Clinical efficacy of S-adenosyl-L-methionine and antihypertensive combination treatment in patients with comorbid course of metabolic-associated steatotic liver disease and arterial hypertension

Objective — to determine the likely effect of S‑adenosyl‑L‑methionine (SAMe) and antihypertensive combination treatment on the clinical course, liver enzymatic activity (the levels of aspartate aminotransferase, alanine aminotransferase, gamma‑glutamyl transpeptidase, alkaline phosphatase), nonalcoholic steatohepatitis activity and the stage of liver fibrosis (LF) stage in patients with metabolic dysfunction‑associated steatotic liver disease (MASLD) and arterial hypertension (AH) comorbid course. Materials and methods. We examined 40 patients with MASLD and AH comorbid course before and after 5 months of the SAMe and antihypertensive combination treatment. The control group comprised 20 apparently healthy people. Patients with viral hepatitis, liver cirrhosis, alcoholic liver disease, AH stage III, and liver fibrosis stage F3—4 were excluded. Liver cytolysis indicators analyses were performed using biochemical techniques. The severity of liver fibrosis was assessed using transient elastography results. Results. Analysis of SAMe and antihypertensive combination treatment in patients with MASLD and AH demonstrated a significant improvement in the clinical course of the disease (reduction in complaints of increased fatigue, headache, general weakness, right upper quadrant pain, sleep disturbance and mood worsening (p<0.05)), significant decrease of systolic blood pressure (p<0.01), diastolic blood pressure (p<0.05), body mass index (p<0.05) and waist‑to‑hip ratio (p=0.05), liver cytolysis indicators such as aspartate aminotransferase (p<0.01), alanine aminotransferase (p<0.01), gamma‑glutamyl transpeptidase (p<0.01) and alkaline phosphatase (p<0.05). Also, a decrease in nonalcoholic steatohepatitis activity (p<0.05) and regression of the liver fibrosis stage (p<0.05) were observed. Conclusions. The results of SAMe and combined antihypertensive therapy show the improvement of the clinical course of the disease, liver function, and the regression of the liver fibrosis stage. Therefore, the inclusion of SAMe in standard antihypertensive therapy of patients with a comorbid course of MASLD and AH is an appropriate treatment method as a pathogenetic drug with a pronounced cytoprotective, anti‑inflammatory, and antifibrotic effect.