Intensity of liver parenchym fibrosis in patients with alcoholic and non-alcoholic steatohepatitis depending on the presence of dysmetabolic iron overload syndrome

Abstract

Objective — to establish the features of iron homeostasis in patients with steatohepatitis of alcoholic and nonalcoholic etiology depending on the presence of dysmetobolic iron overload syndrome, to identify the probable link between ferrokinetics and markers of biochemical syndromes of steatohepatitis, the intensity of endotoxicosis and fibrosing reactions.
 Materials and methods. The study was based on the clinical follow‑up of 125 individuals, including 60 patients with nonalcoholic steatohepatitis and 65 patients with alcoholic steatohepatitis, 25 practically healthy individuals of appropriate age and gender. Depending on the indicators of iron homeostasis, the examined patients were divided into 4 groups: alcoholic steatohepatitis with dysmetabolic iron overload syndrome — 40 patients, 25 patients without dysmetabolic iron overload syndrome; 18 patients with non‑alcoholic steatohepatitis and dysmetabolic iron overload syndrome and 42 patients — without dysmetabolic iron overload syndrome.
 Results. In alcoholic steatohepatitis, activation of collagen anabolism processes was observed through the growth of protein‑bound oxyproline in blood — in the presence of iron overload syndrome 2.5 times (p < 0.05), in the absence — 2.0 times (p < 0.05), as well as a significant increase in the intensity of collagen catabolism — by increasing the content of free oxyproline in blood, respectively — by 1.5 and 1.3 times (p < 0.05), which occurred due to a significant increase in collagenolytic activity of blood plasma (respectively in 1.6 and 1.4 times; p < 0.05) with the presence of a probable intergroup difference (p < 0.05) in all the cases. There was a significant increase in the content of hexosamines in blood: with iron overload syndrome 1.6 times (p < 0.05), in its absence — 1.5 times (p < 0.05), the content of sialic acids, respectively — 1.6 and 1.5 times (p < 0.05), and the accelerated degradation of fucoglycoprotein components of the extracellular matrix. In non‑alcoholic steatohepatitis, activation of collagen synthesis processes with an increase in blood protein‑bound oxyproline was established — in the presence of iron overload syndrome 1.6 times (p < 0.05), in the absence — 1.3 times (p < 0.05), as well as a slight increase in the intensity of collagen breakdown — with an increase in the content of free oxyproline in blood in non‑alcoholic steatohepatitis with iron overload syndrome — 1.2 times (p < 0.05). There was also a significant increase in the content of hexosamines in blood: in the presence of iron overload syndrome by 1.3 times (p < 0.05), in its absence — by 1.2 times (p < 0.05), the content of sialic acids, respectively — in 1.4 and 1.2 times (p < 0.05), and the accelerated degradation of fucoglycoproteins.
 Conclusions. The regularities of liver fibrosis progression in patients with alcoholic steatohepatitis with iron overload syndrome are inextricably linked with the activation of collagen anabolism, the increase in the intensity of collagen catabolism, which occurred due to a significant increase in collagenolytic activity of blood plasma. An important consequence of the activation of cytolysis and inflammation is a significant increase in the content of hexosamines in blood. In patients with nonalcoholic steatohepatitis, there was an activation of collagen synthesis, a slight increase in the intensity of collagen breakdown in the presence of iron overload syndrome, as well as a characteristic increase in blood hexosamines, and the accelerated degradation of fucoglycoproteins.