tetano
Editor, Senior Moderator
Neurogastroenterol Motil
. 2022 Dec 2;e14502.
doi: 10.1111/nmo.14502. Online ahead of print.
Is the Sars-CoV-2 virus a possible trigger agent for the development of achalasia?
Janette Furuzawa-Carballeda[SUP] 1 [/SUP], María E Icaza-Chávez[SUP] 2 [/SUP], Diana Aguilar-León[SUP] 3 [/SUP], Norma Uribe-Uribe[SUP] 3 [/SUP], María C Nuñez-Pompa[SUP] 1 [/SUP], Alonso Trigos-Díaz[SUP] 4 [/SUP], Rodrigo Areán-Sanz[SUP] 4 [/SUP], Dheni A Fernández-Camargo[SUP] 5 6 [/SUP], Enrique Coss-Adame[SUP] 7 [/SUP], Miguel A Valdovinos[SUP] 7 [/SUP], Eduardo Briceño-Souza[SUP] 1 [/SUP], Luis A Chi-Cervera[SUP] 2 [/SUP], Miriam Olivares-Flores[SUP] 3 [/SUP], Gonzalo Torres-Villalobos[SUP] 4 [/SUP]
Affiliations
Abstract
Background: Achalasia is an autoimmune disease whose probable causal agent is a neurotropic virus that chronically infects the myenteric plexus of the esophagus and induces the disease in a genetically susceptible host. The association between achalasia and coronaviruses has not been reported.
Aims: To evaluate the presence of the SARS-CoV-2 virus, the ACE2 expression, the tissue architecture, and immune response in the lower esophageal sphincter muscle (LESm) of achalasia patients who posteriorly had SARS-CoV-2 (achalasia-COVID-19) infection before laparoscopic Heller myotomy (LHM) and compare the findings with type II achalasia patients and transplant donors (controls) without COVID-19.
Methods: The LESm of 7 achalasia-COVID-19 patients (diagnosed by PCR), ten achalasia patients, and ten controls without COVID-19 were included. The presence of the virus was evaluated by in situ PCR and immunohistochemistry. ACE2 receptor expression and effector CD4 T cell and regulatory subsets were determined by immunohistochemistry.
Key results: Coronavirus was detected in 6/7 patients-COVID-19. The SARS-CoV-2 was undetectable in the LESm of the achalasia patients and controls. ACE2 receptor was expressed in all the patients and controls. One patient developed achalasia type II post-COVID-19. The percentage of Th22/Th17/Th1/pDCreg was higher in achalasia and achalasia-COVID-19 pre-HLM vs. controls. The Th2/Treg/Breg cell percentages were higher only in achalasia vs. controls.
Conclusion & inferences: SARS-CoV2 and its receptor expression in the LESm of achalasia patients who posteriorly had COVID-19 but not in the controls suggests that it could affect the myenteric plexus. Unlike achalasia, patients-COVID-19 have an imbalance between effector CD4 T cells and the regulatory mechanisms.
Keywords: CD4 T cells; COVID-19; HSV; achalasia.
. 2022 Dec 2;e14502.
doi: 10.1111/nmo.14502. Online ahead of print.
Is the Sars-CoV-2 virus a possible trigger agent for the development of achalasia?
Janette Furuzawa-Carballeda[SUP] 1 [/SUP], María E Icaza-Chávez[SUP] 2 [/SUP], Diana Aguilar-León[SUP] 3 [/SUP], Norma Uribe-Uribe[SUP] 3 [/SUP], María C Nuñez-Pompa[SUP] 1 [/SUP], Alonso Trigos-Díaz[SUP] 4 [/SUP], Rodrigo Areán-Sanz[SUP] 4 [/SUP], Dheni A Fernández-Camargo[SUP] 5 6 [/SUP], Enrique Coss-Adame[SUP] 7 [/SUP], Miguel A Valdovinos[SUP] 7 [/SUP], Eduardo Briceño-Souza[SUP] 1 [/SUP], Luis A Chi-Cervera[SUP] 2 [/SUP], Miriam Olivares-Flores[SUP] 3 [/SUP], Gonzalo Torres-Villalobos[SUP] 4 [/SUP]
Affiliations
- PMID: 36458526
- DOI: 10.1111/nmo.14502
Abstract
Background: Achalasia is an autoimmune disease whose probable causal agent is a neurotropic virus that chronically infects the myenteric plexus of the esophagus and induces the disease in a genetically susceptible host. The association between achalasia and coronaviruses has not been reported.
Aims: To evaluate the presence of the SARS-CoV-2 virus, the ACE2 expression, the tissue architecture, and immune response in the lower esophageal sphincter muscle (LESm) of achalasia patients who posteriorly had SARS-CoV-2 (achalasia-COVID-19) infection before laparoscopic Heller myotomy (LHM) and compare the findings with type II achalasia patients and transplant donors (controls) without COVID-19.
Methods: The LESm of 7 achalasia-COVID-19 patients (diagnosed by PCR), ten achalasia patients, and ten controls without COVID-19 were included. The presence of the virus was evaluated by in situ PCR and immunohistochemistry. ACE2 receptor expression and effector CD4 T cell and regulatory subsets were determined by immunohistochemistry.
Key results: Coronavirus was detected in 6/7 patients-COVID-19. The SARS-CoV-2 was undetectable in the LESm of the achalasia patients and controls. ACE2 receptor was expressed in all the patients and controls. One patient developed achalasia type II post-COVID-19. The percentage of Th22/Th17/Th1/pDCreg was higher in achalasia and achalasia-COVID-19 pre-HLM vs. controls. The Th2/Treg/Breg cell percentages were higher only in achalasia vs. controls.
Conclusion & inferences: SARS-CoV2 and its receptor expression in the LESm of achalasia patients who posteriorly had COVID-19 but not in the controls suggests that it could affect the myenteric plexus. Unlike achalasia, patients-COVID-19 have an imbalance between effector CD4 T cells and the regulatory mechanisms.
Keywords: CD4 T cells; COVID-19; HSV; achalasia.