ArticleCureus2026
Comparative Analysis of Atherogenic Dyslipidemia Patterns in Alcoholic Versus Metabolic Dysfunction-Associated Steatotic Liver Disease: Implications for Cardiovascular Risk Stratification.
Article in Cureus, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
backgroundAbnormal lipid metabolism is a hallmark of both alcohol-related fatty liver disease (AFLD) and metabolic dysfunction-associated steatotic liver disease (MASLD), both of which heighten cardiovascular risk. However, comparative data on lipid abnormalities between these two conditions remain sparse, especially among South Asian populations.
objectiveTo systematically compare atherogenic lipid profiles between patients with AFLD and MASLD.
methodsThis cross-sectional study enrolled 90 participants, including 30 with AFLD, 30 with MASLD, and 30 healthy controls. Fasting serum samples were assessed for total cholesterol (TC), low-density lipoprotein cholesterol (LDL-C), high-density lipoprotein cholesterol (HDL-C), triglycerides (TG), and non-HDL-C. Additionally, atherogenic indices and lipid ratios were calculated. Group differences were analyzed using ANOVA with post-hoc tests and multivariable regression (α = 0.05).
resultsBoth disease groups showed significant dyslipidemia relative to controls (p < 0.001). MASLD patients exhibited the most unfavorable profile (TC = 220 ± 25 mg/dL, LDL-C = 150 ± 20 mg/dL, TG = 200 ± 50 mg/dL) compared to AFLD (TC = 200 ± 30, LDL-C = 130 ± 25, TG = 180 ± 60 mg/dL) and controls (TC = 180 ± 20, LDL-C = 110 ± 15, TG = 120 ± 40 mg/dL). HDL-C was lowest in AFLD (40 ± 10 mg/dL), intermediate in MASLD (45 ± 8 mg/dL), and highest in controls (55 ± 12 mg/dL). The atherogenic index (log[TG/HDL-C]) was significantly higher in MASLD (0.65 ± 0.18) than in AFLD (0.55 ± 0.21) and controls (0.35 ± 0.15; p < 0.001).
conclusionMASLD is associated with a more severe atherogenic lipid pattern marked by elevated TC, LDL-C, and TG, whereas AFLD features a more pronounced reduction in HDL-C. These distinct profiles suggest differing cardiovascular risk trajectories and support etiology-specific lipid management approaches.
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