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有和没有幽门螺杆菌感染的年轻患者心脏黏膜的炎症及细胞角蛋白7/20染色

Inflammation and cytokeratin 7/20 staining of cardiac mucosa in young patients with and without Helicobacter pylori infection.

作者信息

Oksanen A, Sankila A, von Boguslawski K, Sipponen P, Rautelin H

机构信息

Herttoniemi Municipal Hospital, PL 6300, FIN-00099 Helsinki, Finland.

出版信息

J Clin Pathol. 2005 Apr;58(4):376-81. doi: 10.1136/jcp.2004.020966.

Abstract

BACKGROUND

Both Helicobacter pylori and gastro-oesophageal reflux disease (GORD) may cause inflammation in cardiac mucosa. Intestinal metaplasia (IM) is found more often in GORD associated inflammation than in inflammation caused by H pylori, especially in young individuals.

AIM

To examine morphological differences in chronic inflammation in these two conditions by immunohistochemistry.

PATIENTS/METHODS: Tissue blocks from cardiac mucosa of patients <45 years were available as follows: 10 patients with chronic inflammation of cardiac mucosa (carditis) and H pylori gastritis (group 1); 10 patients with (possibly GORD related) carditis, but normal antrum and corpus (group 2); and 10 patients with non-inflamed cardiac mucosa and normal antrum and corpus (group 3). Haematoxylin and eosin staining and immunohistochemical staining for various inflammatory cells were performed for patients in groups 1 and 2 as follows: CD20 (B cells), CD3 (T cells), CD4 (T helper cells), CD8 (T suppressor cells), CD163 (macrophages), CD138 (plasma cells), and CD117 (mast cells). For all patients, cytokeratin 7/20 (CK7/20) staining was performed.

RESULTS

No clear differences were seen in the morphology of chronic inflammation between groups 1 and 2. In both, plasma cells were most abundant. CK7/20 staining showed no differences between these groups.

CONCLUSION

Helicobacter pylori negative (possibly GORD associated) and H pylori related carditis cannot be distinguished on a morphological basis. The stronger tendency towards IM in the first entity cannot be explained by differences in the type of inflammation. Barrett-type CK7/20 staining seems typical for cardiac mucosa, irrespective of the type of inflammation or presence of IM.

摘要

背景

幽门螺杆菌和胃食管反流病(GORD)均可导致贲门黏膜炎症。肠化生(IM)在GORD相关性炎症中比在幽门螺杆菌引起的炎症中更常见,尤其是在年轻人中。

目的

通过免疫组织化学检查这两种情况下慢性炎症的形态学差异。

患者/方法:可获得45岁以下患者贲门黏膜的组织块如下:10例患有贲门黏膜慢性炎症(贲门炎)和幽门螺杆菌胃炎的患者(第1组);10例患有(可能与GORD相关的)贲门炎但胃窦和胃体正常的患者(第2组);以及10例贲门黏膜无炎症且胃窦和胃体正常的患者(第3组)。对第1组和第2组患者进行苏木精和伊红染色以及针对各种炎症细胞的免疫组织化学染色,如下所示:CD20(B细胞)、CD3(T细胞)、CD4(辅助性T细胞)、CD8(抑制性T细胞)、CD163(巨噬细胞)、CD138(浆细胞)和CD117(肥大细胞)。对所有患者进行细胞角蛋白7/20(CK7/20)染色。

结果

第1组和第2组之间慢性炎症的形态学未见明显差异。在这两组中,浆细胞最为丰富。CK7/20染色在这些组之间未显示差异。

结论

幽门螺杆菌阴性(可能与GORD相关的)和幽门螺杆菌相关性贲门炎在形态学上无法区分。第一种情况下IM的更强倾向不能用炎症类型的差异来解释。无论炎症类型或IM的存在如何,Barrett型CK7/20染色似乎是贲门黏膜的典型特征。

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本文引用的文献

1
Pathologic features of reflux and Helicobacter pylori-associated carditis: a comparative study.
Am J Surg Pathol. 2003 Jul;27(7):960-8. doi: 10.1097/00000478-200307000-00011.
2
Histologic classification of patients based on mapping biopsies of the gastroesophageal junction.
Am J Surg Pathol. 2003 Jul;27(7):929-36. doi: 10.1097/00000478-200307000-00008.
3
Increased risk of noncardia gastric cancer associated with proinflammatory cytokine gene polymorphisms.
Gastroenterology. 2003 May;124(5):1193-201. doi: 10.1016/s0016-5085(03)00157-4.
5
Is intestinal metaplasia of the stomach reversible?
Gut. 2003 Jan;52(1):1-4. doi: 10.1136/gut.52.1.1.
6
Cytokeratin and DAS-1 immunostaining reveal similarities among cardiac mucosa, CIM, and Barrett's esophagus.
Am J Gastroenterol. 2002 Oct;97(10):2514-23. doi: 10.1111/j.1572-0241.2002.06033.x.
7
Etiology of intestinal metaplasia at the gastroesophageal junction.
Surg Endosc. 2003 Jan;17(1):43-8. doi: 10.1007/s00464-002-8944-1. Epub 2002 Oct 8.
9
Carcinogenesis at the gastroesophageal junction: free radicals at the frontier.
Gastroenterology. 2002 May;122(5):1518-20. doi: 10.1053/gast.2002.33368.

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