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Carditis: a manifestation of gastroesophageal reflux disease
R Der1, D D Tsao-Wei, T Demeester
1Department of Surgical Pathology, Foregut Surgery, Keck School of Medicine at the University of Southern California, Los Angeles, USA.
Insights
Chronic inflammation in cardiac mucosa (CM) is linked to acid reflux, not Helicobacter pylori infection. H. pylori can cause acute inflammation in CM, especially in men with severe carditis and no distal gastritis.
Area of Science:
- Gastroenterology
- Pathology
Background:
- Cardiac mucosa (CM) is found in the gastroesophageal junction.
- Carditis is defined as inflammation of CM.
Purpose of the Study:
- To investigate the association between carditis, acid reflux, and Helicobacter pylori infection.
- To determine the role of H. pylori in the pathogenesis of carditis.
Main Methods:
- Analysis of 141 patients with CM in biopsy samples.
- Classification of carditis as acute or chronic based on inflammatory cell count.
- Quantification of esophageal acid exposure using 24-hour pH testing.
- Assessment for H. pylori presence and gastritis in gastric biopsies.
Main Results:
- All cases showed significant chronic inflammation in CM.
- 79% of patients with carditis had no evidence of gastritis.
- Severe chronic inflammation in CM correlated with higher esophageal acid exposure.
- Acute inflammation in CM was associated with distal gastritis and H. pylori.
- Men with carditis had higher acid exposure than women, particularly those with severe inflammation and no distal gastritis.
Conclusions:
- Chronic carditis is strongly associated with acid reflux.
- H. pylori is not a significant cause of chronic carditis.
- H. pylori infection can lead to acute inflammation in CM superimposed on chronic inflammation.
Abstract:
This series consists of 141 patients in whom cardiac mucosa (CM) was present in biopsy samples from the gastroesophageal junctional region. Inflammation of CM, irrespective of its exact anatomic location, was defined as carditis and classified as acute or chronic based on the number of inflammatory cells present. In all cases, CM showed significant chronic inflammation. One hundred and eleven (79%) of the 141 patients with carditis showed no evidence of gastritis in biopsy samples from the gastric antrum and body. Helicobacter pylori was present in 20 of 141 (14%) patients; of these, 17 had evidence of a pangastritis, with 15 of these patients also showing H. pylori in CM. Patients with severe chronic inflammation in CM had a significantly higher acid exposure of the lower esophagus as quantitated by a 24-hour pH test than those with mild chronic inflammation in CM. Acute inflammation was uncommon in CM; it was present in only 26 of 141 (18.4%) patients. There was no significant difference in acid exposure of the lower esophagus between patients with and without acute inflammation in CM. The presence of acute inflammation in CM was significantly associated with distal gastritis and H. pylori infection. Men with carditis had quantitatively higher acid exposure of the lower esophagus than did women with this disorder. This difference was greatest in men with severe inflammation in CM who had no evidence of distal gastritis. These findings provide evidence that chronic inflammation in CM is strongly associated with acid reflux and that H. pylori is not a significant etiologic factor in carditis. They also show that in patients with CM in whom H. pylori gastritis develops, the infection frequently spreads to involve CM, resulting in acute inflammation with neutrophils that is superimposed on the chronic inflammation already present.