Samo Salih, Hamo Falak, Hamza Ameer, Yadlapati Rena, Kahrilas Peter J, Wozniak Ann
Division of Gastroenterology, Hepatology, and Motility, The University of Kansas School of Medicine, Kansas City, Kansas, USA.
Department of Pathology, The University of Kansas School of Medicine, Kansas City, Kansas, USA.
Am J Gastroenterol. 2024 May 1;119(5):987-990. doi: 10.14309/ajg.0000000000002669. Epub 2024 Jan 24.
Achalasia has been linked to viruses. We have observed cases of rapid-developing achalasia post-coronavirus disease 2019 (COVID-19).
We aimed to prospectively evaluate esophageal muscle for severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) from patients with rapid-onset achalasia post-COVID-19 and compare them with achalasia predating COVID-19 and achalasia with no COVID-19.
Compared with long-standing achalasia predating COVID-19 and long-standing achalasia with no COVID-19, the subjects with achalasia post-COVID-19 had significantly higher levels of messenger RNA for the SARS-CoV-2 nucleocapsid (N) protein, which correlated with a significant increase in the inflammatory markers NOD-like receptor family pyrin domain-containing 3 and tumor necrosis factor.
SARS-CoV-2, the virus responsible for COVID-19, is a possible trigger for achalasia.
贲门失弛缓症与病毒有关。我们观察到2019冠状病毒病(COVID-19)后出现快速进展的贲门失弛缓症病例。
我们旨在对COVID-19后快速发病的贲门失弛缓症患者的食管肌肉进行前瞻性评估,以检测严重急性呼吸综合征冠状病毒2(SARS-CoV-2),并将其与COVID-19之前的贲门失弛缓症患者以及无COVID-19的贲门失弛缓症患者进行比较。
与COVID-19之前的长期贲门失弛缓症患者和无COVID-19的长期贲门失弛缓症患者相比,COVID-19后贲门失弛缓症患者的SARS-CoV-2核衣壳(N)蛋白信使核糖核酸水平显著更高,这与炎症标志物含NOD样受体家族吡咯结构域蛋白3和肿瘤坏死因子的显著增加相关。
导致COVID-19的病毒SARS-CoV-2可能是贲门失弛缓症的触发因素。