MAFLD and ASCVD: Plasma Heparin Cofactor II Activity as an Anti-liver Fibrosis Biomarker

Shimabukuro, Michio

doi:10.5551/jat.ed227

Cited by 1 publication

(1 citation statement)

References 11 publications

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“…35 MAFLD disrupts the natural equilibrium between energy intake and expenditure in the body, causing fat to accumulate in the liver and vascular walls and ultimately leading to fatty liver, liver insulin resistance, and atherosclerotic cardiovascular disease (ASCVD). [36][37][38][39][40][41][42] When hepatic steatosis modifies hepatocytokine secretion, it creates a complementary reciprocal condition that affects fatty acid metabolism and insulin resistance in various tissues, including skeletal muscle, cardiovascular smooth muscle, adipose tissue, and the liver. 43 Previous studies have shown that NAFLD is independently associated with chronic macrovascular and microvascular complications, especially with PAD in T2DM 44,45 and its mechanism may involve dyslipidemia, increased insulin resistance, modifications in hemostaticfibrinolytic factors, elevated proinflammatory cytokines, and dysbiosis.…”

Section: Discussionmentioning

confidence: 99%

Association Between Metabolic Dysfunction-Associated Fatty Liver Disease and MACCEs in Patients with Diabetic Foot Ulcers: An Ambispective Longitudinal Cohort Study

Huang,

Li,

Zhai

et al. 2024

DMSO

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Aim Metabolic dysfunction-related fatty liver disease (MAFLD) is closely related to metabolic disorders. However, the relationship between MAFLD and the prognosis in diabetic foot ulcers (DFUs) remains unclear. This study aimed to explore the association between MAFLD and the risk of major adverse cardiac and cerebral events (MACCEs) in patients with DFUs. Methods 889 inpatients with DFUs (PEDIS/TEXAS mild and above) were included in this study from 2013 to 2023. All participants were placed into non-MAFLD ( n = 643) and MAFLD ( n = 246) groups and followed up every 6 months for 10.9 years with a median of 63 months through in-person outpatient interviews and family fixed-line telephone visits. The association between MAFLD and the risk of MACCEs was evaluated through Multivariate Cox regression analyses, Stratified analyses and Kaplan-Meier survival analyses. Results Of the 889 subjects, 214 (24.07%) experienced MACCEs. Multivariate Cox regression analysis showed that MAFLD was independently associated with MACCEs ( P < 0.001), of which with non-fatal myocardial infarction ( P = 0.04), non-fatal stroke ( P = 0.047), coronary artery revascularization ( P = 0.002), heart failure (P = 0.029), and all-cause mortality ( P = 0.021), respectively. The stratified analysis revealed that compared with non-MAFLD (HR=1), DFUs with MAFLD had a 2.64-fold increased risk for MACCEs (P <0.001; P for interaction = 0.001) in peripheral arterial disease (PAD) subgroup. Kaplan-Meier analysis evidenced that the MAFLD group had a higher cumulative incidence of MACCEs (log-rank, all P < 0.05). Conclusion MAFLD is a high-risk factor for MACCEs in patients with DFUs. The findings will remind clinicians to pay more attention to MAFLD in patients with DFUs, especially in patients with DFUs combined with PAD as early as possible in clinical practice and adopt timely effective intervention strategies to prevent the occurrence of MACCEs to improve the clinical prognosis in patients with DFUs.

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