[Autoimmune reactions in diseases of the digestive system organs]

To examine content, diagnostic and prognostic role of autologous antibodies in gastrointestinal diseases (GID).

Enzyme immunoassay was used to measure content of autologous antibodies to N+/K+ ATPase (Aab) of gastric parietal cells, mitochondria, microsomes, tissue transglutaminase in blood serum of 196 patients with gastric, gallbladder, small and large intestinal diseases. Aab relations with heterologous antibodies were studied with kits provided by Bektor-Best (Novosibirsk), DRG-Diagnostics, Orgentec (Germany) and others.

In GID high circulation of Aab to parietal cells (Ab-PC) was detected in 42% cases, mean content being 217 +/- 32.4 U/ml, 10 U/ml in the control. Maximal concentration (180 = 340 U/ml) occurred in hepatic cirrhosis, celiac disease, atrophic gastritis. In exacerbations of pancreatitis, colelithiasis and duodenal ulcer ab-PC concentration was 190-210 U/ml, in remission--6-12 U/ml. Minimal concentration (8-38 U/ml) was seen in polyps, gastric cancer, nonspecific ulcerative colitis. For primary biliary cirrhosis more typical was high A/ab concentration to mitochondria (in 83%; 200 U.ml), for autoimmune hepatitis--Aab to microsomes (in 81%; 170 U/ml), in celial disease--Aab to tissue transglutaminase (93%, 75 U/ml). High autoantibodies concentration in GID is accompanied with overcirculation of heteroantibodies to infectious-toxic agents confirming their role in development of autoimmune processes.

GID are associated with high circulation of autologous antibodies--markers of systemic humoral autoimmune reactions differing in duration, severity, site of lesion, form, stage, disease duration. Maximal detection rate and concentration of serum autologous antibodies were observed in hepatic cirrhosis, active hepatitis, celiac disease, atrophic gastritis, exacerbations of cholelithiasis, ulcer, pancreatitis. Estimation of Aab concentration is essential for diagnosis, prognosis of autoimmune diseases, it reflects intensity and duration of autoimmune reactions in GID.