Pleiotropic effects of Ursosan in non-alcoholic fatty liver disease and metabolic syndrome

Pirogova, I. Yu.; Yakovleva, S. V.; Neujmina, T.V.; Lotos,

doi:10.26442/2414-3529_2018.1.7-14

Cited by 4 publications

(1 citation statement)

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“…[90]. УДХК уменьшает выраженность стеатоза печени по данным неинвазивных методов исследования [91,92,93,86], высокие дозы УДХК уменьшают выраженность балонной дистрофии [94]. УДХК…”

Section: эпидемиологияunclassified

Non-alcoholic fatty liver disease in adults: clinic, diagnostics, treatment. Guidelines for therapists, third version

Лазебник

Голованова

Туркина

et al. 2021

jour

102

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Section: эпидемиологияunclassified

Non-alcoholic fatty liver disease in adults: clinic, diagnostics, treatment. Guidelines for therapists, third version

Лазебник

Голованова

Туркина

et al. 2021

jour

102

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Steatohepatitises: etiological variants, principles of diagnosis and management

Дичева

Andreev

Парцваниа-Виноградова

et al. 2022

Medicinskij sovet

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Steatohepatitises is an etiologically heterogeneous group of pathological changes in the liver, which are characterized by the inflammatory infiltration of the hepatic parenchyma with underlying fatty degeneration of hepatocytes. Whatever is the etiological cause, the clinical significance of steatohepatitis involves the formation of liver fibrosis and, as a result, an increased risk of developing liver cirrhosis and hepatocellular carcinoma, which are life-threatening conditions. It is common practice to identify the following etiological variants of steatohepatitis: metabolic (55–65% of cases), alcoholic (45–55% of cases) and drug-induced (approximately 5% of cases). The pathogenetic basis of metabolic steatohepatitis lies in the mechanisms of increased lipolysis, excess free fatty acid pool and reduced β-oxidation stemming from obesity and insulin resistance. Pathogenetic factors mediating the development of alcoholic steatohepatitis are the toxic activity of acetaldehyde and increased CYP2E1 activity. Intake of some hepatotoxic drugs increases lipogenesis in hepatocytes and disrupts the electron transport chain, which leads to the formation of liver steatosis followed by transformation into steatohepatitis. Whatever is the etiological varient, steatohepatitis is asymptomatic in the prevailing majority of cases. However, some patients may present complaints of weakness, discomfort, or indolent pain in the right hypochondrium. A detailed history taking is essential for the establishment of the etiological cause of liver damage. Laboratory tests allow to diagnose steatohepatitis in increased levels of hepatic transaminases, usually not exceeding 2–3 times the normal values. In addition to liver enzymes, increased levels of alkaline phosphatase and GGTP can also be observed in steatohepatitis. Ultrasound imaging is the most accessible instrumental tool in clinical practice to establish the primary diagnosis of hepatic steatosis. Indirect elastometry is an equally informative non-invasive method for diagnosing steatohepatitis, which allows to measure both the degree of steatosis (the function of determining the ultrasonic controlled attenuation parameter (CAP) and liver fibrosis.

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Non-alcoholic fatty liver disease and cardiovascular risks: A review

Kotovskaya

2023

Consilium Medicum

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Non-alcoholic fatty liver disease (NAFLD) is the most common chronic liver disease. NAFLD may be associated with concomitant metabolic disorders (obesity, type 2 diabetes mellitus, dyslipidemia) and is often considered a hepatic manifestation of metabolic syndrome. In addition to hepatic morbidity and mortality, NAFLD is closely associated with asymptomatic and overt cardiovascular disease (CVD), leading to increased cardiovascular morbidity and mortality, and the more severe the hepatic disorder, the higher the risk. This review describes the main pathophysiological mechanisms linking NAFLD and CVD, discusses the role of NAFLD as a CVD risk factor, and addresses non-drug and drug therapies for NAFLD in the context of cardiovascular risk reduction. NAFLD makes patients candidates for more intensive therapeutic intervention to reduce hepatic and cardiovascular risks. Lifestyle modifications, including weight loss, increased physical activity, and nutritional adjustment, form the basis of NAFLD treatment. Correction of cardiovascular risk factors includes statins, antihypertensive agents, preferably renin-angiotensin system blockers. Ursodeoxycholic acid has therapeutic potential for beneficial effects on hepatic disorders and reducing cardiovascular risk.

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Pleiotropic effects of Ursosan in non-alcoholic fatty liver disease and metabolic syndrome

Cited by 4 publications

References 0 publications

Non-alcoholic fatty liver disease in adults: clinic, diagnostics, treatment. Guidelines for therapists, third version

Non-alcoholic fatty liver disease in adults: clinic, diagnostics, treatment. Guidelines for therapists, third version

Steatohepatitises: etiological variants, principles of diagnosis and management

Non-alcoholic fatty liver disease and cardiovascular risks: A review

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