Immunometabolic drivers of metabolic dysfunction-associated steatotic liver disease in non-obese people living with human immunodeficiency virus

Figure 1 Study flow chart. HIV: Human immunodeficiency virus; VCTE: Vibration-controlled transient elastography; INSTI: Integrase strand transfer inhibitors.

Figure 2 Adjusted multivariate logistic regression analysis of metabolic dysfunction-associated steatotic liver disease risk factors in overall human immunodeficiency virus patients. Variables included in the model are gender, age, group, body mass index, alanine aminotransferase, high-density lipoprotein, triglyceride-glucose, glucose, cluster of differentiation (CD) 4 cell count ≥ 350 cells/μL, and CD4/CD8 ratio. OR: Odds ratio; CI: Confidence interval; BMI: Body mass index; HDL: High-density lipoprotein; ALT: Alanine aminotransferase; TyG: Triglyceride-glucose.

Figure 3 Longitudinal changes in hepatic, metabolic, and immunological parameters among non-obese people with human immunodeficiency virus (12-month follow-up). A: Ultrasound attenuation parameter; B: Liver stiffness measurement; C: Alanine aminotransferase; D: Body mass index; E: Glucose; F: High-density lipoprotein; G: Triglyceride-glucose; H: Cluster of differentiation (CD) 4 cell count; I: CD4/CD8 ratio. Data are presented as mean ± SD. The mixed-effects model analysis showed that none of the unmarked indicators were statistically significant. INSTIs: Integrase strand transfer inhibitors-based regime group; Switch: Switching-to-integrase strand transfer inhibitors-based regime groups; Non-INSTIs: Non-integrase strand transfer inhibitors-based regime group; UAP: Ultrasound attenuation parameter; LSM: Liver stiffness measurement; ALT: Alanine aminotransferase; BMI: Body mass index; HDL: High-density lipoprotein; TyG: Triglyceride-glucose; CD: Cluster of differentiation.