ARTERIAL STIFFNESS AND HEPATIC FIBROSIS IN NASH HAVE INDEPENDENTLY SIGNIFICANT, BILATERAL CORRELATION IN ADULTS WITH TYPE 2 DIABETES
Thursday, May 7, 2020
11:30 AM – 11:45 AM
Participants should be aware of the following financial/non-financial relationships: Shashi Panicker, MD, PhD, MSc: Disclosure information not submitted.
Objective : Background: The association of nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH) with cardiovascular disease (CVD) in type 2 diabetes (T2D) patients remains controversial because of several contradictory studies. Objective: To study the association of hepatic fibrosis, assessed by liver stiffness measurement (LSM), with arterial stiffness (AS), and to evaluate cardiometabolic risk factors to identify predictors of CVD in T2D patients. AS, a surrogate marker of subclinical atherosclerosis, is associated with left ventricular dysfunction.
Methods: Methods: Adults with T2D without history of alcohol consumption, hepatitis or intake of hepatotoxic drugs were enrolled. All underwent clinical assessment, biochemical tests, LSM, and AS measurement. NASH was diagnosed by combining NAFLD Fibrosis Score and LSM by Transient Elastography (TE with FibroScan), and AS was assessed with aortic pulse wave velocity (PWV).
Results: Results NASH with fibrosis was present in 35% of women and 26% of men (n=613).The risk of AS was significantly high in both genders (OR 5.6, 95% CI 3.4 – 9.2, p < 0.0001) and increased with the severity of NASH (moderate NASH with LSM < 9 kPa, OR 3.5, 95% CI 1.9 - 6.4, p< 0.0001, vs severe NASH with LSM ≥9 kPa, OR 9.8, 95% CI 4.4 - 21.6, p < 0.0001). The association of NASH with AS remained significant in multivariate analysis (R2 0.435, F 20.86, t 5.74, p < 0.0005). AS was an independent predictor for liver fibrosis (R2 0.55, F 32.85, t 5.74, p< 0.0005). Serum albumin significantly predicted both NASH (OR 7.9, 95% CI 3.47- 17.9, p< 0.0001) and AS (OR 3.6, 95% CI 1.24-10.38, p = 0.018).
Discussion/Conclusion: Discussion: Age, hypertension, liver stiffness, and hypoalbuminemia were highly significant predictors of CVD in T2D. A significant, direct bilateral association between AS and liver fibrosis in NASH was observed, independent of cardiometabolic risk factors. Greater severity of NASH worsened AS and vice-versa. This association has been missed in previous studies that have used ultrasound which assessed hepatic steatosis instead of fibrosis. In multivariate analysis, hypoalbuminemia was a significant, independent risk factor for both liver fibrosis and AS. No previous study has correlated serum albumin as a significant independent predictor for both liver fibrosis and subclinical atherosclerosis in patients with T2D.
Conclusion: Subclinical atherosclerosis and fibrosis in NASH have an independent bilateral correlation in T2D. Recognition of specific biomarkers like albumin, which participate in the pathophysiological mechanisms which cause fibrosis in NASH and CVD, may lead to novel therapeutic interventions for both complications in T2D.