Lauwers Gregory Y, Mino Mari, Ban Shinichi, Forcione David, Eatherton Desiree E, Shimizu Michio, Sevestre Henri
Gastrointestinal Pathology Service, Department of Pathology, Division of Gastroenterology, Massachusetts General Hospital, Boston, MA 02114, USA.
Am J Surg Pathol. 2005 Apr;29(4):437-42. doi: 10.1097/01.pas.0000155155.46434.da.
Cervical inlet patch (CIP) is defined by the presence of gastric mucosa within the first few centimeters of the esophagus. Several endoscopic series have demonstrated a frequent association of CIP with Barrett's esophagus (BE) suggesting a pathogenetic link. A histochemical study reporting the presence of acid mucin in CIP, including sulfomucin, supports this hypothesis. We evaluated mucin core protein expression and cytokeratins 7 and 20 (CK7/CK20) pattern in biopsies of CIP, normal antrum, and BE to comment on a possible relationship of CIP with BE. We observed that both lesions have similar cytokeratin patterns with mixed CK7/CK20 reactivity on the surface and pits and lone CK7 positivity in the glands. MUC5AC was strongly expressed on the surface and pits but not in the glands of CIP and antral mucosa. Within BE, MUC5AC positivity was noted not only on the surface and pits but also in the glands. MUC6 similarly decorated the glands of CIP and BE. MUC2 was expressed rarely in CIP with goblet cells but conspicuously on the surface and pits of BE. MUC5B was seen in both CIP and BE and rarely in the antral mucosa. The similarities between CIP and BE but not with normal antral mucosa fits with the hypothesis that both lesions may originate from submucosal esophageal mucous glands. Two pathogenetic pathways can be entertained: focal upper esophageal mucosal misdevelopment in pediatric population and patchy metaplastic replacement of squamous mucosa in adults with gastroesophageal reflux disease.
宫颈入口处斑块(CIP)定义为食管最初几厘米内存在胃黏膜。多项内镜系列研究表明,CIP与巴雷特食管(BE)频繁相关,提示存在致病联系。一项关于CIP中酸性黏蛋白(包括硫黏蛋白)存在情况的组织化学研究支持了这一假说。我们评估了CIP活检组织、正常胃窦和BE中黏蛋白核心蛋白表达及细胞角蛋白7和20(CK7/CK20)模式,以探讨CIP与BE之间可能的关系。我们观察到,这两种病变具有相似的细胞角蛋白模式,表面和小凹处CK7/CK20呈混合反应,腺体中仅CK7呈阳性。MUC5AC在CIP和胃窦黏膜的表面和小凹处强烈表达,但在腺体中不表达。在BE中,不仅在表面和小凹处,而且在腺体中均发现MUC5AC呈阳性。MUC6同样分布于CIP和BE的腺体中。MUC2在有杯状细胞的CIP中很少表达,但在BE的表面和小凹处明显表达。MUC5B在CIP和BE中均可见,在胃窦黏膜中很少见。CIP与BE之间的相似性而非与正常胃窦黏膜的相似性,符合这两种病变可能均起源于食管黏膜下黏液腺的假说。可以考虑两种致病途径:儿童人群中食管上段黏膜的局灶性发育异常,以及成人胃食管反流病患者鳞状黏膜的斑片状化生替代。