Bechi P, Romagnoli P, Bacci S, Dei R, Amorosi A, Cianchi F, Masini E
Istituti di Clinica Chirurgica e DC, Dipartimenti di Anatomia Umana ed Istologia, e di Farmacologia Preclinica e Clinica, Università di Firenze, Florence, Italy.
Am J Gastroenterol. 1996 Nov;91(11):2338-43.
A "gastrin link" has been suggested to explain the statistically relevant association between Helicobacter pylori and duodenal ulcer. Given the well known, although not entirely clarified, relationships between gastrin and histamine, the purpose of this study was to assess whether gastric mucosal histamine pathways and, more specifically, histamine-storing cells are involved in the Helicobacter pylori-duodenal ulcer route.
Fasting serum gastrin, gastric mucosal histamine content, and mucosal density of both enterochromaffin-like cells and mast cells were compared in 11 H. pylori-positive, non-duodenal ulcer subjects, in 16 duodenal ulcer patients (all H. pylori positive), and in 11 H. pylori-negative control subjects.
Fasting serum gastrin concentration and mucosal histamine content were significantly higher in the duodenal ulcer group than in controls, whereas H. pylori-positive, non-ulcer subjects had values that were intermediate between those of the other two groups. Enterochromaffin-like cell density was significantly greater in duodenal ulcer patients than in the other groups.
These results demonstrate the involvement of histamine pathways in H. pylori infection and duodenal ulcer. The most original finding in this study was that enterochromaffin-like cell density is three times greater in duodenal ulcer patients than in H. pylori-positive, non-ulcer subjects. This could explain the previous report of an exaggerated acid response to gastrin in duodenal ulcer patients when compared with H. pylori-positive, non-ulcer subjects and thus provide further insight into the pathogenesis of ulcers.
有人提出“胃泌素联系”来解释幽门螺杆菌与十二指肠溃疡之间具有统计学意义的关联。鉴于胃泌素与组胺之间的关系已为人熟知，尽管尚未完全阐明，本研究的目的是评估胃黏膜组胺途径，更具体地说，储存组胺的细胞是否参与幽门螺杆菌 - 十二指肠溃疡的发病过程。
比较了11名幽门螺杆菌阳性、无十二指肠溃疡的受试者、16名十二指肠溃疡患者（均为幽门螺杆菌阳性）和11名幽门螺杆菌阴性对照受试者的空腹血清胃泌素、胃黏膜组胺含量以及肠嗜铬样细胞和肥大细胞的黏膜密度。
十二指肠溃疡组的空腹血清胃泌素浓度和黏膜组胺含量显著高于对照组，而幽门螺杆菌阳性、无溃疡的受试者的值介于其他两组之间。十二指肠溃疡患者的肠嗜铬样细胞密度显著高于其他组。
这些结果表明组胺途径参与了幽门螺杆菌感染和十二指肠溃疡的发病过程。本研究最原始的发现是，十二指肠溃疡患者的肠嗜铬样细胞密度比幽门螺杆菌阳性、无溃疡的受试者高三倍。这可以解释之前的报告，即与幽门螺杆菌阳性、无溃疡的受试者相比，十二指肠溃疡患者对胃泌素的酸反应过度，从而为溃疡的发病机制提供进一步的见解。
