Akademik Veri Yönetim Sistemi
SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY, cilt.40, sa.10, ss.1149-1156, 2005 (SCI-Expanded)
Objective. Acid secretion produced by a heterotopic gastric mucosal patch (HGMP) in the proximal esophagus, instead of gastric acid, may be responsible for laryngopharyngeal reflux (LPR), passing the upper esophageal sphincter. The aim of this study was to investigate the prevalence of HGMP in the proximal esophagus in patients with posterior laryngitis indicating the presence of LPR in comparison with a control group and to elucidate the possible role of this lesion in the pathogenesis of LPR. Material and methods. A total of 36 consecutive patients with posterior laryngitis diagnosed on laryngoscopic examination were enrolled in the study. Esophagoscopy and ambulatory 24-h intra-esophageal dual-probe pH monitoring were performed in all patients. During endoscopy, special attention was paid to the proximal part of the esophagus, and the proximal electrode for pH monitoring was placed in this region under endoscopic view. The control group comprised 660 consecutive patients who had undergone upper gastrointestinal endoscopy for the usual indications. When HGMP was found, biopsies were taken for histological confirmation. Results. HGMP was detected in 5 out of 36 patients. One out of five patients with patches was excluded from the study because the histopathology of this patient's patch revealed antral-type mucosa, which is not capable of acid secretion. Thus a total of 35 patients were included in the study, yielding a HGMP prevalence of 11.4% (4/35). Compared with the prevalence of the control group (1.6%), a significant difference was observed (p< 0.005). pH monitoring showed that 45.4% of the patients had abnormal proximal acid reflux. All of four HGMP (+) patients with posterior laryngitis revealed significantly higher abnormal proximal reflux compared to the patients without patches ( p< 0.05). Conclusions. This first preliminary study may suggest that HGMP in the cervical esophagus could play a role in the pathogenesis of LPR, at least in a minor group of patients with posterior laryngitis, depending on its capability to produce acid in situ, although isolated proximal reflux could not be demonstrated. This finding may need to be supported by further studies with larger patient populations and using acid stimulation tests.