The impact of metabolic health on non-alcoholic fatty liver disease (NAFLD). A single center experience.


Journal

Clinics and research in hepatology and gastroenterology
ISSN: 2210-741X
Titre abrégé: Clin Res Hepatol Gastroenterol
Pays: France
ID NLM: 101553659

Informations de publication

Date de publication:
05 2022
Historique:
received: 19 08 2021
revised: 24 12 2021
accepted: 14 02 2022
pubmed: 2 3 2022
medline: 15 6 2022
entrez: 1 3 2022
Statut: ppublish

Résumé

The role of patients' metabolic clinical and biochemical profile in NAFLD has not been extensively explored. 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. 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. 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 γ-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). Metabolically healthy NAFLD patients presented with a favorable biochemical profile; 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 metabolically healthy NAFLD may not constitute a benign condition and patients could potentially be at increased risk of metabolic syndrome and liver disease progression.

Sections du résumé

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 γ-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 profile; 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 metabolically healthy NAFLD may not constitute a benign condition and patients could potentially be at increased risk of metabolic syndrome and liver disease progression.

Identifiants

pubmed: 35227957
pii: S2210-7401(22)00039-0
doi: 10.1016/j.clinre.2022.101896
pii:
doi:

Substances chimiques

Cholesterol, HDL 0
Triglycerides 0
Glucose IY9XDZ35W2

Types de publication

Journal Article Observational Study

Langues

eng

Sous-ensembles de citation

IM

Pagination

101896

Informations de copyright

Copyright © 2022 Elsevier Masson SAS. All rights reserved.

Déclaration de conflit d'intérêts

Declaration of Competing Interests The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.

Auteurs

Anna Boulouta (A)

Division of Gastroenterology, Department of Internal Medicine, University Hospital of Patras, Patras 26504, Greece.

Ioanna Aggeletopoulou (I)

Division of Gastroenterology, Department of Internal Medicine, University Hospital of Patras, Patras 26504, Greece.

Stavros Kanaloupitis (S)

Division of Gastroenterology, Department of Internal Medicine, University Hospital of Patras, Patras 26504, Greece.

Efthymios P Tsounis (EP)

Division of Gastroenterology, Department of Internal Medicine, University Hospital of Patras, Patras 26504, Greece.

Vasileios Issaris (V)

Division of Gastroenterology, Department of Internal Medicine, University Hospital of Patras, Patras 26504, Greece.

Konstantinos Papantoniou (K)

Division of Gastroenterology, Department of Internal Medicine, University Hospital of Patras, Patras 26504, Greece.

Anastasios Apostolos (A)

Division of Gastroenterology, Department of Internal Medicine, University Hospital of Patras, Patras 26504, Greece.

Paraskevas Tsaplaris (P)

Division of Gastroenterology, Department of Internal Medicine, University Hospital of Patras, Patras 26504, Greece.

Ploutarchos Pastras (P)

Division of Gastroenterology, Department of Internal Medicine, University Hospital of Patras, Patras 26504, Greece.

Christos Sotiropoulos (C)

Division of Gastroenterology, Department of Internal Medicine, University Hospital of Patras, Patras 26504, Greece.

Aggeliki Tsintoni (A)

Department of Internal Medicine, University Hospital of Patras, Patras 26504, Greece.

Georgia Diamantopoulou (G)

Division of Gastroenterology, Department of Internal Medicine, University Hospital of Patras, Patras 26504, Greece.

Konstantinos Thomopoulos (K)

Division of Gastroenterology, Department of Internal Medicine, University Hospital of Patras, Patras 26504, Greece.

Marina Michalaki (M)

Division of Endocrinology, Diabetes and Metabolic Diseases, Department of Internal Medicine, University of Patras, Patras 26504, Greece.

Christos Triantos (C)

Division of Gastroenterology, Department of Internal Medicine, University Hospital of Patras, Patras 26504, Greece. Electronic address: chtriantos@upatras.gr.

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Classifications MeSH