• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

相似文献

1
Gastrin and antral G cells in course of Helicobacter pylori eradication: six months follow up study.幽门螺杆菌根除过程中的胃泌素和胃窦G细胞:六个月随访研究
World J Gastroenterol. 2005 Jul 21;11(27):4140-7. doi: 10.3748/wjg.v11.i27.4140.
2
Somatostatin and D cells in patients with gastritis in the course of Helicobacter pylori eradication: a six-month, follow-up study.幽门螺杆菌根除过程中胃炎患者的生长抑素与D细胞:一项为期六个月的随访研究。
Eur J Gastroenterol Hepatol. 2003 Jul;15(7):755-66. doi: 10.1097/01.meg.0000059153.68845.1a.
3
Epidermal growth factor and transforming growth factor alpha in duodenal ulcer and non-ulcer dyspepsia patients before and after Helicobacter pylori eradication.幽门螺杆菌根除前后十二指肠溃疡和非溃疡性消化不良患者的表皮生长因子和转化生长因子α
Scand J Gastroenterol. 1998 Feb;33(2):143-51. doi: 10.1080/00365529850166860.
4
Basal and stimulated gastrin and pepsinogen levels after eradication of Helicobacter pylori: a 1-year follow-up study.幽门螺杆菌根除后基础和刺激状态下胃泌素及胃蛋白酶原水平:一项为期1年的随访研究。
Eur J Gastroenterol Hepatol. 1999 Feb;11(2):189-200. doi: 10.1097/00042737-199902000-00022.
5
Helicobacter pylori and impaired gastric secretory functions associated with duodenal ulcer and atrophic gastritis.幽门螺杆菌与十二指肠溃疡和萎缩性胃炎相关的胃分泌功能受损。
J Physiol Pharmacol. 1997 Sep;48(3):365-73.
6
Helicobacter pylori eradication improves gastric histology and decreases serum gastrin, pepsinogen I and pepsinogen II levels in patients with duodenal ulcer.根除幽门螺杆菌可改善十二指肠溃疡患者的胃组织学状况,并降低其血清胃泌素、胃蛋白酶原I和胃蛋白酶原II水平。
J Gastroenterol Hepatol. 2008 Nov;23(11):1666-71. doi: 10.1111/j.1440-1746.2007.04983.x. Epub 2007 Jun 7.
7
Effect of Helicobacter pylori eradication on antral gastrin- and somatostatin-immunoreactive cell density and gastrin and somatostatin concentrations.幽门螺杆菌根除对胃窦胃泌素和生长抑素免疫反应性细胞密度以及胃泌素和生长抑素浓度的影响。
Scand J Gastroenterol. 1993 Oct;28(10):858-64. doi: 10.3109/00365529309103125.
8
Antral and fundic D-cell numbers in Helicobacter pylori infection.幽门螺杆菌感染时胃窦和胃底D细胞数量
Eur J Gastroenterol Hepatol. 1997 Apr;9(4):361-5. doi: 10.1097/00042737-199704000-00008.
9
Hormonal, secretory and morphological alterations in gastric mucosa in the course of Helicobacter pylori eradication in patients with duodenal ulcer and non-ulcer dyspepsia.十二指肠溃疡和非溃疡性消化不良患者根除幽门螺杆菌过程中胃黏膜的激素、分泌及形态学改变
J Physiol Pharmacol. 1997 Jun;48 Suppl 3:1-56.
10
Effect of Helicobacter pylori eradication on antral somatostatin cell density in humans.幽门螺杆菌根除对人体胃窦部生长抑素细胞密度的影响。
Eur J Gastroenterol Hepatol. 1998 Apr;10(4):289-91. doi: 10.1097/00042737-199804000-00003.

引用本文的文献

1
The Impact of Sex on the Response to Proton Pump Inhibitor Treatment.性别对质子泵抑制剂治疗反应的影响
Pharmaceuticals (Basel). 2023 Dec 12;16(12):1722. doi: 10.3390/ph16121722.
2
The morphological and immunohistochemical spectrum of gastric biopsies of patients with absorptive hypercalciuria.吸收性高钙尿症患者胃活检的形态学和免疫组织化学特征
BMJ Open Gastroenterol. 2015 Feb 6;1(1):e000004. doi: 10.1136/bmjgast-2014-000004. eCollection 2014.
3
Helicobacter pylori infection, gastrin and cyclooxygenase-2 in gastric carcinogenesis.幽门螺杆菌感染、胃泌素与环氧化酶-2在胃癌发生中的作用
World J Gastroenterol. 2014 Sep 28;20(36):12860-73. doi: 10.3748/wjg.v20.i36.12860.
4
Helicobacter pylori infection stimulates intestinalization of endocrine cells in glandular stomach of Mongolian gerbils.幽门螺杆菌感染会刺激蒙古沙鼠腺胃内分泌细胞的肠化生。
Cancer Sci. 2006 Oct;97(10):1015-22. doi: 10.1111/j.1349-7006.2006.00273.x.
5
Expression of cytokeratins in Helicobacter pylori-associated chronic gastritis of adult patients infected with cagA+ strains: an immunohistochemical study.细胞角蛋白在感染cagA+菌株的成年患者幽门螺杆菌相关性慢性胃炎中的表达:一项免疫组织化学研究
World J Gastroenterol. 2006 Mar 28;12(12):1865-73. doi: 10.3748/wjg.v12.i12.1865.

本文引用的文献

1
Anti-CagA and anti-VacA antibodies in Helicobacter pylori-infected patients with and without peptic ulcer disease in Serbia and Montenegro.塞尔维亚和黑山幽门螺杆菌感染患者中有无消化性溃疡疾病的抗CagA和抗VacA抗体情况
Scand J Gastroenterol. 2004 Mar;39(3):222-6. doi: 10.1080/00365520310008403.
2
Effect of Helicobacter pylori infection on gastric acid secretion and meal-stimulated serum gastrin in children.幽门螺杆菌感染对儿童胃酸分泌及进餐刺激血清胃泌素的影响。
Helicobacter. 2004 Apr;9(2):100-5. doi: 10.1111/j.1083-4389.2004.00205.x.
3
Chronic Helicobacter pylori infection results in gastric hypoacidity and hypergastrinemia in wild-type mice but vagally induced hypersecretion in gastrin-deficient mice.慢性幽门螺杆菌感染在野生型小鼠中导致胃酸过少和高胃泌素血症,但在胃泌素缺乏的小鼠中导致迷走神经诱导的胃酸分泌过多。
Regul Pept. 2003 Oct 15;115(3):161-70. doi: 10.1016/s0167-0115(03)00167-8.
4
Somatostatin and D cells in patients with gastritis in the course of Helicobacter pylori eradication: a six-month, follow-up study.幽门螺杆菌根除过程中胃炎患者的生长抑素与D细胞:一项为期六个月的随访研究。
Eur J Gastroenterol Hepatol. 2003 Jul;15(7):755-66. doi: 10.1097/01.meg.0000059153.68845.1a.
5
Enhanced somatostatin secretion into the gastric juice with recovery of basal acid output after Helicobacter pylori eradication in gastric ulcers.胃溃疡患者根除幽门螺杆菌后,胃液中生长抑素分泌增加,基础胃酸分泌恢复。
J Gastroenterol Hepatol. 2003 May;18(5):505-11. doi: 10.1046/j.1440-1746.2003.03008.x.
6
Eradication of Helicobacter pylori increases nocturnal intragastric acidity during dosing with rabeprazole, omeprazole, lansoprazole and placebo.在使用雷贝拉唑、奥美拉唑、兰索拉唑和安慰剂治疗期间,根除幽门螺杆菌会增加夜间胃内酸度。
Aliment Pharmacol Ther. 2003 Mar 15;17(6):775-83. doi: 10.1046/j.1365-2036.2003.01488.x.
7
Long-term Helicobacter pylori colonization produces G cell hyperplasia and carcinoid tumor in Mongolian gerbils.长期幽门螺杆菌定植会在蒙古沙鼠体内产生胃泌素细胞增生和类癌肿瘤。
J Cell Mol Med. 2000 Oct-Dec;4(4):308-309. doi: 10.1111/j.1582-4934.2000.tb00133.x.
8
Helicobacter pylori and gut hormones.幽门螺杆菌与肠道激素
J Gastroenterol. 2002;37(2):77-86. doi: 10.1007/s005350200000.
9
[Particular features of the relationship of Helicobacter pylori and G cells in patients with duodenal ulcer, with special reference to the Helicobacter pylori strain].十二指肠溃疡患者中幽门螺杆菌与G细胞关系的特殊特征,特别提及幽门螺杆菌菌株
Lik Sprava. 2001 Jul-Aug(4):176-7.
10
Gastrin induces CXC chemokine expression in gastric epithelial cells through activation of NF-kappaB.胃泌素通过激活核因子κB诱导胃上皮细胞中CXC趋化因子的表达。
Am J Physiol Gastrointest Liver Physiol. 2001 Sep;281(3):G735-42. doi: 10.1152/ajpgi.2001.281.3.G735.

幽门螺杆菌根除过程中的胃泌素和胃窦G细胞:六个月随访研究

Gastrin and antral G cells in course of Helicobacter pylori eradication: six months follow up study.

作者信息

Sokic-Milutinovic Aleksandra, Todorovic Vera, Milosavljevic Tomica, Micev Marjan, Drndarevic Neda, Mitrovic Olivera

机构信息

Clinic for Gastroenterology and Hepatology, Institute for Digestive Diseases, Clinical Center of Serbia, Belgrade 11000, Serbia and Montenegro.

出版信息

World J Gastroenterol. 2005 Jul 21;11(27):4140-7. doi: 10.3748/wjg.v11.i27.4140.

DOI:10.3748/wjg.v11.i27.4140
PMID:16015680
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4615433/
Abstract

AIM

To assess long-term effects of Helicobacter pylori (H pylori) eradication on antral G cell morphology and function in patients with and without duodenal ulcer (DU).

METHODS

Consecutive dyspeptic patients referred to the endoscopy entered the study. Out of 39 H pylori positive patients, 8 had DU (H pylori +DU) and 31 gastritis (H pylori +G). Control groups consisted of 11 uninfected dyspeptic patients (CG1) and 7 healthy volunteers (CG2). Basal plasma gastrin (PGL), antral tissue gastrin concentrations (ATGC), immunohistochemical and electron microscopic characteristics of G cells were determined, prior to and 6 mo after therapy.

RESULTS

We demonstrated elevated PGL in infected patients compared to uninfected controls prior to therapy. Elevated PGL were registered in all H pylori+patients (H pylori +DU: 106.78+/-22.72 pg/mL, H pylori +G: 74.95+/-15.63, CG1: 68.59+/-17.97, CG2: 39.24+/-5.59 pg/mL, P<0.01). Successful eradication (e) therapy in H pylori+patients lead to significant decrease in PGL (H pylori+DU: 59.93+/-9.40 and H pylori +Ge: 42.36+/-10.28 pg/mL, P<0.001). ATGC at the beginning of the study were similar in infected and uninfected patients and eradication therapy lead to significant decrease in ATGC in H pylori +gastritis, but not in DU patients. In the H pylori +DU patients, the mean number of antral G cells was significantly lower in comparison with all other groups (P<0.01), but after successful eradication was close to normal values found in controls. By contrast, G cell number and volume density were significantly decreased (P<0.01) in H pylori +Ge group after successful eradication therapy (294+/-32 and 0.31+/-0.02, respectively), in comparison to values before eradication (416+/-40 and 0.48+/-0.09). No significant change of the G cell/total endocrine cell ratio was observed during the 6 mo of follow up in any of the groups. A reversible increase in G cell secretory function was seen in all infected individuals, demonstrated by a more prominent secretory apparatus. However, differences between DU and gastritis group were identified.

CONCLUSION

H pylori infection induces antral G cell hyperfunction resulting in increased gastrin synthesis and secretion. After eradication therapy complete morphological and functional recovery is observed in patients with gastritis. In the DU patients some other factors unrelated to the H pylori infection influence antral G cell morphology and function.

摘要

目的

评估幽门螺杆菌(H pylori)根除对十二指肠溃疡(DU)患者和非DU患者胃窦G细胞形态及功能的长期影响。

方法

连续纳入因消化不良接受内镜检查的患者。39例H pylori阳性患者中,8例患有DU(H pylori+DU),31例为胃炎(H pylori+G)。对照组包括11例未感染的消化不良患者(CG1)和7名健康志愿者(CG2)。在治疗前及治疗后6个月测定基础血浆胃泌素(PGL)、胃窦组织胃泌素浓度(ATGC)、G细胞的免疫组化及电子显微镜特征。

结果

治疗前,与未感染对照组相比,感染患者的PGL升高。所有H pylori阳性患者(H pylori+DU:106.78±22.72 pg/mL,H pylori+G:74.95±15.63,CG1:68.59±17.97,CG2:39.24±5.59 pg/mL,P<0.01)的PGL均升高。H pylori阳性患者成功根除(e)治疗后,PGL显著降低(H pylori+DU:59.93±9.40和H pylori+Ge:42.36±10.28 pg/mL,P<0.001)。研究开始时,感染和未感染患者的ATGC相似,根除治疗导致H pylori+胃炎患者的ATGC显著降低,但DU患者未降低。H pylori+DU患者的胃窦G细胞平均数量与所有其他组相比显著降低(P<0.01),但成功根除后接近对照组的正常水平。相比之下,成功根除治疗后,H pylori+Ge组的G细胞数量和体积密度显著降低(P<0.01)(分别为294±32和0.31±0.02),与根除前的值(416±40和0.48±0.09)相比。在随访的6个月中,任何一组的G细胞/总内分泌细胞比率均未观察到显著变化。所有感染个体均可见G细胞分泌功能的可逆性增加,表现为分泌装置更突出。然而,DU组和胃炎组之间存在差异。

结论

H pylori感染诱导胃窦G细胞功能亢进,导致胃泌素合成和分泌增加。根除治疗后,胃炎患者的形态和功能完全恢复。在DU患者中,一些与H pylori感染无关的其他因素影响胃窦G细胞的形态和功能。