Pharmacotherapy of Nonalcoholic Fatty Liver Disease (MASLD)

Fájlok
Metabolic dysfunction-associated steatotic liver disease (MASLD), previously termed nonalcoholic fatty liver disease (NAFLD), represents the most prevalent chronic liver disorder globally, affecting nearly 30% of adults. MASLD encompasses a spectrum of hepatic abnormalities, ranging from benign fat accumulation (steatosis) to more advanced stages such as metabolic dysfunction-associated steatohepatitis (MASH), progressive fibrosis, cirrhosis, and even hepatocellular carcinoma. The pathogenesis of MASLD is multifactorial, shaped by metabolic imbalances, genetic predispositions, and environmental influences. Major risk factors include insulin resistance, obesity, type 2 diabetes mellitus, and dyslipidemia. Diagnosis is commonly achieved through imaging studies, non-invasive biomarkers, and, in some cases, liver biopsy. While lifestyle modification remains the first-line intervention, pharmacologic treatment is indicated in individuals with MASH or significant fibrosis. Recent therapeutic advances include agents such as GLP-1 receptor agonists, SGLT2 inhibitors, PPAR agonists, and resmetirom—a thyroid hormone receptor-β agonist that has recently gained approval. Additional compounds targeting hepatic inflammation, fibrosis, and gut microbiota are under clinical investigation. Innovative approaches like combination regimens and individualized therapy are being explored to accommodate the heterogeneous nature of the disease and improve outcomes. Ongoing research efforts are focused on refining diagnostic tools, enhancing patient stratification, and expanding the therapeutic arsenal for MASLD.(1.13 MB)
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Metabolic dysfunction-associated steatotic liver disease (MASLD), previously termed nonalcoholic fatty liver disease (NAFLD), represents the most prevalent chronic liver disorder globally, affecting nearly 30% of adults. MASLD encompasses a spectrum of hepatic abnormalities, ranging from benign fat accumulation (steatosis) to more advanced stages such as metabolic dysfunction-associated steatohepatitis (MASH), progressive fibrosis, cirrhosis, and even hepatocellular carcinoma. The pathogenesis of MASLD is multifactorial, shaped by metabolic imbalances, genetic predispositions, and environmental influences. Major risk factors include insulin resistance, obesity, type 2 diabetes mellitus, and dyslipidemia. Diagnosis is commonly achieved through imaging studies, non-invasive biomarkers, and, in some cases, liver biopsy. While lifestyle modification remains the first-line intervention, pharmacologic treatment is indicated in individuals with MASH or significant fibrosis. Recent therapeutic advances include agents such as GLP-1 receptor agonists, SGLT2 inhibitors, PPAR agonists, and resmetirom—a thyroid hormone receptor-β agonist that has recently gained approval. Additional compounds targeting hepatic inflammation, fibrosis, and gut microbiota are under clinical investigation. Innovative approaches like combination regimens and individualized therapy are being explored to accommodate the heterogeneous nature of the disease and improve outcomes. Ongoing research efforts are focused on refining diagnostic tools, enhancing patient stratification, and expanding the therapeutic arsenal for MASLD.

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Kulcsszavak
pharmacotherapy, nonalcoholic fatty liver disease, MASLD, Metabolic dysfunction-associated steatotic liver disease
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