Carditis: a relevant marker of gastroesophageal reflux disease. Data from a prospective central European multicenter study on histological and endoscopic diagnosis of esophagitis (histoGERD trial)

Abstract

The columnar-lined mucosa at the gastroesophageal junction may contain an inflammatory infiltrate, commonly referred to as carditis (or cardia gastritis). The etiology of carditis is not entirely clear since published data are conflicting. Some authors believe it to be secondary to gastroesophageal reflux disease (GERD) and others to Helicobacter pylori gastritis. This prospective study aims at clarifying the relationship between carditis and the histological, clinical, and endoscopic findings of GERD, in a large cohort of individuals negative for H. pylori infection. Eight hundred and seventy-three individuals (477 females and 396 males, median age 53 years) participated in this study. Biopsy material was systematically sampled from above and below the gastroesophageal junction. Reflux-associated changes of the esophageal squamous epithelium were assessed according to the Esohisto consensus guidelines. Grading of carditis was performed according to the Updated Sydney System, known from the histological evaluation of gastritis. In total, 590 individuals (67.5%) had chronic carditis. Of these, 468 (53.6%) had mild chronic inflammation, with 321 individuals (68.6%) showing no or minimal changes on endoscopic examination (Los Angeles Categories N and M). The presence of chronic carditis was associated with several GERD-related parameters of the esophageal squamous epithelium (P < 0.0001), and data retained statistical significance even when analysis was restricted to individuals with mild chronic carditis and/or endoscopically normal mucosa. Chronic carditis was also associated with the presence of intestinal metaplasia (P < 0.0001). In addition, chronic carditis had a statistically significant association with patients' symptoms of GERD (P = 0.0107). This observation remained valid for mild chronic carditis in all patients (P = 0.0038) and in those with mild chronic carditis and normal endoscopic mucosa (P = 0.0217). In conclusion, chronic carditis appears to be the immediate consequence of GERD, correlating with patients' symptoms and endoscopic diagnosis. These results are valid in individuals with nonerosive reflux disease, which indicates a higher sensitivity of histological diagnosis. Our findings may impact the routine assessment of reflux patients.

Unraveling the identity of gastric cardiac cancer

“…Second, although distal esophageal cardiac mucosa may undergo intestinal metaplasia, the frequency of goblet cell or intestinal metaplasia is much lower than that seen in long-segment BE and EAC. [17][18][19] Third, the prevalence of goblet cell or intestinal metaplasia in cardiac mucosa adjacent to EAC was reported to be about 50% in American and British patients. 61,63 The evidence suggests that at least two phenotypes of EAC exist: that is, one with a high prevalence and one with a low prevalence of goblet cells or intestinal metaplasia.…”

“…The prevalence of intestinal metaplasia of those glands appears to be lower than that in long‐segment BE 15‐17 . The length of superficial esophageal cardiac glands may increase, as a result of aging, obesity and gastroesophageal reflux disease 18,19 …”

“…First, cardiac mucosa with distal esophageal extension is common and known to be associated with aging and reflux diseases (Figures 1‐3). Second, although distal esophageal cardiac mucosa may undergo intestinal metaplasia, the frequency of goblet cell or intestinal metaplasia is much lower than that seen in long‐segment BE and EAC 17‐19 . Third, the prevalence of goblet cell or intestinal metaplasia in cardiac mucosa adjacent to EAC was reported to be about 50% in American and British patients 61,63 .…”

“…[15][16][17] The length of superficial esophageal cardiac glands may increase, as a result of aging, obesity and gastroesophageal reflux disease. 18,19 There is overwhelming evidence of the congenital nature of gastric cardiac mucosa in fetuses, neonates and adults in various racial and ethnic populations, 8 such as Japanese, 9 Korean, 20 Dutch, 21,22 German, 23 American, [24][25][26] and Chinese. 13 Investigators with the viewpoint F I G U R E 1 Schematic drawing of gastric cardia 3 cm below and 2 cm above the gastroesophageal junction (GEJ) at the angle of His [Color figure can be viewed at wileyonlinelibrary.com] F I G U R E 2 A, Gastric cardiac mucosa with mucous and mucoxyntic glands distal to the gastroesophageal junction (GEJ).…”

Clinical course of gastroesophageal reflux disease and impact of treatment in symptomatic young patients

“…More recently, the presence of IM at the EGJ has been recognized as a marker of progressive disease. 84,85 Medical therapy is unable to prevent the development of BE or induce the regression of IM, the precursor of visible BE. Also, current endoscopic therapies cannot reduce and correct a hiatal hernia, and their effects on histopathology, including prevention of EAC, are unknown.…”