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http://ir.nhri.org.tw/handle/3990099045/15505
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| Title: | Reply |
| Authors: | Yen, FS;Hwu, CM;Hsu, CC |
| Contributors: | Institute of Population Health Sciences;National Center for Geriatrics and Welfare Research |
| Abstract: | Reply. We are grateful to Cheng Han Ng1 for carefully reading our article and providing valuable comments.2 We also agree that there is a signi fi cant interrelationship between diabetes and liver cirrhosis. Asia has one of the highest burdens of diabetes mellitus and liver cirrhosis in the world.3,4 Moreover, patients with liver cirrhosis, as a result of substantial liver damage, have altered drug metabolism and excretion, making the treatment of diabetes in cirrhotic patients more complex.1 This is why we have dedicated much of our time in recent years to performing diabetes treatment – related research for patients with liver cirrhosis.5 Although the use of subcutaneous semaglutide in patients with nonalcoholic steatohepatitis did not signi fi cantly improve the fi brosis stage,6 our study showed that the use of glucagon-like peptide-1 receptor agonist (GLP-1 RA) in patients with cirrhosis was associated with a signi fi cantly reduced risk of cirrhosis decompensation, liver failure, cardiovascular events, and mortality. However, as Ng1 pointed out, our cohort of patients with cirrhosis was primarily owing to viral hepatitis. Therefore, our fi ndings may not be directly applicable to patients with cirrhosis resulting from metabolic-associated fatty liver disease. Interestingly, a similar study by Simon et al7 found that 64.3% of their cirrhosis patients had the condition as a result of nonalcoholic fatty liver disease. Their research showed that the use of GLP-1 RA was associated with a signi fi -cantly lower risk of hepatic decompensation events in patients with liver cirrhosis. These 2 studies suggest that the use of GLP-1 RA in patients with cirrhosis, whether caused by nonalcoholic fatty liver disease or viral hepatitis, may reduce the risk of cirrhosis decompensation and liver-related complications. However, because these were observational studies, there must be other unknown confounding factors. The results can only indicate an association, not a causal relationship. Randomized controlled trials are needed to validate our fi ndings. In addition, it requires further mechanistic research 1 on whether GLP-1 RA works by modulating the gut microbiota to reduce intestinal ammonia, or by improving the brain gamma-aminobutyric acid transmitter imbalance to potentially reduce the risk of hepatic encephalopathy in cirrhotic patients; and on whether GLP-1 RA can reduce portal pressure and subsequently attenuate the risk of cirrhosis decompensation. |
| Date: | 2024-04 |
| Relation: | Clinical Gastroenterology and Hepatology. 2024 Apr;22(4):902-903. |
| Link to: | http://dx.doi.org/10.1016/j.cgh.2023.10.018 |
| JIF/Ranking 2023: | http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=1542-3565&DestApp=IC2JCR |
| Cited Times(Scopus): | https://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85186882456 |
| Appears in Collections: | [許志成] 期刊論文
[許志成] 期刊論文
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Size | Format | |
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| PUB37913938.pdf | | 55Kb | Adobe PDF | 36 | View/Open |
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