Some aspects of the pathogenesis of hepatic encephalopathy

Abstract

Aim. To study the pathogenesis of hepatic encephalopathy in patients with cirrhosis of the liver. Material and methods.141 patients with liver cirrhosis complicated by hepatic encephalopathy were examined. The diagnosis was established on the basis of anamnesis, clinical, biochemical, instrumental, virological methods of research, including the study of the level of pro-inflammatory cytokines and ammonia in the blood serum. Results and discussion. The level of interleukin-6 in patients with liver cirrhosis in the stage of decompensation averaged 118 ± 14 pg/ml (p < 0,01), and increased to 194 ± 14 pg/ml (p < 0,05) in hepatic encephalopathy. Levels of tumor necrosis factor – α almost doubled. The level of tumor necrosis factor (TNF-α) in patients with liver cirrhosis in the stage of decompensation averaged 121 ± 12 pg/ml (p < 0,001), while in patients with hepatic encephalopathy it made 244 ± 17 pg/ml (p < 0,005). A similar picture was also observed when studying the ammonia in blood serum. In liver cirrhosisin the stage of decompensation level of ammonia was 93,1 + 4,2 (p < 0,001). In patients with hepatic encephalopathy, a decrease in the number of bifidobacteria, lactobacteria and eubacteria by 3-4 times compared with the norm was revealed. At the same time, the number of pathogenic microflora and yeast fungi increased. Conclusion. In the pathogenesis of hepatic encephalopathy, a high content of pro-inflammatory cytokines and nitrogenous compounds play an important role as a result of the syndrome of increased bacterial growth and persistence of Helicobacter pylori in the gastric mucosa.