Основними причинами стеатогепатиту печінки є вплив на неї токсичних речовин, ендокринні порушення, неправильне харчування. Особливе місце серед токсичних агентів займає алкоголь. Мета – дослідити зміни основних показників червоної крові при стеатогепатиті різної етіології. Матеріал і методи. Проведено клінічне спостереження за 60 хворими на алкогольну хворобу печінки та неалкогольний стеатогепатит. Серед обстежених 53,3 % становили чоловіки, 46,7 % – жінки. Усіх хворих було поділено на дві групи: до першої (І) ввійшли 33 % пацієнтів з алкогольною хворобою печінки (алкогольним стеатогепатитом – АСГ), до другої (ІІ) – 67 % хворих із неалкогольною жировою хворобою печінки (неалкогольний стеатогепатит – НАСГ). Контрольну групу склали 20 практично здорових осіб (ПЗО), в яких не виявлено гострих чи хронічних захворювань та алергічних проявів. Результати. При дослідженні показників клінічного аналізу крові встановлено, що вміст еритроцитів у периферичній крові хворих на НАСГ був у межах норми, а у хворих на АСГ даний показник був вірогідно нижчий за показник у ПЗО на 9,0 % (p<0,05). Разом з тим, вміст гемоглобіну у хворих цієї ж групи вірогідно відрізнявся від вікової норми і був істотно нижчий від показника у ПЗО на 8,5 % (p<0,05), а це свідчить, що в частини хворих на АСГ встановлено анемічний синдром. Висновок. Перебіг алкогольного стеатогепатиту у 25,0 % випадків супроводжується анемічним синдромом легкого ступеня, незважаючи на істотне вірогідне підвищення в сироватці крові вмісту заліза, феритину, насичення трансферину залізом. Причому, в 15,0 % хворих на АСГ анемія зумовлена дефіцитом вітаміну B12, а у 10,0 % – гемолізом еритроцитів. Описано, що на тлі ожиріння перебіг неалкогольного стеатогепатиту характеризується невірогідним зростанням показників вмісту заліза в сироватці крові, вмісту феритину та насичення трансферину залізом за відсутності клініко-лабораторних ознак анемії.

The retrospective analysis of 378 medical records of inpatients with steatohepatitis (SH) depending on its etiology was performed to identify and study the type of anaemic conditions (AC). Among patients with SH of mixed (including alcoholic) etiology anaemia was found in 32.2% of cases, in patients with alcoholic (ASH) - in 36.3%, in patients with non-alcoholic SH (NASH) - in 22.0 % of cases. Macrocytic, hyperchromic anaemia prevailed in patients with anaemia of all groups: in patients with SH of mixed etiology - in 47.9%, in patients with ASH - 56.8%, NASH - 71.4%. Normocytic, normochromic anaemia was registered in 52.1% with mixed etiology of SH, in patients with ASH - 43.2%, NASH - 28.6%.The prospective study of 125 patients with SH showed that anaemia was found in 40.0% of patients with ASH, among patients with SH of mixed (including alcoholic) etiology anaemia was found in 32.0%, among patients with NASH the result was 21.7%. The following types of anaemia were found in ASH: vitamin B12 - deficient - in 17.5% of cases, anaemia of chronic disease - in 10.0% of cases and Zieve's syndrome - in 12.5% of cases. Three types of anaemia were found in patients with SH of mixed etiology: vitamin B12 - deficient - in 16.0% of cases, anaemia of chronic disease - in 8.0% and Zieve's syndrome - in 8.0% of patients. The structure of anaemias in patients with NASH accompanied by obesity of I-II degrees is as follows: B12 - deficient anaemia - in 15.0% of cases, anaemia of chronic disease - in 6.7% of people. In patients with NASH, H. pylory contamination was present in 84.6% of patients with anaemic syndrome (AS), including 100% of patients with B12-deficient anaemia. With ASH, H. pylory contamination was present in 80.0% with anaemia, including 100% of patients with B12-deficient anaemia. In patients with SH of mixed etiology, H. pylory contamination was present in 100.0% of people with AS.

Aim of the study: To establish the effectiveness of discrete plasmapheresis in the treatmentof patients with nonalcoholic fatty liver disease accompanied by hyperferritinemia andconcomitant obesity.Material and methods. The study is based on the clinical observations of 18 patientswith non-alcoholic steatohepatitis accompanied by hyperferritinemia and concomitantobesity. Each patient was undergoing the basic therapy as well as the sessions of discreteplasmapheresis for 10-14 days, which led to the removal of 17-20% of the volume ofcirculating plasma during each procedure, the total of which amounts to about 1-1.5 ofthe circulating plasma volume.Results. As a result of the two-week treatment, the patients' well-being improvedsignificantly, their efficiency increased, and previously elevated levels of ferritin (1.29times in men and 1.21 in women) and serum iron (2.7 times) decreased. The initiallyelevated level of total cholesterol also decreased significantly (2.34 times), and due toVLDL (7.86 times) and triacylglycerols – 9.78 times. The atherogenic factor decreasedfrom 3.8 to 1.5. (2.5 times). The sizeable decrease was observed in the uric acid content– 1.77 times, ALT activity – 1.55 times, LDH – 1.77 times, LF – 1.42 times, GGTP – 4.0times (p <0.05).Conclusions. Inclusion of the discrete plasmapheresis sessions to the treatmentprogram of non-alcoholic steatohepatitis at comorbidity with hyperferritemia andobesity enables to reduce significantly the initially elevated blood levels of ferritin,serum iron, LPVLD, triacylglycerols, cholesterol, AAT, LDHG, AP, GGTF activity.

The aim: to study some histopathological changes in the liver affected by steatohepatitis of various etiologies with the presence of anemia. Material and methods. Liver biopsies were analyzed in 30 patients with non-alcoholic steatohepatitis (NASH) and 20 patients with alcoholic steatohepatitis (ASH). The morphological examination of the liver was carried out according to the standard methods. The histopathological features of the liver were established on the basis of hematoxylin and eosin staining method, with confirmation, if necessary, by the histochemical methods - staining for fat (method with Sudan-III) and collagen fibers (method with chromotropic-water blue by NZ Slinchenko). Microspectrophotometric studies were performed using a cytological analyzer with software "VideoTest - Size 5.0" (2000). Results. A number of parameters revealed the statistical differences in the average trends with the use of the nonparametric Mann-Whitney method (p<0.05). The highest rate of hepatocyte necrosis was observed in the patients with ASH with anemia, in particular, more than a third of hepatocytes in these patients had signs of colic necrosis, which was more pronounced in ASH than in NASH. NASH with anemia was accompanied by more pronounced necrosis of hepatocytes than NASH without anemia. In ASH without anemia, the percentage of affected hepatocytes was on average approximately the same as in NASH without anemia. Fatty dystrophy of hepatocytes was observed in all the patients with NASH and ASH, but the severity of the general pathological process was not the same. Conclusions. Due to the comorbidity of fatty liver disease with anemia in both NASH and ASH, a much higher percentage of hepatocytes affected by reversible swelling are formed, which coincides with the tendency for hepatocyte oncosis. Anemia affects the nature of connective tissue growth in NASH and ASH (in ASH, the specific volume of connective tissue was higher than in NASH). At the same time, the intensity of regenerative processes in the liver (ductal reactions of the liver) is most pronounced in patients with anemia, and most - in ASH.

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.