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诱导性炎症掩盖了胃病变中低级别异型增生的潜在存在。

-induced inflammation masks the underlying presence of low-grade dysplasia on gastric lesions.

机构信息

Department of Gastroenterology and Digestive Endoscopy, National Institute of Gastroenterology "S De Bellis", Research Hospital, Castellana Grotte 70013, Italy.

Sergio Coletta Department of Clinical Pathology, National Institute of Gastroenterology "S De Bellis", Research Hospital, Castellana Grotte 70013, Italy.

出版信息

World J Gastroenterol. 2020 Jul 14;26(26):3834-3850. doi: 10.3748/wjg.v26.i26.3834.

DOI:10.3748/wjg.v26.i26.3834
PMID:32774061
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7383846/
Abstract

BACKGROUND

infection has been associated with a long-term risk of precancerous gastric conditions (PGC) even after eradication.

AIM

To investigate the efficacy of High-Resolution White-Light Endoscopy with Narrow-Band Imaging in detecting PGC, before/after eradication.

METHODS

We studied 85 consecutive patients with -related gastritis with/without PGC before and 6 mo after proven eradication. Kimura-Takemoto modified and endoscopic grading of gastric intestinal metaplasia classifications, were applied to assess the endoscopic extension of atrophy and intestinal metaplasia. The histological result was considered to be the gold standard. The Sydney System, the Operative-Link on Gastritis-Assessment, and the Operative-Link on Gastric-Intestinal Metaplasia were used for defining histological gastritis, atrophy and intestinal metaplasia, whereas dysplasia was graded according to World Health Organization classification. Serum anti-parietal cell antibody and anti-intrinsic factor were measured when autoimmune atrophic gastritis was suspected.

RESULTS

After eradication histological signs of mononuclear/polymorphonuclear cell infiltration and Mucosal Associated Lymphoid Tissue-hyperplasia, disappeared or decreased in 100% and 96.5% of patients respectively, whereas the Operative-Link on Gastritis-Assessment and Operative-Link on Gastric-Intestinal Metaplasia stages did not change. Low-Grade Dysplasia prevalence was similar on random biopsies before and after eradication (17.6% 10.6%, = 0.19), but increased in patients with visible lesions (0% 22.4%, < 0.0001). At a multivariate analysis, the probability for detecting dysplasia after resolution of -related active inflammation was higher in patients with regression or reduction of Mucosal Associated Lymphoid Tissue hyperplasia, greater alcohol consumption, and anti-parietal cell antibody and/or anti-intrinsic factor positivity [odds ratio (OR) = 3.88, 95% confidence interval (CI): 1.31-11.49, = 0.01; OR = 3.10, 95%CI: 1.05-9.12, = 0.04 and OR = 5.47, 95%CI: 1.33-22.39, < 0.04, respectively].

CONCLUSION

High-Resolution White-Light Endoscopy with Narrow-Band Imaging allows an accurate diagnosis of Low-Grade Dysplasia on visible lesions after regression of -induced chronic gastritis. Patients with an overlap between autoimmune/-induced gastritis may require more extensive gastric mapping.

摘要

背景

即使在根除后,感染仍与癌前胃部疾病(PGC)的长期风险相关。

目的

研究高分辨率白光内镜联合窄带成像技术在根除前后检测 PGC 的效果。

方法

我们研究了 85 例伴有/不伴有 PGC 的 -相关胃炎患者,在根治后 6 个月进行了内镜检查。Kimura-Takemoto 改良内镜胃黏膜肠上皮化生分类法和内镜胃黏膜萎缩分类法被用于评估萎缩和肠上皮化生的内镜下延伸程度。组织学结果被视为金标准。悉尼系统、胃炎评估操作链接和胃黏膜肠上皮化生操作链接用于定义组织学胃炎、萎缩和肠上皮化生,而异型增生则根据世界卫生组织分类进行分级。当怀疑自身免疫性萎缩性胃炎时,检测血清壁细胞抗体和内因子抗体。

结果

根除后,单核/多形核细胞浸润和黏膜相关淋巴组织增生的组织学征象 100%和 96.5%的患者分别消失或减少,而胃炎评估操作链接和胃黏膜肠上皮化生操作链接分期没有变化。根治后随机活检的低级别异型增生发生率与根治前相似(17.6% 10.6%, = 0.19),但在有可见病变的患者中增加(0% 22.4%, < 0.0001)。多变量分析显示,在 -相关活动性炎症消退后,黏膜相关淋巴组织增生消退或减少、酒精摄入量增加、壁细胞抗体和/或内因子阳性的患者,检测到异型增生的可能性更高[比值比(OR)=3.88,95%置信区间(CI):1.31-11.49, = 0.01;OR=3.10,95%CI:1.05-9.12, = 0.04;OR=5.47,95%CI:1.33-22.39, < 0.04]。

结论

高分辨率白光内镜联合窄带成像技术可准确诊断 -诱导的慢性胃炎消退后可见病变的低级别异型增生。自身免疫性胃炎/-诱导性胃炎重叠的患者可能需要更广泛的胃黏膜活检。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6be3/7383846/c3de5e6b5dab/WJG-26-3834-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6be3/7383846/9135c3b27c1c/WJG-26-3834-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6be3/7383846/34609e0f3c96/WJG-26-3834-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6be3/7383846/907d3835e34f/WJG-26-3834-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6be3/7383846/c3de5e6b5dab/WJG-26-3834-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6be3/7383846/9135c3b27c1c/WJG-26-3834-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6be3/7383846/34609e0f3c96/WJG-26-3834-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6be3/7383846/907d3835e34f/WJG-26-3834-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6be3/7383846/c3de5e6b5dab/WJG-26-3834-g004.jpg

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