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.
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Chongqing Med Univ, Bishan Hosp, Dept Gastroenterol, Chongqing, Peoples R ChinaChongqing Med Univ, Bishan Hosp, Dept Gastroenterol, Chongqing, Peoples R China
Rong, Li
Zou, Junyan
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Southwest Univ, Med Res Inst, Chongqing, Peoples R China
Southwest Univ, Publ Hlth Hosp, Med Res Inst, Chongqing, Peoples R ChinaChongqing Med Univ, Bishan Hosp, Dept Gastroenterol, Chongqing, Peoples R China
Zou, Junyan
Ran, Wei
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Southwest Univ, Publ Hlth Hosp, Med Res Inst, Chongqing, Peoples R ChinaChongqing Med Univ, Bishan Hosp, Dept Gastroenterol, Chongqing, Peoples R China
Ran, Wei
Qi, Xiaohong
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Baoshan Peoples Hosp Yunnan Prov, Dept Gen Surg, Baoshan, Yunnan, Peoples R ChinaChongqing Med Univ, Bishan Hosp, Dept Gastroenterol, Chongqing, Peoples R China
Qi, Xiaohong
Chen, Yaokai
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Southwest Univ, Publ Hlth Hosp, Med Res Inst, Chongqing, Peoples R ChinaChongqing Med Univ, Bishan Hosp, Dept Gastroenterol, Chongqing, Peoples R China
Chen, Yaokai
Cui, Hongjuan
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Southwest Univ, Med Res Inst, Chongqing, Peoples R ChinaChongqing Med Univ, Bishan Hosp, Dept Gastroenterol, Chongqing, Peoples R China
Cui, Hongjuan
Guo, Jinjun
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Chongqing Med Univ, Bishan Hosp, Dept Gastroenterol, Chongqing, Peoples R ChinaChongqing Med Univ, Bishan Hosp, Dept Gastroenterol, Chongqing, Peoples R China
机构:
Royal Adelaide Hosp, Dept Gastroenterol & Hepatol, Adelaide, SA, AustraliaRoyal Adelaide Hosp, Dept Gastroenterol & Hepatol, Adelaide, SA, Australia
Gill, M. G.
Bate, J. P.
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Royal Adelaide Hosp, Dept Gastroenterol & Hepatol, Adelaide, SA, AustraliaRoyal Adelaide Hosp, Dept Gastroenterol & Hepatol, Adelaide, SA, Australia
Bate, J. P.
Tse, E.
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Royal Adelaide Hosp, Dept Gastroenterol & Hepatol, Adelaide, SA, AustraliaRoyal Adelaide Hosp, Dept Gastroenterol & Hepatol, Adelaide, SA, Australia