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TOPLINE:
METHODOLOGY:
- The etiology of achalasia is unclear. Studies have suggested an immune reaction to viral infections, including SARS-CoV-2, as a potential cause.
- Researchers studied four adults who developed achalasia within 5 months of SARS-CoV-2 infection (group 1), six with longstanding achalasia predating SARS-CoV-2 infection (group 2), and two with longstanding achalasia with no known SARS-CoV-2 infection (group 3).
- They tested for the presence of SARS-CoV-2 nucleocapsid (N) and spike (S) proteins, as well as inflammatory markers, in esophageal muscle tissue isolated from the participants.
TAKEAWAY:
- Group 1 patients (confirmed or suspected post–COVID-19 achalasia) had the highest levels of the N protein in all four cases and higher levels of the S protein in the two confirmed cases. No N or S protein was detected in group 3.
- The presence of mRNA for SARS-CoV-2 N protein correlated with a significant increase in the inflammatory markers of NOD-like receptor family pyrin domain-containing 3 and tumor necrosis factor. There were no differences in interleukin 18 in groups 1 and 2.
- The S protein was detected in all muscle tissue samples from group 1. It was also detected in some (but not all) samples from group 2 and to a much lesser degree. The presence of S protein was irrespective of the SARS-CoV-2 vaccination status.
IN PRACTICE:
“Our findings not only show the continued presence of SARS-CoV-2 proteins in esophageal muscle tissue isolated from subjects with achalasia post infection, but they further correlate this with the presence of a sustained inflammatory response,” the authors wrote.
SOURCE:
The study, with first author Salih Samo, MD, MS, Division of Gastroenterology, Hepatology, and Motility, University of Kansas School of Medicine, Kansas City, Kansas, was published online on January 24, 2024, in the American Journal of Gastroenterology.
LIMITATIONS:
The sample size was small, and it was not known which SARS-CoV-2 variant each patient had. The study cannot definitively confirm that SARS-CoV-2 is causative for achalasia.
DISCLOSURES:
The study had no specific funding. Samo reported relationships with Castle Biosciences, Sanofi, Evoke, and EndoGastric Solutions.
A version of this article appeared on Medscape.com.
TOPLINE:
METHODOLOGY:
- The etiology of achalasia is unclear. Studies have suggested an immune reaction to viral infections, including SARS-CoV-2, as a potential cause.
- Researchers studied four adults who developed achalasia within 5 months of SARS-CoV-2 infection (group 1), six with longstanding achalasia predating SARS-CoV-2 infection (group 2), and two with longstanding achalasia with no known SARS-CoV-2 infection (group 3).
- They tested for the presence of SARS-CoV-2 nucleocapsid (N) and spike (S) proteins, as well as inflammatory markers, in esophageal muscle tissue isolated from the participants.
TAKEAWAY:
- Group 1 patients (confirmed or suspected post–COVID-19 achalasia) had the highest levels of the N protein in all four cases and higher levels of the S protein in the two confirmed cases. No N or S protein was detected in group 3.
- The presence of mRNA for SARS-CoV-2 N protein correlated with a significant increase in the inflammatory markers of NOD-like receptor family pyrin domain-containing 3 and tumor necrosis factor. There were no differences in interleukin 18 in groups 1 and 2.
- The S protein was detected in all muscle tissue samples from group 1. It was also detected in some (but not all) samples from group 2 and to a much lesser degree. The presence of S protein was irrespective of the SARS-CoV-2 vaccination status.
IN PRACTICE:
“Our findings not only show the continued presence of SARS-CoV-2 proteins in esophageal muscle tissue isolated from subjects with achalasia post infection, but they further correlate this with the presence of a sustained inflammatory response,” the authors wrote.
SOURCE:
The study, with first author Salih Samo, MD, MS, Division of Gastroenterology, Hepatology, and Motility, University of Kansas School of Medicine, Kansas City, Kansas, was published online on January 24, 2024, in the American Journal of Gastroenterology.
LIMITATIONS:
The sample size was small, and it was not known which SARS-CoV-2 variant each patient had. The study cannot definitively confirm that SARS-CoV-2 is causative for achalasia.
DISCLOSURES:
The study had no specific funding. Samo reported relationships with Castle Biosciences, Sanofi, Evoke, and EndoGastric Solutions.
A version of this article appeared on Medscape.com.
TOPLINE:
METHODOLOGY:
- The etiology of achalasia is unclear. Studies have suggested an immune reaction to viral infections, including SARS-CoV-2, as a potential cause.
- Researchers studied four adults who developed achalasia within 5 months of SARS-CoV-2 infection (group 1), six with longstanding achalasia predating SARS-CoV-2 infection (group 2), and two with longstanding achalasia with no known SARS-CoV-2 infection (group 3).
- They tested for the presence of SARS-CoV-2 nucleocapsid (N) and spike (S) proteins, as well as inflammatory markers, in esophageal muscle tissue isolated from the participants.
TAKEAWAY:
- Group 1 patients (confirmed or suspected post–COVID-19 achalasia) had the highest levels of the N protein in all four cases and higher levels of the S protein in the two confirmed cases. No N or S protein was detected in group 3.
- The presence of mRNA for SARS-CoV-2 N protein correlated with a significant increase in the inflammatory markers of NOD-like receptor family pyrin domain-containing 3 and tumor necrosis factor. There were no differences in interleukin 18 in groups 1 and 2.
- The S protein was detected in all muscle tissue samples from group 1. It was also detected in some (but not all) samples from group 2 and to a much lesser degree. The presence of S protein was irrespective of the SARS-CoV-2 vaccination status.
IN PRACTICE:
“Our findings not only show the continued presence of SARS-CoV-2 proteins in esophageal muscle tissue isolated from subjects with achalasia post infection, but they further correlate this with the presence of a sustained inflammatory response,” the authors wrote.
SOURCE:
The study, with first author Salih Samo, MD, MS, Division of Gastroenterology, Hepatology, and Motility, University of Kansas School of Medicine, Kansas City, Kansas, was published online on January 24, 2024, in the American Journal of Gastroenterology.
LIMITATIONS:
The sample size was small, and it was not known which SARS-CoV-2 variant each patient had. The study cannot definitively confirm that SARS-CoV-2 is causative for achalasia.
DISCLOSURES:
The study had no specific funding. Samo reported relationships with Castle Biosciences, Sanofi, Evoke, and EndoGastric Solutions.
A version of this article appeared on Medscape.com.