Gut: 在健康的志愿者中,免疫组化证实贲门扩张的机制为鳞状上皮向柱状上皮化生,向心性肥胖加剧了这一机制

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中文版

GUT

在健康的志愿者中,免疫组化证实贲门扩张的机制为鳞状上皮向柱状上皮化生,向心性肥胖加剧了这一机制
 

摘要:

引言  最近,我们发现在健康志愿者中贲门黏膜的长度与年龄和肥胖相关。我们通过检测扩张的贲门的免疫组化特点,来确定此类扩张是否是由食管远端柱状上皮化生引发的。
 

方法我们采用52名健康志愿者的鳞柱状上皮交界处、胃窦、胃体部位的活检组织进行研究。52名志愿者均为幽门螺杆菌阴性,且参与了我们早期的生理学研究,均不伴有食管裂孔疝、胃食管反流、Barrett’s食管与贲门肠上皮化生(IM)。我们观察了鳞状上皮、贲门、鳞柱交界处、胃窦和胃体黏膜中的炎症细胞密度和异型性,并将切片染色,观察了CDX-2、绒毛蛋白、TFF-3、肝--LI)钙粘蛋白、粘蛋白MUC1 Muc-2  Muc-5ac等蛋白。另外,采用15名伴有或不伴有肠化的Barrett’s食管患者活检组织作为对照组,进行黏膜染色与评分。免疫组化特点与肥胖参数和高精度PH值测定记录相关。
 

结果贲门黏膜的炎性渗出强度与非肠化生的Barrett’s食管黏膜相似,但较其他的上消化道GI粘膜强。贲门黏膜免疫染色最接近非肠化的Barrett’s食管,表现为略弱的CDX-2染色。在食管远端的鳞状上皮中,柱状上皮分化标志物(TFF-3LI-cadherin)有明显的表达,并且与向心性肥胖相关(相关系数分别为CC=0.604,p=0.001CC=0.462,p=0.002)。另外,TFF-3在食管远端鳞状上皮的表达与食管括约肌以下区域的近端延伸的胃内酸度相关(CC =−0.538, p= 0.001)

 

结论以上发现与健康志愿者的贲门扩张和食管远端鳞柱化生是一致的,并且在向心性肥胖患者中更加明显。贲门扩张的化生起源可能在相当大的程度上与幽门螺杆菌感染非相关的或胃食管反流的贲门腺癌有关。

摘自Gut 2015;0:1–10. doi:10.1136/gutjnl-2014-308914

(译 田书信 郑勇)

石河子大学医学院第一附属医院消化内科

原文链接:http://gut.bmj.com/content/early/2015/03/24/gutjnl-2014-308914.full 

 

 

英文版

GUT

In healthyvolunteers, immunohistochemistry supports squamous to columnar metaplasia asmechanism of expansion of cardia, aggravated by central obesity
 

Introduction Recently, weshowed that the length of cardiac mucosa in healthy volunteers correlated withage and obesity. We have now examined the immunohistological characteristics ofthis expanded cardia to determine whether it may be due to columnar metaplasiaof the distal oesophagus.
 

Methods We used the squamocolumnar junction (SCJ), antraland body biopsies from the 52 Helicobacter pylori-negative healthy volunteerswho had participated in our earlier physiological study and did not have hiatushernia, transsphincteric acid reflux, Barrett's oesophagus or intestinalmetaplasia (IM) at cardia. The densities of inflammatory cells andreactive atypia were scored at squamous, cardiac and oxyntocardiac mucosa ofSCJ, antrum and body. Slides were stained for caudal type homeobox 2(CDX-2), villin, trefoil factor family 3 (TFF-3) and liver–intestine(LI)-cadherin, mucin MUC1, Muc-2 and Muc-5ac. In addition, biopsies from15 Barrett's patients with/without IM were stained and scored ascomparison. Immunohistological characteristics were correlated withparameters of obesity and high-resolution pH metry recording.

 

Results Cardiac mucosa had a similarintensity of inflammatory infiltrate to non-IM Barrett's and greater than anyof the other upper GI mucosae. The immunostaining pattern of cardiac mucosamost closely resembled non-IM Barrett's showing only slightly weaker CDX-2 immunostaining.In distal oesophageal squamous mucosa, expression of markers of columnardifferentiation (TFF-3 and LI-cadherin) was apparent and these correlated withcentral obesity (correlation coefficient (CC)=0.604, p=0.001 and CC=0.462,p=0.002, respectively). In addition, expression of TFF-3 in distal oesophagealsquamous mucosa correlated with proximal extension of gastric acidity withinthe region of the lower oesophageal sphincter (CC=−0.538, p=0.001).

Conclusions These findings are consistent with expansion of cardia inhealthy volunteers occurring by squamo columnar metaplasia of distal oesophagusand aggravated by central obesity. This metaplastic origin of expandedcardia may be relevant to the substantial proportion of cardia adenocarcinomas unattributableto H. pylori or transsphincteric acid reflux.

FromGut 2015;0:1–10.doi:10.1136/gutjnl-2014-308914
 

Original connection
http://gut.bmj.com/content/early/2015/03/24/gutjnl-2014-308914.full

 
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