Helicobacter pylori non-cytotoxic genotype enhances mucosal gastrin and mast cell tryptase

Helicobacter pylori non-cytotoxic genotype enhances mucosal gastrin and mast cell tryptase
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DOI:
10.1136/jcp.52.3.210
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发表时间:
1999-03-01
影响因子:
3.4
通讯作者:
Plebani, M
Plebani, M
中科院分区:
医学3区
文献类型:
--
作者:
Basso, D;Navaglia, F;Plebani, M

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目的 - 确定幽门螺杆菌基因型与胃泌素、生长抑素、类胰蛋白酶和组胺水平的胃粘膜变异之间的关联(如果有的话)。方法 - 对 49 名十二指肠溃疡患者和 48 名非溃疡性消化不良患者进行了研究。为了鉴定幽门螺杆菌基因型,通过聚合酶链式反应分析了 cagA 基因和 vacA 等位基因 m1、m2、s1 和 s2 的存在。在胃窦粘膜活检中测量胃泌素、生长抑素、类胰蛋白酶和组胺。结果 - 57 名患者感染幽门螺杆菌(30 名患者患有十二指肠溃疡,27 名患者患有非溃疡性消化不良)。幽门螺杆菌感染患者的胃泌素和类胰蛋白酶升高,但仅胃泌素的变化具有统计学意义;生长抑素和组胺不受幽门螺杆菌感染的影响。在非溃疡性消化不良患者中,cagA 基因的缺失和 vacA 等位基因 s2 和 m2 的存在与较高的类胰蛋白酶值和较小程度的胃泌素相关。在十二指肠溃疡患者中未发现这些关联。 结论 - 幽门螺杆菌的 cagA 阴性 s2m2 菌株对胃粘膜的危险可能比其他幽门螺杆菌菌株低,因为它能增强胃粘膜肥大细胞产生类胰蛋白酶。这种酶被认为可以刺激组织更新并有利于伤口愈合。
Aims - To determine the association, if any, between H pylori genotype and the gastric mucosal variations in the levels of gastrin, somatostatin, tryptase, and histamine.Methods - 49 patients affected by duodenal ulcer and 48 by non-ulcer dyspepsia were studied. To identify the H pylori genotype, the presence of the cagA gene and vacA alleles m1, m2, s1, and s2 were analysed by polymerase chain reaction. Gastrin, somatostatin, tryptase, and histamine were measured in antral mucosal biopsies.Results - 57 patients were infected with H pylori (30 with duodenal ulcer and 27 with non-ulcer dyspepsia). Gastrin and tryptase were increased in patients with H pylori infection, although the variations were statistically significant only for gastrin; somatostatin and histamine were not influenced by H pylori infection. In patients with non-ulcer dyspepsia the absence of the cagA gene and the presence of vacA alleles s2 and m2 were associated with higher values of tryptase and to a lesser extent of gastrin. These associations were not found in patients with duodenal ulcer.Conclusions - The cagA negative s2m2 strain of H pylori may be less dangerous for the gastric mucosa than other H pylori strains since it enhances tryptase production by gastric mucosal mast cells; this enzyme is thought to stimulate tissue turnover and favour wound healing.