Diagnosis and treatment of metabolic-associated fatty liver disease in patients with type 2 diabetes mellitus. Review

• Published in: Clinical Endocrinology and Endocrine Surgery no. 3; pp. 62 - 69
• Main Author: Tkach, S. M.
• Format: Journal Article
• Language: English
• Published: 30.09.2023
• ISSN: 1818-1384; 2519-2582
• DOI: 10.30978/CEES-2023-3-62

Metabolic‑associated fatty liver disease (MAFLD) is a new clinical definition of fatty liver disease that changes the definition of non‑alcoholic fatty liver disease (NAFLD) from a disease of exclusion to a disease of inclusion, in which the main pathogenic processes originate from metabolic dysfunction, primarily in type 2 diabetes mellitus (T2DM) and obesity. In recent years, MAFLD has become an epidemic and is closely associated with T2DM and a significant synergistic increase in the risk of cardiovascular disease. The presence of MAFLD significantly increases the risk of T2DM development, and the risk of new onset of T2DM in patients with MAFLD doubles. When managing patients with MAFLD and T2DM, the presence of fibrous nonalcoholic steatohepatitis (NASH) should be actively detected, for which non‑invasive indicators should first be used, such as FIB‑4 and FNI, which are available at the level of primary care. Despite evidence of utility in improving diagnosis, the effectiveness of many of the above non‑invasive tests for detecting fibrosis, particularly in unselected populations with advanced fibrosis, is low and generally remains uncertain at the primary care level. Modifications of lifestyle and diet have traditionally been considered the best therapeutic option for MAFLD in T2DM, with weight loss of ≥7% significantly improving steatosis, leading to reductions in NASH activity and glycemia. At the same time, only 40% of patients achieve this goal and reduce the activity of steatohepatitis, emphasizing the difficulty in treating MAFLD only by lifestyle changes. Nevertheless, mandatory dietary and lifestyle modification should still be recommended for patients with MAFLD, along with antidiabetic drugs that can reduce liver enzyme activity, inflammation, and fibrosis, such as PPARγ inhibitors, SGLT‑2i, GLP‑1 RA, as well as dual GIP and GLP‑1 RA agonists.