassay using kits made in Belarus Institute of Bioorganic Chemistry. Registration of chemoluminescence was conducted on chemiluminometer LBK 1251 (Finland) by M. Wilson (1985) method.


RESULTS
In moderate AVH at the height of intoxication a low Re-antibodies level was recorded irrespective of the disease etiology. To convalescence this level went up. PL reserves in AVH patients were low except patients with AVH C who had unaffected neutrophil reverves in relation to LPS binding. At the height of AVH, HDLP EBA was very high in all the groups with normalization to convalescence. In VHC high HDLP EBA persisted as long as the disease course. A significant rise of beta2-microglobulin was seen in all the groups of AVH patients, its severity correlating with the degree of the disease severity.


CONCLUSIONS
One of the leading factors in development of indoxication in AVH patients is a lipopolysaccharide complex of gram-negative intestinal bacteria actively coming into blood flow due to hepatocyte cytolysis. In response to LPS action there appeared a stereotypic adaptation complex of reactions in the form of activation of cellular and humoral immune response.
Pak
S G
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Volchkova
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Umbetova
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D000208:Acute Disease; D000222:Adaptation, Physiological / Q000276:immunology; D000328:Adult; D019446:Endotoxemia / Q000209:etiology / Q000276:immunology*; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D006017:Glycolipids / Q000097:blood / Q000276:immunology*; D006525:Hepatitis, Viral, Human / Q000150:complications / Q000276:immunology*; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood / Q000276:immunology; D008070:Lipopolysaccharides / Q000097:blood / Q000276:immunology*; D008075:Lipoproteins, HDL / Q000097:blood; D008297:Male; D009504:Neutrophils / Q000276:immunology*; D001613:beta 2-Microglobulin / Q000097:blood / Q000276:immunology
D006017:Glycolipids; D007074:Immunoglobulin G; D008070:Lipopolysaccharides; D008075:Lipoproteins, HDL; C055264:Re-glycolipid; D001613:beta 2-Microglobulin