ГИПЕРАММОНИЕМИЯ У ПАЦИЕНТОВ НА ДОЦИРРОТИЧЕСКОЙ СТАДИИ: КЛИНИЧЕСКАЯ РЕАЛЬНОСТЬ?

Ammonia belongs to the common neuro- and cytotoxic metabolites in the human. It is established that ammonia has hepatotoxic properties. Ammonia induces the formation of oxygen active forms, reduces the activity of endothelial NO synthase, dose-dependently decreases the cellular metabolism and proliferation of stellate cells, and promotes fibrogenesis, disturbance of intrahepatic hemodynamics and, accordingly, the formation of portal hypertension. The article demonstrates causes of hyperammonemia in pathological conditions and disturbance of physiological functions. The increased level of ammonia is associated not only with various neuropsychiatric disorders in liver cirrhosis, but also is shown in patients with chronic liver disease (CLD) at the precirrhosis stage. The presence of minimal hepatic encephalopathy in patients with chronic hepatitis is a cognitive impairment, which manifests as a de-crease in concentration, in particular when driving. The effect on hyperammonemia becomes a target for therapy in steatohepatitis of various etiologies. The use of the oral form of L-ornithine-L-aspartate effectively reduces the level of ammonia in the blood, improves cognitive function and positively affects the functional state of the liver in patients with CLD at the precirrhotsis stage.