Impact of Cardiometabolic Risk Factors Control on Cardiovascular–Kidney–Metabolic Axis in Chronic Hepatitis B
Karen Cheuk‐Ying Ho, Rex Wan‐Hin Hui, Matthew Shing‐Hin Chung, Wai‐Kay Seto, Man‐Fung Yuen, Lung‐Yi MakABSTRACT
Background
The impact of cardiometabolic risk factors (CMRFs) on the cardiovascular–kidney–metabolic (CKM) axis in chronic hepatitis B (CHB) remains poorly defined.
Methods
We conducted a prospective analysis enrolling patients with CHB who were on nucleos(t)ide analogues (NUCs). CMRFs were defined as per established criteria; poorly‐controlled CMRFs were defined with specific cut‐offs measured across 5 years. Study outcomes include fibrosis progression (liver stiffness [LS] increase by ≥ 20%), liver‐related events (LREs), chronic kidney disease (CKD) progression, major adverse cardiovascular events (MACE), and all‐cause mortality.
Results
A total of 714 NUC‐treated patients (median age: 61.0 [54.5–66.7] years; 69.6% male; 90.5% undetectable HBV DNA, median NUCs duration of 14.1 [11.3–16.5] years) were followed up for 9.7 (7.2–10.2) years. LREs occurred in 112 (15.7%) patients, with annual incidence rate of 1.62 events per 100 person‐years. All‐cause mortality was observed in 86 (12%) patients, including 47 (6.6%) liver‐related mortality. The number or types of CMRFs did not display a linear positive relationship with adverse clinical outcomes. The presence of ≥ 1 poorly controlled CMRFs is independently associated with LREs (aHR: 2.001, 95% CI: 1.350–2.965), MACE (aHR: 1.042, 95% CI: 1.030–1.081), and all‐cause mortality (aHR: 2.082, 95% CI: 1.006–4.310), whereas patients having ≥ 2 and ≥ 3 poorly controlled CMRFs are independently associated with CKD progression (aOR: 1.887, 95% CI: 1.115–3.221) and fibrosis progression (aOR: 1.624, 95% CI: 1.164–2.266), respectively. The results remain robust in patients without advanced fibrosis (LS ≤ 10 kPa) at baseline.
Conclusion
Active optimization of CMRFs should be an integral component of CHB management in addition to NUCs therapy.