Carditis at the interface between GERD and Helicobacter pylori infection
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U Peitz1, M Vieth, P Malfertheiner
1Department of Gastroenterology, Hepatology and Infectiology, Otto-von-Guericke University, Magdeburg, Germany. ulrich.peitz@medizin.uni-magdeburg.de
Insights
Carditis, gastric cardia inflammation, is a histological diagnosis. Its causes, like H. pylori infection and GERD, and clinical relevance remain controversial, requiring further study.
Area of Science:
- Gastroenterology
- Histopathology
Background:
- Carditis is inflammation of the gastric cardia, a histological diagnosis.
- Its causes, primarily Helicobacter pylori infection and gastroesophageal reflux disease (GERD), and their interactions are debated.
- The clinical significance of carditis regarding symptoms and cancer risk is unclear due to anatomical variations and conflicting study data.
Purpose of the Study:
- To evaluate the histological criteria for carditis, potentially adapting the updated Sydney classification.
- To investigate the controversial roles of H. pylori and GERD in carditis development and inflammation.
- To clarify the clinical relevance and cancer risk associated with carditis.
Main Methods:
- Review and adaptation of histological criteria from the updated Sydney classification for the gastric cardia.
- Analysis of existing literature on H. pylori infection and GERD in relation to carditis.
- Examination of anatomical variations in the esophagogastric junction and cardia-type mucosa (CM) development.
Main Results:
- Carditis diagnosis relies on histological criteria, with proposed adaptation from the Sydney classification.
- H. pylori gastritis commonly involves the gastric cardia.
- The contribution of GERD to carditis in H. pylori-negative individuals is highly controversial, with reported prevalence in GERD patients ranging widely (10-97%).
Conclusions:
- Carditis, due to its high frequency and low specificity, is not currently considered a distinct clinical entity.
- Metaplastic cardia-type mucosa may develop in the esophagus due to GERD.
- Further research with precise biopsy protocols is needed to understand carditis's role in esophagogastric junction cancer incidence.
Abstract:
Inflammation of the gastric cardia ('carditis') is a histological diagnosis. It seems reasonable to transfer histological criteria of the updated Sydney classification from the distal stomach to the cardia as long as a special classification of inflammation of the esophagogastric junction is lacking. The two best characterized causes of carditis are Helicobacter pylori infection and gastroesophageal reflux disease (GERD). However, the causal contribution and interference of these two factors are highly controversial, as is the clinical relevance of carditis in terms of eliciting symptoms or conferring an increased cancer risk. Variability of studies on carditis is based on conflicting concepts of the normal anatomy of the esophagogastric junction. Cardia-type mucosa (CM) apparently exists at birth as a tiny circular area, and extends to a larger area in adulthood. This implies that cardia-type mucosa is largely metaplastic. Metaplastic CM may evolve in the lower esophagus as a consequence of GERD. It is a general phenomenon that H. pylori-induced gastritis also involves the gastric cardia, irrespective whether the cardia is lined by fundus-type mucosa or CM. The contribution of GERD to inflammation of CM in H. pylori-negative individuals is, however, highly controversial. Prevalence of carditis in GERD patients fluctuates between 10 and 97%. Hence, because of its high frequency and low specificity, carditis can currently not be considered as a clinical entity. The role of carditis for the increasing incidence of cancer of the esophagogastric junction requires careful studies that include accurate description of the area with adequate biopsy protocols.
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