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Multicenter Study
. 2024 Jul 15;38(9):1323-1332.
doi: 10.1097/QAD.0000000000003903. Epub 2024 Apr 18.

The effect of weight gain and metabolic dysfunction-associated steatotic liver disease on liver fibrosis progression and regression in people with HIV

Affiliations
Multicenter Study

The effect of weight gain and metabolic dysfunction-associated steatotic liver disease on liver fibrosis progression and regression in people with HIV

Giovanni Guaraldi et al. AIDS. .

Erratum in

Abstract

Objective: People with HIV (PWH) have high risk of liver fibrosis. We investigated the effect of weight gain and metabolic dysfunction-associated steatotic liver disease (MASLD) on liver fibrosis dynamics.

Design: Multicenter cohort study.

Methods: Fibrosis progression was defined as development of significant fibrosis [liver stiffness measurement (LSM) ≥8 kPa], or transition to cirrhosis (LSM ≥13 kPa), for those with significant fibrosis at baseline. Fibrosis regression was defined as transition to LSM less than 8 kPa, or to LSM less than 13 kPa for those with cirrhosis at baseline. MASLD was defined as hepatic steatosis (controlled attenuation parameter >248 dB/m) with at least one metabolic abnormality. A continuous-time multistate Markov model was used to describe transitions across fibrosis states.

Results: Among 1183 PWH included from three centers (25.2% with viral hepatitis coinfection), baseline prevalence of significant fibrosis and MASLD was 14.4 and 46.8%, respectively. During a median follow-up of 2.5 years (interquartile range 1.9-3.5), the incidence rate of fibrosis progression and regression was 2.8 [95% confidence interval (CI) 2.3-3.4] and 2.2 (95% CI 1.9-2.6) per 100 person-years, respectively. In Markov model, weight gain increased the odds of fibrosis progression [odds ratio (OR) 3.11, 95% CI 1.59-6.08], whereas weight gain (OR 0.30, 95% CI 0.10-0.84) and male sex (OR 0.32, 95% CI 0.14-0.75) decreased the odds of fibrosis regression. On multivariable Cox regression analysis, predictors of fibrosis progression were weight gain [adjusted hazard ratio (aHR) 3.12, 95% CI 1.41-6.90] and MASLD (aHR 2.72, 95% CI 1.05-7.02).

Conclusion: Fibrosis transitions are driven by metabolic health variables in PWH, independently of viral hepatitis coinfection and antiretroviral class therapy.

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Conflict of interest statement

G.G. received a research grant and speaker honoraria from Gilead, ViiV, Merck and Jansen and attended advisory boards of Gilead, ViiV and Merck. J.R. has received honoraria for consulting or speaking at educational events from Abvie, Boehringer, Galapagos, Gilead, Merck, Janssen, Theratechnologies and ViiV. G.S. has acted as speaker for Merck, Gilead, Abbvie, Novo Nordisk, Pfizer, served as an advisory board member for Pfizer, Merck, Novo Nordisk, Gilead, and has received unrestricted research funding from Theratecnologies Inc. J.M., S.R., F.M., F.C., J.B., A.D., J.C., F.M., M.D.M., D.K., W.E., S.C., C.M. have nothing to disclose.

Figures

None
Graphical abstract
Fig. 1
Fig. 1
Alluvial plot showing the transition of patients through the stages of liver fibrosis during follow-up visits.

Comment in

References

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