Akbayir Nihat, Sökmen H Mehmet, Caliş Asli Batur, Bölükbaş Cengiz, Erdem Levent, Alkim Canan, Sakiz Damlanur, Mungan Zeynel
Department of Gastroenterology, Sişli Etfal Training and Research Hospital, Istanbul, Turkey.
Scand J Gastroenterol. 2005 Oct;40(10):1149-56. doi: 10.1080/00365520510023468.
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.
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.
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).
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.
位于食管上段的异位胃黏膜斑（HGMP）产生的酸分泌，而非胃酸，可能通过食管上括约肌导致喉咽反流（LPR）。本研究的目的是调查与对照组相比，提示存在LPR的喉后部炎症患者食管上段HGMP的患病率，并阐明该病变在LPR发病机制中的可能作用。
本研究共纳入36例经喉镜检查确诊为喉后部炎症的连续患者。所有患者均接受了食管镜检查和24小时动态食管双探头pH监测。在内镜检查过程中，特别关注食管上段，并在内镜直视下将pH监测的近端电极放置在该区域。对照组包括660例因常见适应证接受上消化道内镜检查的连续患者。发现HGMP时，取活检进行组织学确诊。
36例患者中有5例检测到HGMP。5例有黏膜斑的患者中有1例被排除在研究之外，因为该患者黏膜斑的组织病理学显示为胃窦型黏膜，不具备酸分泌能力。因此，共有35例患者纳入研究，HGMP患病率为11.4%（4/35）。与对照组患病率（1.6%）相比，差异有统计学意义（p<0.005）。pH监测显示，45.4%的患者近端酸反流异常。所有4例患有喉后部炎症的HGMP（+）患者的近端反流异常明显高于无黏膜斑的患者（p<0.05）。
这项初步研究可能表明，食管上段的HGMP可能在LPR的发病机制中起作用，至少在一小部分喉后部炎症患者中如此，这取决于其原位产酸能力，尽管未能证实存在孤立的近端反流。这一发现可能需要更多患者参与的进一步研究以及酸刺激试验的支持。
