Autoimmune liver diseases and diabetes: A propensity score matched analysis and a proportional meta-analysis
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Background and Aims: Patients with some chronic liver diseases have increased risk of diabetes. Whether this is also the case for patients with autoimmune liver diseases is unknown. The study aimed to calculate risk and worldwide prevalence of diabetes in patients with autoimmune hepatitis (AIH), primary biliary cholangitis (PBC) and primary sclerosing cholangitis (PSC). Methods: We performed a case–control study using data from the United Kingdom Biobank (UKB) and compared frequency of type 1 diabetes (T1D) and type 2 diabetes (T2D) in AIH and PBC with age-, sex-, BMI- and ethnicity-matched controls. Next, we performed a systematic review and proportional meta-analysis searching PubMed, Embase, Cochrane Library and Web of Science (inception to 1 May 2022 [AIH]; 20 August 2022 [PBC]; 11 November 2022 [PSC]). The pooled prevalence of diabetes was calculated using an inverse method random effects model. Results: Three hundred twenty-eight AIH patients and 345 PBC patients were identified in UKB and risk of T1D and T2D significantly increased compared with matched controls. Our systematic search identified 6914 records including the UKB study. Of these, 77 studies were eligible for inclusion comprising 36 467, 39 924 and 4877 individuals with AIH, PBC and PSC, respectively. The pooled prevalence of T1D was 3.8% (2.6%–5.7%), 1.7% (0.9%–3.1%), 3.1% (1.9%–4.8%) and of T2D 14.8% (11.1%–19.5%), 18.1% (14.6%–22.2%), 6.3% (2.8%–13.3%) in patients with AIH, PBC and PSC, respectively. Conclusions: Patients with autoimmune liver diseases have increased risk of diabetes. Increased awareness of diabetes risk in patients with autoimmune liver diseases is warranted.
| Originalsprog | Engelsk |
|---|---|
| Tidsskrift | Liver International |
| Vol/bind | 43 |
| Udgave nummer | 11 |
| Sider (fra-til) | 2479-2491 |
| Antal sider | 13 |
| ISSN | 1478-3223 |
| DOI | |
| Status | Udgivet - 2023 |
Bibliografisk note
Funding Information:
A.H.J. and N.J.W.A. were supported by Novo Nordisk Foundation Excellence Emerging Investigator Grant—Endocrinology and Metabolism (application no. NNF19OC0055001), European Foundation for the Study of Diabetes Future Leader Award (NNF21SA0072746) and Independent Research Fund Denmark, Sapere Aude (1052‐00003B). Novo Nordisk Foundation Center for Protein Research is supported financially by the Novo Nordisk Foundation (Grant agreement NNF14CC0001). The funding was not involved in this study.
Funding Information:
J.B. reports personal fees from AbbVie, Celgene, Pfizer, Samsung Bioepis, Pharmacosmos, Ferring and Galapagos; grants and personal fees from Janssen, MSD, Takeda, Tillots Pharma and Bristol Myers Squibb; and grants from Novo Nordisk. H.Y. has been principal investigator in clinical trials run by Gilead and Cymabay. L.L.G. reports grants or contracts from Novo Nordisk, Gilead, Sobi and Pfizer; and receiving consulting fees from Novo Nordisk, Astra Zeneca, Sobi, Pfizer and Becton Dickinson. N.J.W.A. has received funding, served on scientific advisory panels, and or speakers bureaus for Boehringer Ingelhiem, MSD/MERC, Novo Nordisk and Mercodia. A.H.J., M.W.S. and A.B. declare no competing interests.
Funding Information:
This research uses data provided by patients and collected by the NHS as part of their care and support. Copyright © (2023), NHS England. Re‐used with the permission of UK Biobank. This research used data assets made available by National Safe Haven as part of the Data and Connectivity National Core Study, led by Health Data Research UK in partnership with the Office for National Statistics and funded by UK Research and Innovation. We acknowledge the UKB and the study participants. This research has been conducted using the UK Biobank Resource under Application Number 61785. All authors had full access to the data and accept responsibility to submit for publication.
Publisher Copyright:
© 2023 The Authors. Liver International published by John Wiley & Sons Ltd.
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