栓子堵塞胃底腺息肉中的腺管出口。
Plugs clog the glandular outlets in fundic gland polyps.
作者信息
Rubio Carlos A
机构信息
Gastrointestinal and Liver Pathology Research Laboratory, Department of Pathology, Karolinska Institute and University Hospital, Stockholm, Sweden.
出版信息
Int J Clin Exp Pathol. 2009 Sep 10;3(1):69-74.
A systematic histologic analysis of 62 gastric fundic gland polyps (FGP) was carried out. All FGP (100%) showed foveolar cells with hypertrophic cytoplasm. In 95% of the FGP, parietal cells ballooned into the lumen and in 93%, exfoliated anucleated structures with eosinophilic granules were found. Plugs of anucleated structures with eosinophilic granules, most likely derived from exfoliated parietal cells, were found to clog the outlets of the glands in 86% of the FGP. None of the 30 control gastric biopsies without FGP had similar cellular aberrations. FGP seems to evolve by cellular aberrations affecting parietal cells. This is not surprising considering that genetic mutations are recorded in FGP with a common APC/b-catenin pathway in both FAP and sporadic cases. The genetic mutations in FGP might alter the biological behavior of the parietal cells, leading to increased exfoliation with clogging of the outlets of the glands. Thus, the blocking of the glandular outflow by plugs of anucleated structures with eosinophilic granules is the most likely cause for the cystic accumulation of "normal" glandular secretions.
对62个胃底腺息肉（FGP）进行了系统的组织学分析。所有FGP（100%）均显示小凹细胞的细胞质肥大。95%的FGP中，壁细胞向管腔内膨出，93%的FGP中发现有含嗜酸性颗粒的无核脱落结构。在86%的FGP中，发现含嗜酸性颗粒的无核结构栓子（很可能来源于脱落的壁细胞）堵塞了腺管的出口。30例无FGP的对照胃活检标本均无类似的细胞异常。FGP似乎是由影响壁细胞的细胞异常演变而来。考虑到在家族性腺瘤性息肉病（FAP）和散发性病例中，FGP均存在常见的APC/β-连环蛋白途径的基因突变，这并不奇怪。FGP中的基因突变可能改变壁细胞的生物学行为，导致脱落增加并堵塞腺管出口。因此，含嗜酸性颗粒的无核结构栓子阻塞腺管流出是“正常”腺分泌液囊性积聚的最可能原因。
Zotero 插件