Association between plasminogen activator inhibitor-1 in young adulthood and nonalcoholic fatty liver disease in midlife: CARDIA.

Autor: Campbell PT; Department of Medicine, Northwestern University, Chicago, IL, USA., VanWagner LB; Division of GI & Hepatology, Northwestern University, Chicago, IL, USA.; Department of Preventive Medicine, Northwestern Universtiy, Chicago, IL, USA., Colangelo LA; Department of Preventive Medicine, Northwestern Universtiy, Chicago, IL, USA., Lewis CE; Department of Epidemiology, University of Alabama at Birmingham, Birmingham, AL, USA., Henkel A; Division of GI & Hepatology, Northwestern University, Chicago, IL, USA., Ajmera VH; Division of GI & Hepatology, University of California San Diego, San Diego, CA, USA., Lloyd-Jones DM; Department of Medicine, Northwestern University, Chicago, IL, USA.; Department of Preventive Medicine, Northwestern Universtiy, Chicago, IL, USA., Vaughan DE; Department of Medicine, Northwestern University, Chicago, IL, USA.; Department of Preventive Medicine, Northwestern Universtiy, Chicago, IL, USA., Khan SS; Department of Preventive Medicine, Northwestern Universtiy, Chicago, IL, USA.
Jazyk: angličtina
Zdroj: Liver international : official journal of the International Association for the Study of the Liver [Liver Int] 2020 May; Vol. 40 (5), pp. 1111-1120. Date of Electronic Publication: 2020 Mar 11.
DOI: 10.1111/liv.14417
Abstrakt: Background: Prior studies have demonstrated a cross-sectional association between elevated plasminogen activator inhibitor-1 (PAI-1) levels and nonalcoholic fatty liver disease (NAFLD). However, there are no prospective longitudinal assessments of the association between PAI-1 and NAFLD. We aimed to describe the association between PAI-1 levels in early adulthood with NAFLD in midlife.
Methods: Among the 5115 participants in the coronary artery risk development in young adults (CARDIA) study, participants were randomly selected from a subset that was free of obesity, diabetes and hypertension at the 1992-1993 exam and attended the 2005-2006 exam (n = 996). A subset of participants (n = 896) also had CT liver fat measured (2010-2011). Participants with secondary causes of steatosis were excluded (n = 87). NAFLD was defined as liver attenuation ≤51 Hounsfield units. Logistic regression models assessed the association between PAI-1 and NAFLD.
Results: Of 809 participants, 53% were female, 37% black with a mean age of 32 years. Median PAI-1 level at 1st assessment (1992-1993) was 23.4 ng/mL among participants with NAFLD vs 11.9 ng/mL among those without NAFLD (P < .0001). Median PAI-1 level at 2nd assessment (2005-2006) was 55.6 ng/mL among participants with NAFLD vs 19.5 ng/mL among those without NAFLD (P < .0001). Higher PAI-1 levels were independently associated with NAFLD (1st assessment adjusted OR [AOR] 2.16 per 1 standard deviation higher log(PAI-1) level (95% confidence interval [CI] 1.63-2.85); 2nd assessment AOR 2.71 (95% CI 2.03-3.61)).
Conclusions: Plasma PAI-1 levels in young adulthood were independently associated with NAFLD in midlife. Further studies may indicate whether PAI-1 plays a role in NAFLD pathophysiology.
(© 2020 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.)
Databáze: MEDLINE
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