Haruma K, Sumii K, Okamoto S, Yoshihara M, Sumii M, Kajiyama G, Wagner S
First Dept. of Internal Medicine, Hiroshima University School of Medicine, Japan.
Scand J Gastroenterol. 1995 Jun;30(6):550-3. doi: 10.3109/00365529509089788.
Recent studies on the role of Helicobacter pylori in the pathogenesis of duodenal ulcers have focused on the mechanism by which H. pylori infections cause exaggerated gastrin release.
We determined meal-stimulated serum gastrin concentrations and antral somatostatin content in 24 asymptomatic volunteers (6 H. pylori-infected, 18 H. pylori-uninfected). Somatostatin content was determined by radioimmunoassay in biopsy specimens obtained from the antrum.
Fasting and integrated 2-h gastrin concentrations were significantly higher in H. pylori-positive volunteers than in H. pylori-negative volunteers (fasting, 111 +/- 16.3 pmol/l versus 53.4 +/- 3.5 pmol/l; p < 0.05; integrated 2-h, 267 +/- 41.2 pmol/l versus 70.1 +/- 2.1 pmol/l; p < 0.01). Antral somatostatin content was 0.764 +/- 0.173 ng/mg and 2.931 +/- 0.414 ng/mg in H. pylori-positive and -negative volunteers, respectively (p < 0.01).
Low antral somatostatin content may cause hypergastrinemia in asymptomatic healthy volunteers, and H. pylori may contribute to the pathogenesis of duodenal ulcer, through this mechanism.
近期关于幽门螺杆菌在十二指肠溃疡发病机制中作用的研究聚焦于幽门螺杆菌感染导致胃泌素过度释放的机制。
我们测定了24名无症状志愿者（6名幽门螺杆菌感染，18名未感染）餐后刺激的血清胃泌素浓度和胃窦部生长抑素含量。通过放射免疫分析法测定从胃窦部获取的活检标本中的生长抑素含量。
幽门螺杆菌阳性志愿者的空腹及2小时综合胃泌素浓度显著高于幽门螺杆菌阴性志愿者（空腹时，分别为111±16.3 pmol/L和53.4±3.5 pmol/L；p<0.05；2小时综合值，分别为267±41.2 pmol/L和70.1±2.1 pmol/L；p<0.01）。幽门螺杆菌阳性和阴性志愿者的胃窦部生长抑素含量分别为0.764±0.173 ng/mg和2.931±0.414 ng/mg（p<0.01）。
胃窦部生长抑素含量低可能导致无症状健康志愿者出现高胃泌素血症，幽门螺杆菌可能通过此机制促成十二指肠溃疡的发病。
