Differential diagnostics and correction of metabolic and immunological disorders in patients with hepatic cirrhosis, complicated hepatosplenomegalia and portal hypertension
Abstract
Summary: The study of the role of the spleen in the pathogenesis of liver cirrhosis is important for treatment. Currently available literature data indicate the role of altered spleen functions in the pathogenesis of liver cirrhosis. The aim of this study was to clarify the features of the etiology and pathogenetic disorders in patients with hepatosplenomegaly. Materials and methods. We investigated the uniform elements of blood and blood serum from 58 patients with hepatosplenomegaly amid cirrhosis, portal hypertension complicated. Patients were divided into two groups depending on the antigenic load: I - patients with liver cirrhosis against the background of hepatitis viruses HBV/HCV and II - patients with autoimmune hepatitis against the background of herpes viruses CMV/VEB. Treatment of patients included the use of antiherpetic immunoglobulins and hematopoietic cord blood progenitor cells. Results. In patients of group I was detected an increase in the spontaneous oxidative activity of neutrophils and depletion of the oxidative reserve in oxygen-dependent phagocytosis. It activated the signaling pathways of pro-inflammatory cytokines IL-6 (an increase of 60 times). We found an increased content of CD22+ -plasma B-lymphocyte that elevated synthesized concentrations of IgA. In patients of group II were found an increase in the activity of C3 and a decrease in the C4-components of complement; thrombocytopenia due to the presence of platelet autoantibodies; increased synthesis of immunoglobulins IgM, IgG, increased synthesis of IFN-. All patients showed disturbances in the metabolism of amino acids in various metabolic cycles - ornithine, which disrupted the formation of urea and indicates the accumulation of ammonia, which can enhance the cytotoxic effect in group I; methionine with a violation of the formation of cystine from cysteine and the accumulation of homocysteine, which enhances the synthesis of IFN-γ, which was increased in group II by 4 times. Conclusions. Some etiological and pathogenetic features of the formation of liver cirrhosis complicated by portal hypertension and recurrent bleeding from varicose veins of the esophagus were revealed. The immunological and metabolic changes verified by us correlated with the disappearance of the clinical manifestations of the disease, improved well-being, and the absence of recurrence of bleeding.
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