Thyroid-stimulating hormone is an independent risk factor of non-alcoholic fatty liver disease.
hypothyroidism
liver fibrosis
non‐alcoholic fatty liver disease
thyroid‐stimulating hormone
Journal
JGH open : an open access journal of gastroenterology and hepatology
ISSN: 2397-9070
Titre abrégé: JGH Open
Pays: Australia
ID NLM: 101730833
Informations de publication
Date de publication:
Jun 2020
Jun 2020
Historique:
received:
20
08
2019
accepted:
03
09
2019
entrez:
10
6
2020
pubmed:
10
6
2020
medline:
10
6
2020
Statut:
epublish
Résumé
Hypothyroidism might play a crucial role in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). The association of subclinical hypothyroidism with NAFLD has been inconsistent. The relationship of NAFLD with thyroid function parameters and subclinical hypothyroidism was determined. This cross-sectional study included 70 patients with subclinical hypothyroidism and 70 controls with euthyroidism matched according to gender, age, and body mass index (BMI). NAFLD was diagnosed via abdominal ultrasonography. The association between NAFLD and subclinical hypothyroidism was analyzed. The prevalence of NAFLD was significantly higher in patients with subclinical hypothyroidism than in those with euthyroidism. Multivariate analysis showed that subclinical hypothyroidism was an independent risk factor of NAFLD adjusted by metabolic-related factors, such as BMI, triglyceride, high-density lipoprotein-cholesterol, hypertension, and diabetes. Thyroid-stimulating hormone (TSH) was an independent risk factor of NAFLD adjusted by the same metabolic-related factors, but free thyroxine (FT4) was not a risk factor. The FIB-4 index, a noninvasive marker of liver fibrosis was significantly higher in patients with subclinical hypothyroidism than in those with euthyroidism. Compared with patients with euthyroidism, the proportion of the FIB-4 index ≥2.67 was significantly higher, and the proportion of the FIB-4 index <1.30 was lower in patients with subclinical hypothyroidism. TSH elevation even within the euthyroid range is an independent risk factor of NAFLD and may influence the progression of liver fibrosis, even with a normal FT4 level.
Sections du résumé
BACKGROUND AND AIM
OBJECTIVE
Hypothyroidism might play a crucial role in the pathogenesis of non-alcoholic fatty liver disease (NAFLD). The association of subclinical hypothyroidism with NAFLD has been inconsistent. The relationship of NAFLD with thyroid function parameters and subclinical hypothyroidism was determined.
METHODS
METHODS
This cross-sectional study included 70 patients with subclinical hypothyroidism and 70 controls with euthyroidism matched according to gender, age, and body mass index (BMI). NAFLD was diagnosed via abdominal ultrasonography. The association between NAFLD and subclinical hypothyroidism was analyzed.
RESULTS
RESULTS
The prevalence of NAFLD was significantly higher in patients with subclinical hypothyroidism than in those with euthyroidism. Multivariate analysis showed that subclinical hypothyroidism was an independent risk factor of NAFLD adjusted by metabolic-related factors, such as BMI, triglyceride, high-density lipoprotein-cholesterol, hypertension, and diabetes. Thyroid-stimulating hormone (TSH) was an independent risk factor of NAFLD adjusted by the same metabolic-related factors, but free thyroxine (FT4) was not a risk factor. The FIB-4 index, a noninvasive marker of liver fibrosis was significantly higher in patients with subclinical hypothyroidism than in those with euthyroidism. Compared with patients with euthyroidism, the proportion of the FIB-4 index ≥2.67 was significantly higher, and the proportion of the FIB-4 index <1.30 was lower in patients with subclinical hypothyroidism.
CONCLUSIONS
CONCLUSIONS
TSH elevation even within the euthyroid range is an independent risk factor of NAFLD and may influence the progression of liver fibrosis, even with a normal FT4 level.
Identifiants
pubmed: 32514444
doi: 10.1002/jgh3.12264
pii: JGH312264
pmc: PMC7273701
doi:
Types de publication
Journal Article
Langues
eng
Pagination
400-404Informations de copyright
© 2019 The Authors. JGH Open: An open access journal of gastroenterology and hepatology published by Journal of Gastroenterology and Hepatology Foundation and John Wiley & Sons Australia, Ltd.
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