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Cause of death by fibrosis stage in 959 patients with biopsy-proven NAFLD
  1. Ying Shang1,
  2. Camilla Akbari2,
  3. Maja Dodd2,
  4. Patrik Nasr3,
  5. Johan Vessby4,
  6. Fredrik Rorsman4,
  7. Stergios Kechagias3,
  8. Per Stål1,5,
  9. Mattias Ekstedt3,
  10. Hannes Hagström1,5
  1. 1Department of Medicine, Huddinge, Karolinska Institutet, Stockholm, Sweden
  2. 2Department of Medicine, Karolinska Institutet, Stockholm, Sweden
  3. 3Department of Gastroenterology and Hepatology and Department of Health, Medicine, and Caring Sciences, Linköping University, Linköping, Sweden
  4. 4Department of Gastroenterology and Hepatology, Uppsala University Hospital, Uppsala, Sweden
  5. 5Division of Hepatology, Department of Upper GI, Karolinska University Hospital, Stockholm, Sweden
  1. Correspondence to Dr Ying Shang, Department of Medicine, Huddinge, Karolinska Institute, Stockholm, 171 77, Sweden; ying.shang{at}

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We have read with interest the study from Simon et al, where the authors observed a higher mortality rate among patients with biopsy-proven nonalcoholic fatty liver disease (NAFLD) compared with reference controls without NAFLD.1 Importantly, mortality rates exhibited a significant increase as the severity of NAFLD worsened, that is, from simple steatosis, non-fibrotic nonalcoholic steatohepatitis (NASH), non-cirrhotic fibrosis (ie, F1–F3, with or without NASH) to cirrhosis. The leading causes of death were attributable to extrahepatic cancers and liver cirrhosis, while cardiovascular disease and hepatocellular carcinoma had a comparatively lesser impact. This extensive study of patients with NAFLD reveals higher mortality rates across different NAFLD stages but does not stratify causes of death within the respective pre-cirrhotic fibrosis stages (F0–F3). Owing to the long natural history of NAFLD, for example, patients with F0 and F1 may never experience liver-related events.2–4 For that reason, to assess the distribution of causes of death based on fibrosis stage, we retrospectively leveraged the granular data from a cohort of 959 patients …

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  • Twitter @YingShang1, @hanneshagstrom

  • Contributors Study concept and design: YS and HH. Acquisition of data: CA, MD, PN, JV, FR, SK, PS, ME and HH. Statistical analysis and drafting of manuscript: YS. Interpretation of data and critical revision: All authors.

  • Funding YS was supported by Mag-Tarm Fonden, Karolinska Institutet Research Funding and Region Stockholm. HH was supported by grants from Stockholm City County, The Swedish Cancer Society and The Swedish Research Council.

  • 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.