Multi-component infusion hepatoprotectors for liver damage

• Main Authors: E. I. Sas, V. B. Grinevich
• Format: Article
• Language: Russian
• Published: Remedium Group LLC 2019-05-01
• Series: Медицинский совет
• Subjects: drug-induced liver injury; side effect; amber acid; remaxol
• Online Access: https://www.med-sovet.pro/jour/article/view/3009
• ISSN: 2079-701X; 2658-5790

Drug-induced liver injuries (DILI) remain today one of the most pressing problems not only in gastroenterology, but also in all therapy. Up to 10% of the changes in laboratory parameters can be attributed to the use of drugs. The importance of DILI has increased significantly in recent years, due to the increase in the number of over-the-counter medicines on the pharmaceutical market, as well as non-compliance with the methods and modes of administration. There are common links in the pathogenesis of DILI, including hypoxia, de-energization (deficit of ATP production), damage to hepatocyte membranes and suppression of antioxidant protection. Therefore, pathogenetic pharmacotherapy and prevention of liver damage are based on drugs with an action mechanism aimed at eliminating one or more links in the pathogenesis. One of these drugs is Remaxol, which includes antihypoxantantioxidants of metabolic type: natural metabolites, substrates and cofactors involved in energy metabolism. Remaxol was administered to 30 patients with duodenal ulcer (DU) in the acute phase in addition to the main eradication therapy in the case of cytolytic syndrome by the end of the first week of therapy intravenously dripping at a rate of 40-60 drops/min in a daily dose of 400 ml for 10 days a day. Against the background of Remaxol application, the patients with DILI had stabilization of the main biochemical parameters: the level of AST, ALT, direct bilirubin, GGT and alkaline phosphatase. These changes were accompanied by a positive dynamics of the general state of health. The use of Remaxol in patients with DILI will allow to achieve clinical and biochemical remission, preventing the development of severe liver damage, and contributes to the preservation of the recommended duration of treatment of the underlying disease.