Background: The role of patients' metabolic clinical and biochemical profile in NAFLD has not been extensively explored.Aims: The aim of the study was to assess the role of metabolic health in NAFLD patients and to examine liver disease progression in these populations.Methods: The medical charts of 569 patients diagnosed with fatty liver were thoroughly reviewed; 344 patients were excluded because of other chronic liver diseases. Metabolically healthy people were defined as those who met none of the following criteria: blood pressure > 130/85 mmHg or under hypertension treatment, fasting glucose > 100 mg/dl or under diabetes treatment, serum triglycerides > 150 mg/dl, high density lipoprotein-cholesterol <40/50 mg/dl for men/women. Study participants were followed-up over a median period of 22 months.Results: The present observational case-control study included 225 NAFLD patients; 14 (6.2%) were metabolically healthy. Metabolically healthy participants were younger (p = 0.006), had lower age at diagnosis (p = 0.002), lower levels of g-GT (p = 0.013), fasting glucose (p <0.001) and triglycerides (p <0.001) and higher HDL-cholesterol (p = 0.005) compared to metabolically non-healthy. By the last follow up assessment, 8 metabolically healthy patients had developed dyslipidemia; 1 patient (14.4%) had presented liver disease progression compared to 8 patients (10.5%) from the unhealthy group (p = 0.567). In multivariate analysis, diabetes mellitus (p = 0.017) and hemoglobin levels (p = 0.009) were the sole independent predictors of disease progression. No significant difference was observed in liver disease progression-free survival rates among the two patient groups (p = 0.503).Conclusions: Metabolically healthy NAFLD patients presented with a favorable biochemical pro-file; however, they were diagnosed with NAFLD at a younger age and the liver disease progression risk was similar to that of metabolically unhealthy patients. These findings suggest that metabol-ically healthy NAFLD may not constitute a benign condition and patients could potentially be at increased risk of metabolic syndrome and liver disease progression.(c) 2022 Elsevier Masson SAS. All rights reserved.
机构:
Univ Texas Hlth Sci Ctr San Antonio, Div Endocrinol, San Antonio, TX 78284 USAUniv Texas Hlth Sci Ctr San Antonio, Diabet Div, San Antonio, TX 78284 USA
Ali, Rafeeq
Cusi, Kenneth
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机构:
Univ Texas Hlth Sci Ctr San Antonio, Diabet Div, San Antonio, TX 78284 USA
Audie L Murphy Mem Vet Adm Med Ctr, San Antonio, TX 78284 USAUniv Texas Hlth Sci Ctr San Antonio, Diabet Div, San Antonio, TX 78284 USA