Compensated advanced chronic liver disease in patients with metabolic dysfunction-associated steatotic liver disease: association with cardiometabolic factors

Aim . Тo study cardiometabolic factors and the PNPLA3 I148M (rs738409 C>G) gene polymorphism in association with the compensated advanced chronic liver disease (cACLD) in patients with metabolic dysfunction-associated steatotic liver disease (MASLD). Materials and methods . А retrospective cross-sectional study was conducted. The total of 108 patients with MASLD (33 men and 75 women aged 28 to 89 years) involved were divided into two groups based on results of transient elastography: group 1 – with the presence of cACLD (liver stiffness ≥ 8.0 kPa) – 18 patients and group 2 – without cACLD (<8.0 kPa) – 90 patients. Cardiometabolic risk factors and the PNPLA3 I148M (rs738409 C>G) gene polymorphism were studied in both groups. Odds ratios (OR) and 95% confidence intervals (CI) were calculated, and a logistic regression model was constructed for the detection of cACLD. Results . Compared to group 2, patients with cACLD had statistically significant higher prevalence of: arterial hypertension ( p < 0.05), type 2 diabetes mellitus ( p < 0.01), obesity ( p < 0.05), dyslipidemia ( p < 0.05), and PNPLA3 gene polymorphism ( p < 0.05). The OR for cACLD in individuals with arterial hypertension was 5.58 (95% CI: 1.21–25.71; p < 0.05), with type 2 diabetes mellitus – 4.58 (95% CI: 1.59–13.21; p < 0.01), with obesity – 3.83 (95% CI: 1.17–12.52; p < 0.05), with dyslipidemia – 6.12 (95% CI: 1.33–28.20; p < 0.05), in the presence of a polymorphic variant of the PNPLA3 gene in a hetero or homozygous state – 3.9 (95% CI: 1.28–11.89; p < 0.05). The binary logistic regression model for detecting cACLD included type 2 diabetes mellitus, dyslipidemia, and waist circumference. The area under the ROC curve was 0.81 (95% CI: 0.70–0.92), sensitivity was 72.2%, specificity was 74.4%, and accuracy was 84.3%. Conclusion . Type 2 diabetes mellitus, dyslipidemia, and waist circumference are the determining factors for the development of cACLD in patients with MASLD. The PNPLA3 I148M gene polymorphism does not play a leading role in the development of progressive MASLD in the study cohort.