Chamouard P, Walter P, Wittersheim C, Demuynck P, Meunier O, Baumann R
Service d'Hépato-Gastroentérologie et d'Assistance Nutritive, CHRU Hautepierre, Strasbourg, France.
Eur J Gastroenterol Hepatol. 1997 Apr;9(4):361-5. doi: 10.1097/00042737-199704000-00008.
Helicobacter pylori infection is associated with an exaggeration of gastrin release following meals or bombesin stimulation attributed to a defect of somatostatin secretion of antral D-cells. Nevertheless, these modifications of gastric physiology do not explain the increase of gastric acid secretion which is only observed in duodenal ulcer patients. The inhibitory effect of somatostatin secretion of fundic D-cells on parietal cells is well known. The aim of our prospective study was to compare the number of fundic D-cells and likewise the number of antral G-cells and D-cells between patients with duodenal ulcer and healthy subjects with and without H. pylori infection.
The numbers of D-cells and G-cells were compared between 19 infected patients with duodenal ulcer and 20 healthy subjects, 10 with and 10 without H. pylori infection. Fundic mucosal biopsy specimens were examined using immunohistochemical techniques specific for the presence of somatostatin, antral mucosal biopsy specimens for the presence of gastrin and somatostatin.
The number of G-cells was significantly lower (P = 0.0012) in duodenal ulcer patients by comparison with infected subjects and controls. The number of antral D-cells was significantly less (P < 0.0001) in duodenal ulcer patients (mean of 10 random fields = 0.45 +/- 0.04) than in either asymptomatic infected patients (0.65 +/- 0.07) or uninfected controls (0.88 +/- 0.10). The number of fundic D-cells was significantly lower (P < 0.0001) in duodenal ulcer patients (mean = 0.20 +/- 0.03) than in either asymptomatic infected subjects (0.29 +/- 0.05) or controls (0.73 +/- 0.09); here the difference between the two groups of infected subjects was not significant. Multivariate analysis showed that the presence of H. pylori infection of the fundic mucosa did not influence the number of fundic D-cells.
Changes in the number of fundic and antral D-cells induced by H. pylori infection did not explain abnormalities of gastric acid secretion usually observed in duodenal ulcer patients; it is suggested that pre-existing abnormalities in the regulation of parietal cell or increase of parietal cell mass are involved.
幽门螺杆菌感染与餐后或蛙皮素刺激后胃泌素释放增加有关，这归因于胃窦D细胞生长抑素分泌缺陷。然而，这些胃生理学改变并不能解释仅在十二指肠溃疡患者中观察到的胃酸分泌增加。胃底D细胞分泌的生长抑素对壁细胞的抑制作用是众所周知的。我们前瞻性研究的目的是比较十二指肠溃疡患者与有或无幽门螺杆菌感染的健康受试者之间胃底D细胞数量，以及同样地胃窦G细胞和D细胞数量。
比较19例感染幽门螺杆菌的十二指肠溃疡患者与20例健康受试者（10例感染幽门螺杆菌，10例未感染）的D细胞和G细胞数量。使用针对生长抑素存在的免疫组织化学技术检查胃底黏膜活检标本，使用针对胃泌素和生长抑素存在的免疫组织化学技术检查胃窦黏膜活检标本。
与感染受试者和对照组相比，十二指肠溃疡患者的G细胞数量显著降低（P = 0.0012）。十二指肠溃疡患者胃窦D细胞数量（10个随机视野的平均值 = 0.45 ± 0.04）显著少于无症状感染患者（0.65 ± 0.07）或未感染对照组（0.88 ± 0.10）（P < 0.0001）。十二指肠溃疡患者胃底D细胞数量（平均值 = 0.20 ± 0.03）显著低于无症状感染受试者（0.29 ± 0.05）或对照组（0.73 ± 0.09）（P < 0.0001）；两组感染受试者之间的差异不显著。多变量分析表明，胃底黏膜幽门螺杆菌感染的存在不影响胃底D细胞数量。
幽门螺杆菌感染引起的胃底和胃窦D细胞数量变化不能解释十二指肠溃疡患者中通常观察到的胃酸分泌异常；提示壁细胞调节预先存在的异常或壁细胞数量增加与之有关。
