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Diabetes is the strongest risk factor of hepatic fibrosis in lean patients with non-alcoholic fatty liver disease
  1. Huiyul Park1,
  2. Eileen L Yoon2,
  3. Seon Cho3,
  4. Dae Won Jun2,
  5. Eun-Hee Nah3
  1. 1Department of Family Medicine, Eulji University Hospital in Uijeongbu, Uijeongbu-si, Korea (the Republic of)
  2. 2Department of Internal Medicine, Hanyang University College of Medicine, Seoul, Korea (the Republic of)
  3. 3Department of Laboratory Medicine, Health Promotion Research Institute, Seoul, Korea (the Republic of)
  1. Correspondence to Professor Dae Won Jun, Department of Internal Medicine, Hanyang University College of Medicine, Seongdong-gu, Seoul 133-792, Korea (the Republic of); noshin{at}hanyang.ac.kr; Dr Eun-Hee Nah, Department of Laboratory Medicine, Health Promotion Research Institute, Gangseo-gu, Seoul 07572, Republic of Korea; cellonah{at}hanmail.net

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We read the commentary by Francque and Wong1 with great interest. They pointed out that metabolic dysfunction could be the main factor associated with an increased risk of hepatic fibrosis among lean patients with non-alcoholic fatty liver disease (NAFLD). However, it is unclear whether the definition of metabolic dysfunction would also fit lean patients, who are less likely to have metabolic risks.2 Herein, we evaluated the fibrosis burden in lean patients with NAFLD according to the presence of each metabolic dysfunction component.

We analysed participants in a community-based cohort, all of whom have undergone magnetic resonance elastography (MRE) for their health check-up (N=6775, 100% single ethnic Korean). Fatty liver was diagnosed by ultrasonography. The prevalence of NAFLD and lean (body mass index <23) NAFLD in all subjects was 35.2% and 3.7%, respectively. The mean liver stiffness value was lower in lean patients with NAFLD than in non-lean patients (2.26±0.55 vs 2.39±0.53, p<0.001) (online supplemental table 1). However, there was no difference in the prevalence of both significant (MRE …

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Footnotes

  • HP and ELY are joint first authors.

  • HP and ELY contributed equally.

  • DWJ and E-HN contributed equally.

  • Contributors Guarantor of the article: DWJ. Concept and design: DWJ. Data collection and management: ELY, SC, E-HN. Interpretation of data: DWJ. Writing of the manuscript: HP. Supervision: DWJ, E-HN. All authors have approved the final version of the manuscript.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.

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