Author information

¹NAFLD Research Center, Division of Gastroenterology. University of California at San Diego, La Jolla, CA, United States of America.

²Department of Medicine, Yong Loo Lin School of Medicine, National University of Singapore, Singapore.

³Division of Gastroenterology and Hepatology, Department of Medicine, National University Health System, Singapore.

⁴Johns Hopkins University Bloomberg School of Public Health, Baltimore, Maryland, United States of America.

⁵University of California San Diego School of Medicine, San Diego, California, United States of America.

⁶Laboratory of Pathology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland, United States of America.

⁷Liver Institute Northwest, Seattle, Washington, United States of America.

⁸Cleveland Clinic, Cleveland, Ohio, United States of America.

⁹Division of Gastrointestinal and Liver Diseases, University of Southern California, United States of America.

¹⁰Division of Gastroenterology, Duke University Medical Center, Durham, North Carolina, United States of America.

¹¹Indiana University School of Medicine, Indianapolis, Indiana, United States of America.

¹²Saint Louis University, St. Louis, Missouri, United States of America.

¹³Virginia Commonwealth University School of Medicine, Richmond, Virginia, United States of America.

¹⁴Division of Epidemiology, Department of Family Medicine and Public Health, University of California at San Diego, San Diego, CA, United States of America.

Abstract

Background: There are limited data on the progression of liver stiffness measurement (LSM) by vibration-controlled transient elastography (VCTE) in people with type 2 diabetes (T2DM) versus those without T2DM in biopsy-proven metabolic dysfunction-associated steatotic liver disease (MASLD). We examined LSM progression in participants with T2DM versus those without T2DM in a large, prospective, multicenter cohort study.

Approach and results: This study included 1,231 adult participants (62% female) with biopsy-proven MASLD who had VCTEs at least one year apart. LSM progression and regression were defined by a ≥ 20% increase and an upward or downward change, respectively, in the LSM category in the Baveno VII categories for compensated advanced chronic liver disease, compared between participants with T2DM (n=680) versus no T2DM (n=551) at baseline. The mean (±SD) age and BMI were 51.8 (±12.0) years and 34.0 (±6.5) kg/m2, respectively. The median (IQR) time between the first and last VCTE measurements was 4.1(2.5-6.5) years. Participants with T2DM had higher LSM progression at 4-years (12% vs. 10%), 6-years (23% vs. 16%), and 8-years (50% vs. 39%), p=0.04. Using a multivariable Cox proportional hazards model adjusted for multiple confounders, the presence of T2DM remained an independent predictor of LSM progression (adjusted HR 1.35, 95% CI 1.01-1.81, p=0.04). T2DM was not associated with LSM regression (p=0.71). Mean HbA1c was significantly associated with LSM progression (p=0.003) and regression (p=0.02).

Conclusion: Utilizing serial VCTE data from a multicenter study of participants with biopsy-proven MASLD, we demonstrate that T2DM and HbA1c are associated with LSM progression.