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Effect of proton pump inhibitor therapy on inflammatory changes in the gastric cardia (carditis)
Shailender Singh1, Ajay Bansal, Srinivas Puli
1University of Kansas School of Medicine and Veterans Affairs Medical Center, Kansas City, Kansas, Missouri 64128, USA.
Insights
Proton pump inhibitor (PPI) therapy did not significantly reduce inflammation in the gastric cardia. These findings suggest gastroesophageal reflux disease (GERD) may not be a primary cause of carditis.
Area of Science:
- Gastroenterology
- Pathology
Background:
- The causes of gastric cardia inflammation (carditis) are debated.
- Gastroesophageal reflux disease (GERD) and H. pylori infection are potential etiological factors.
Purpose of the Study:
- To assess the impact of acid suppression on histological changes in the gastric cardia.
- To evaluate the efficacy of proton pump inhibitors (PPIs) in managing carditis.
Main Methods:
- Gastric cardia biopsies from reflux patients were analyzed before and after PPI therapy.
- The updated Sydney classification was used to score histological findings.
- Carditis, intestinal metaplasia, and atrophy scores were compared pre- and post-treatment.
Main Results:
- No significant reduction in carditis scores was observed after prolonged PPI therapy (mean 30 months).
- Mean mononuclear and neutrophil scores showed a slight, non-significant increase post-PPI therapy.
- Intestinal metaplasia and atrophy scores remained unchanged.
Conclusions:
- Acid suppressive therapy with PPIs did not significantly decrease carditis scores.
- GERD is unlikely to be a major factor in the pathogenesis of gastric cardia inflammation.
Abstract:
The etiology of inflammation of the gastric cardia (carditis) is controversial, and gastroesophageal reflux disease (GERD) and H. pylori infection have been proposed as etiological factors. This study aimed to investigate the effect of acid suppression on histological changes in the gastric cardia. Gastric cardia biopsies of reflux patients were evaluated at baseline and after proton pump inhibitor (PPI) therapy. The updated Sydney classification was used to score the biopsies, and carditis scores (pre- and post-PPI therapy) were compared. A total of 31 patients were included, of which 5 patients were excluded, as cardiac mucosa was not documented in either pre- or post-PPI biopsies. The mean duration of PPI therapy was 30 months (SE, 3.04 months). There was no significant change in carditis scores post-PPI therapy. The mean mononuclear and neutrophil scores were 1.23 and 0.35 pre-PPI therapy and 1.73 and 0.62 post-PPI therapy, respectively. No change in mean intestinal metaplasia and atrophy scores was identified. In conclusion, acid suppressive therapy with PPI did not lead to a significant reduction in carditis scores. These results suggest that GERD probably does not play a major role in the pathogenesis of inflammation in the gastric cardia.
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