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Gut. 1992 Sep;33(9):1162-5. doi: 10.1136/gut.33.9.1162.
2
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Helicobacter pylori infection and serum pepsinogen A, pepsinogen C, and gastrin in gastritis and peptic ulcer: significance of inflammation and effect of bacterial eradication.幽门螺杆菌感染与胃炎和消化性溃疡患者血清胃蛋白酶原A、胃蛋白酶原C及胃泌素的关系:炎症的意义及细菌根除的影响
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Treatment of Helicobacter pylori infection favourably affects gastric mucosal superoxide dismutases.幽门螺杆菌感染的治疗对胃黏膜超氧化物歧化酶有积极影响。
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Effect of Helicobacter pylori eradication on gastric histology, serum gastrin and pepsinogen I levels, and gastric emptying in patients with gastric ulcer.幽门螺杆菌根除对胃溃疡患者胃组织学、血清胃泌素和胃蛋白酶原I水平以及胃排空的影响。
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8
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引用本文的文献

1
Prostaglandin E2 in gastric mucosa of children with Helicobacter pylori gastritis: relation to thickness of mucus gel layer.幽门螺杆菌胃炎患儿胃黏膜中的前列腺素E2:与黏液凝胶层厚度的关系
J Clin Pathol. 1993 Sep;46(9):836-9. doi: 10.1136/jcp.46.9.836.

本文引用的文献

1
Protein measurement with the Folin phenol reagent.使用福林酚试剂进行蛋白质测定。
J Biol Chem. 1951 Nov;193(1):265-75.
2
Superficial gastritis; a cause of temporary achlorhydria and hyperpepsinemia.浅表性胃炎;暂时性胃酸缺乏和高胃蛋白酶血症的一个原因。
N Engl J Med. 1958 Oct 2;259(14):682-4. doi: 10.1056/NEJM195810022591406.
3
Pepsinogen release from isolated gastric glands.从分离的胃腺中释放胃蛋白酶原。
Am J Physiol. 1982 Sep;243(3):G218-25. doi: 10.1152/ajpgi.1982.243.3.G218.
4
Pyloric Campylobacter infection and gastroduodenal disease.幽门弯曲杆菌感染与胃十二指肠疾病
Med J Aust. 1985 Apr 15;142(8):439-44. doi: 10.5694/j.1326-5377.1985.tb113444.x.
5
Ingestion of Campylobacter pyloridis causes gastritis and raised fasting gastric pH.摄入幽门弯曲杆菌会导致胃炎并使空腹时胃的pH值升高。
Am J Gastroenterol. 1987 Mar;82(3):192-9.
6
Campylobacter-like organisms in association with symptomatic gastritis in children.与儿童症状性胃炎相关的类弯曲杆菌微生物
J Pediatr. 1986 Jul;109(1):80-3. doi: 10.1016/s0022-3476(86)80579-0.
7
Association of Campylobacter pylori on the gastric mucosa with antral gastritis in children.儿童胃黏膜幽门螺杆菌与胃窦炎的关联。
N Engl J Med. 1987 Jun 18;316(25):1557-61. doi: 10.1056/NEJM198706183162501.
8
Iatrogenic Campylobacter pylori infection is a cause of epidemic achlorhydria.医源性幽门螺杆菌感染是流行性胃酸缺乏症的一个病因。
Am J Gastroenterol. 1988 Sep;83(9):974-80.
9
Campylobacter pylori: prospective analysis of clinical and histological factors associated with colonization of the upper gastrointestinal tract.幽门螺杆菌:上消化道定植相关临床及组织学因素的前瞻性分析
Eur J Clin Invest. 1988 Apr;18(2):133-8. doi: 10.1111/j.1365-2362.1988.tb02403.x.
10
Duodenal ulcer, Campylobacter pylori, and the "leaking roof" concept.十二指肠溃疡、幽门螺杆菌与“漏水屋顶”概念
Lancet. 1988;2(8626-8627):1467-9. doi: 10.1016/s0140-6736(88)90942-7.

小儿幽门螺杆菌感染期间的黏膜消化活性

Mucosal peptic activity during Helicobacter pylori infection in pediatric patients.

作者信息

Yahav J, Oderda G, Diver-Haber A, Keller N, Jonas A

机构信息

Pediatric Gastroenterology Service, Department of Clinical Microbiology, Tel Hashomer, Israel.

出版信息

Gut. 1992 Sep;33(9):1162-5. doi: 10.1136/gut.33.9.1162.

DOI:10.1136/gut.33.9.1162
PMID:1427366
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1379478/
Abstract

Intramucosal peptic activity may participate in the genesis of acute and chronic superficial gastritis. The proteolytic activity of homogenates of gastric mucosa (antrum and body) and duodenum were measured at pH 2.0 (total peptic activity) after exposure to pH 8.0 (pepsinogen) and the activated pepsinogen (pepsin) was calculated in pediatric patients investigated for the presence of Helicobacter pylori (H pylori), 122 antral, 77 stomach body, and 74 duodenal biopsies were examined in 43 H pylori positive patients, 51 controls, and 28 H pylori negative gastritis patients. Activated pepsinogen was significantly reduced in the stomach of H pylori positive patients only. Pepsinogen values were similar in all the anatomical areas tested in all patients. In 13 H pylori positive patients reinvestigated three months after antibiotic therapy, antral mucosal activated pepsinogen activity increased significantly (mean pretreatment 1.56 (1.0) U/mg protein versus mean post-treatment 2.72 (1.7) U/mg protein) and reached values comparable with controls. The decreased activated pepsinogen activity in association with normal pepsinogen content observed in the antrum of H pylori positive gastritis patients indicate local pepsin inactivation or alternately enhanced removal into the gastric lumen or backflow into the circulation.

摘要

黏膜内的胃蛋白酶活性可能参与急慢性浅表性胃炎的发病过程。在研究幽门螺杆菌(Hp)感染情况的儿科患者中,测定了胃黏膜(胃窦和胃体)及十二指肠匀浆在pH 8.0(胃蛋白酶原)处理后于pH 2.0时的蛋白水解活性(总胃蛋白酶活性),并计算活化胃蛋白酶原(胃蛋白酶)的含量。对43例Hp阳性患者、51例对照者和28例Hp阴性胃炎患者的122份胃窦活检组织、77份胃体活检组织及74份十二指肠活检组织进行了检查。仅在Hp阳性患者的胃中,活化胃蛋白酶原显著降低。所有患者所有检测解剖部位的胃蛋白酶原值相似。在13例Hp阳性患者接受抗生素治疗三个月后再次检查,胃窦黏膜活化胃蛋白酶原活性显著增加(治疗前平均为1.56(1.0)U/mg蛋白,治疗后平均为2.72(1.7)U/mg蛋白),并达到与对照者相当的值。在Hp阳性胃炎患者胃窦中观察到的活化胃蛋白酶原活性降低而胃蛋白酶原含量正常,表明存在局部胃蛋白酶失活,或者是胃腔内清除增加或反流进入循环。