BACKGROUND Atherosclerotic cardiovascular disease (ASCVD) is the leading cause of mortality in patients with nonalcoholic fatty liver disease (NAFLD). Weight loss is a key factor for successful NAFLD and CVD therapy. Ursodeoxycholic acid (UDCA), which is one of the first-line therapeutic agents for treatment of NAFLD, is reported to have a beneficial effect on dyslipidemia and ASCVD risk because of antioxidant properties. AIM To evaluate the effects of 6 mo of UDCA treatment on hepatic function tests, lipid profile, hepatic steatosis and fibrosis, atherogenesis, and ASCVD risk in men and women with NAFLD, as well as to assess the impact of > 5% weight reduction on these parameters. METHODS An open-label, multicenter, international noncomparative trial was carried out at primary health care settings and included 174 patients with ultrasound-diagnosed NAFLD who received 15 mg/kg/d UDCA for 6 mo and were prescribed lifestyle modification with diet and exercise. The efficacy criteria were liver enzymes, lipid profile, fatty liver index (FLI), noninvasive liver fibrosis tests (nonalcoholic fatty liver disease fibrosis score and liver fibrosis index), carotid intima-media thickness (CIMT), and ASCVD risk score. To test statistical hypotheses, the Wilcoxon test, paired t -test, Fisher’s exact test, and Pearson's chi-squared test were used. RESULTS The alanine aminotransferase (ALT) level changed by -14.1 U/L (-31.0; -5.3) from baseline to 3 mo and by -6.5 U/L (-14.0; 0.1) from 3 to 6 mo. The magnitude of ALT, aspartate transaminase, and glutamyltransferase decrease was greater during the first 3 mo of treatment compared to the subsequent 3 mo ( P < 0.001, P < 0.01, P < 0.001, respectively). At 6 mo, in the total sample, we observed a statistically significant decrease in body weight and levels of FLI: 84.9 ± 10.4 vs 72.3 ± 17.6, P < 0.001, total cholesterol: 6.03 ± 1.36 vs 5.76 ± 1.21, Р < 0.001, low-density lipoprotein: 3.86 ± 1.01 vs 3.66 ± 0.91, Р < 0.001, and triglyceride: 3.18 (2.00; 4.29) vs 2.04 (1.40; 3.16), Р < 0.001. No effect on nonalcoholic fatty liver disease fibrosis score or liver fibrosis index was found. The CIMT decreased significantly in the total sample (0.985 ± 0.243 vs 0.968 ± 0.237, P = 0.013), whereas the high-density lipoprotein ( Р = 0.036) and 10-year ASCVD risk ( Р = 0.003) improved significantly only in women. Fifty-four patients (31%) achieved > 5% weight loss. At the end of the study, the FLI decreased significantly in patients with (88.3 ± 10.2 vs ...

Portal vein thrombosis (PVT) in patients with liver cirrhosis is a common complication associated with adverse outcomes. Aim. To build a predictive model for PVT in cirrhotic patients. Materials and methods. A single centre case-control study was carried out. From the database of 1512 cirrhotic patients 94 with newly diagnosed PVT based on contrast-enhanced computed tomography were referred to the Case group. Malignant PVT was an exclusion criterion. Patients without PVT were stratified and matched according to sex, age and etiology of cirrhosis; case-control ratio was 1 : 3-4. The prevalence of PVT in the database, clinical, laboratory, instrumental parameters of the groups were evaluated. Logistic regression model was used to estimate association between variables and PVT. Results and discussion. The overall prevalence of PVT was 6.2% with the highest rates among the patients with HBV infection - 16.7%, nonalcoholic steatohepatitis - 15.6%, alcohol abuse in combination with HCV infection - 11.7%. The best predictive model included variables: Child-Pugh classes B-C (coefficient of regression β=1.853, р=0.001), ascites (β=0.460, р=0.003), hepatocellular carcinoma without vascular invasion (β=2.126, р=0.0001), endoscopic band ligation (β=0.774, р=0.003), azygoportal disconnection (β=2.734, р=0.001), portal hypertensive gastropathy (β=0.793, р=0.017), portal vein diameter (β=0.203, р=0.004), and local factors - ulcerative colitis flare, Clostridium difficile enterocolitis, spontaneous bacterial peritonitis, colorectal cancer, splenectomy, cholecystectomy (β=2.075, р=0.017). The model had accuracy 85.8% (95% CI 81.7-89.4%), sensitivity - 55.1% (95% CI 43.4-66.4%), specificity - 95% (95% CI 91.6-97.3%), and AUC - 0.871 (95% CI 0.826-0.916). Conclusion. Child-Pugh classes B-C, severe portal hypertension, hepatocellular carcinoma without vascular invasion, and local factors were estimated as risk factors of PVT in cirrhotic patients.

The National Consensus was prepared with the participation of the National Medical Association for the Study of the Multimorbidity, Russian Scientific Liver Society, Russian Association of Endocrinologists, Russian Association of Gerontologists and Geriatricians, National Society for Preventive Cardiology, Professional Foundation for the Promotion of Medicine Fund PROFMEDFORUM. The aim of the multidisciplinary consensus is a detailed analysis of the course of non-alcoholic fatty liver disease (NAFLD) and the main associated conditions. The definition of NAFLD is given, its prevalence is described, methods for diagnosing its components such as steatosis, inflammation and fibrosis are described. The association of NAFLD with a number of cardio-metabolic diseases (arterial hypertension, atherosclerosis, thrombotic complications, type 2 diabetes mellitus (T2DM), obesity, dyslipidemia, etc.), chronic kidney disease (CKD) and the risk of developing hepatocellular cancer (HCC) were analyzed. The review of non-drug methods of treatment of NAFLD and modern opportunities of pharmacotherapy are presented. The possibilities of new molecules in the treatment of NAFLD are considered: agonists of nuclear receptors, antagonists of pro-inflammatory molecules, etc. The positive properties and disadvantages of currently used drugs (vitamin E, thiazolidinediones, etc.) are described. Special attention is paid to the multi-target ursodeoxycholic acid (UDCA) molecule in the complex treatment of NAFLD as a multifactorial disease. Its anti-inflammatory, anti-oxidant and cytoprotective properties, the ability to reduce steatosis an independent risk factor for the development of cardiovascular pathology, reduce inflammation and hepatic fibrosis through the modulation of autophagy are considered. The ability of UDCA to influence glucose and lipid homeostasis and to have an anticarcinogenic effect has been demonstrated. The Consensus statement has advanced provisions for practitioners to optimize the diagnosis and treatment of NAFLD and related common pathogenetic links of cardio-metabolic diseases.

Цель исследования: оценить влияние урсодезоксихолевой кислоты (УДХК) на воспаление, стеатоз и фиброз печени и факторы атерогенеза у больных неалкогольной жировой болезнью печени (НАЖБП). Материалы и методы. В исследование были включены 139 больных НАЖБП, которые получали 15 мг/кг УДХК (Урсосан ®) в сутки на протяжении 24-х нед. До начала и после окончания исследования были определены показатели функции печени и липидного обмена, индекс стеатоза печени FLI, толщина комплекса интима-медия (ТКИМ) сонных артерий, рассчитан сердечно-сосудистый риск по калькулятору ASCVD 2013. Результаты. На фоне применения УДХК у больных НАЖБП наблюдалось снижение активности АЛТ (р < 0,001), АСТ (р < 0,001), ГГТП (р < 0,001), концентрации общего холестерина (р < 0,001), триглицеридов (р < 0,001), ЛПНП (р < 0,001) в крови, индекса стеатоза печени FLI (р < 0,001). Кроме того, у женщин также снизился показатель ТКИМ (р = 0,048) и десятилетний риск сердечно-сосудистых осложнений по калькулятору ASCVD 2013 (р = 0,022). Выводы. Применение УДХК при НАЖБП приводит к уменьшению активности воспалительных процессов в печени, ее стеатоза, а также улучшает показатели липидного обмена и обладает потенциальными антиатерогенными свойствами. На фоне применения УДХК не было отмечено прогрессирования фиброза печени. Никто из участников наблюдательной программы не достиг нормальной массы тела к ее окончанию, поэтому представленные положительные изменения следует отнести непосредственно к эффектам УДХК. Ключевые слова: неалкогольная жировая болезнь печени, стеатоз, сердечно-сосудистый риск, урсодезоксихолевая кислота, липидный обмен, атеросклероз Конфликт интересов: Заказчиком и спонсором исследования выступило ЗАО «ПРО.МЕД.ЦС Маркетинг» по поручению компании "PRO.MED.CS Praha a.s.". Благодарности: Авторы выражают благодарность ассистенту кафедры пропедевтики внутренних болезней Сеченовского Университета Р.В. Масленникову за ценные комментарии и предложения.

Aim: present clinical guidelines, aimed at general practitioners, gastroenterologists, cardiologists, endocrinologists, comprise up-to-date methods of diagnosis and treatment of non-alcoholic fatty liver disease.Key points. Nonalcoholic fatty liver disease, the most wide-spread chronic liver disease, is characterized by accumulation of fat by more than 5 % of hepatocytes and presented by two histological forms: steatosis and nonalcoholic steatohepatitis. Clinical guidelines provide current views on pathogenesis of nonalcoholic fatty liver disease as a multisystem disease, methods of invasive and noninvasive diagnosis of steatosis and liver fibrosis, principles of nondrug treatment and pharmacotherapy of nonalcoholic fatty liver disease and associated conditions. Complications of nonalcoholic fatty liver disease include aggravation of cardiometabolic risks, development of hepatocellular cancer, progression of liver fibrosis to cirrhotic stage.Conclusion. Progression of liver disease can be avoided, cardiometabolic risks can be reduced and patients' prognosis — improved by the timely recognition of diagnosis of nonalcoholic fatty liver disease and associated comorbidities and competent multidisciplinary management of these patients.