von Rahden Burkhard H A, Stein Hubert J, Becker Karen, Liebermann-Meffert Dorothea, Siewert J Rüdiger
Department of Surgery, Klinikum rechts der Isar, Technical University Munich, Germany.
Am J Gastroenterol. 2004 Mar;99(3):543-51. doi: 10.1111/j.1572-0241.2004.04082.x.
The prevalence of heterotopic gastric mucosa (HGM) in the cervical esophagus is frequently underestimated. Tiny microscopic foci have to be distinguished from a macroscopically visible patch, also called "inlet patch." Symptoms as well as morphologic changes associated with HGM are regarded as a result of the damaging effect of acid, produced by parietal cells in the mostly fundic type of HGM. We herein review the literature and propose a new clinicopathologic classification of esophageal HGM: Most of the carriers of esophageal HGM are asymptomatic (HGM I). Some individuals with HGM in the esophagus complain of dysphagia, odynophagia, or "extraesophageal manifestations" (hoarseness and coughing), without further morphologic findings (HGM II). Still fewer patients are symptomatic due to morphologic changes, i.e., esophageal strictures, webs, or esophagotracheal fistula (HGM III). Malignant transformation via dysplasia (intraepithelial neoplasia, HGM IV) to cervical esophageal adenocarcinoma (HGM V) is exceedingly rare (only 24 reported cases). In contrast to Barrett's esophagus, HGM should not be regarded as a precancerous lesion. Symptoms are more likely to occur in patients with inlet patch, whereas malignant transformation and adenocarcinogenesis can also occur in microscopic HGM foci. Asymptomatic HGM requires neither specific therapy nor endoscopic surveillance. Only in symptomatic cases treatment, i.e., dilatation for (benign) strictures or acid suppression for reflux symptoms, can be recommended. Patients with low-grade dysplasia in HGM might be candidates for surveillance strategies, whereas in cases of high-grade dysplasia and invasive adenocarcinoma oncological treatment strategies must be employed.
颈段食管异位胃黏膜(HGM)的患病率常常被低估。微小的显微镜下病灶必须与肉眼可见的斑块(也称为“入口斑块”)区分开来。与HGM相关的症状以及形态学改变被认为是由大多为胃底型HGM中壁细胞产生的酸的破坏作用所致。我们在此回顾文献并提出一种新的食管HGM临床病理分类:大多数食管HGM携带者无症状(HGM I)。一些食管有HGM的个体主诉吞咽困难、吞咽痛或“食管外表现”(声音嘶哑和咳嗽),且无进一步的形态学发现(HGM II)。因形态学改变(即食管狭窄、蹼或食管气管瘘)而出现症状的患者更少(HGM III)。通过发育异常(上皮内瘤变,HGM IV)至颈段食管腺癌(HGM V)的恶性转化极为罕见(仅报道24例)。与巴雷特食管不同,HGM不应被视为癌前病变。症状更可能出现在有入口斑块的患者中,而恶性转化和腺癌发生也可发生在显微镜下的HGM病灶中。无症状的HGM既不需要特殊治疗也不需要内镜监测。仅在有症状的情况下,可推荐进行治疗,即对(良性)狭窄进行扩张或对反流症状进行抑酸治疗。HGM中存在低级别发育异常的患者可能是监测策略的候选对象,而在高级别发育异常和浸润性腺癌的情况下,必须采用肿瘤治疗策略。