Tham T C, Chen L, Dennison N, Johnston C F, Collins J S, Ardill J E, Buchanan K D
Department of Medicine, The Queen's University of Belfast and Royal Victoria Hospital, Northern Ireland, UK.
Eur J Gastroenterol Hepatol. 1998 Apr;10(4):289-91. doi: 10.1097/00042737-199804000-00003.
As Helicobacter pylori infection is associated with an elevation in plasma gastrin with normal antral gastrin cell counts, an abnormality in antral somatostatin cells may be associated with the infection. We evaluated the effect of eradication of H. pylori on antral somatostatin cell density in the light of antral gastrin cell density and plasma gastrin levels.
Prospective study.
Of 25 dyspeptic patients with H. pylori infection, nine had H. pylori successfully eradicated and the rest remained infected. Antral biopsies were immunostained for somatostatin cells and plasma gastrin measured before and 4 weeks after H. pylori eradication therapy. Ten other dyspeptic patients without H. pylori infection had their somatostatin cell density evaluated as controls.
Somatostatin cell density in the patients without H. pylori infection at the outset was significantly higher than that in the patients with H. pylori infection at the outset (median 57 [18-83] vs. 37 [6-80] cells/mm) respectively (P <0.05). Somatostatin cell density increased after H. pylori eradication (before treatment, median 50 [15-72]; after treatment 71 [39-107] cells/mm) (P < 0.05) but was unchanged with persistent H. pylori infection. Plasma gastrin decreased after H. pylori eradication (before treatment, median 70 [45-100]; after treatment 30 [10-100] ng/l) (P < 0.05) but was unchanged with persistent H. pylori infection.
Following eradication of H. pylori, there is an increase in somatostatin cell density with a fall in plasma gastrin. This supports the theory that H. pylori infection results in a decrease in somatostatin cell density and, as the latter is an inhibitor of gastrin cells, this results in an increased plasma gastrin.
由于幽门螺杆菌感染与血浆胃泌素升高相关,而胃窦部胃泌素细胞计数正常,因此胃窦部生长抑素细胞异常可能与该感染有关。我们根据胃窦部胃泌素细胞密度和血浆胃泌素水平,评估了根除幽门螺杆菌对胃窦部生长抑素细胞密度的影响。
前瞻性研究。
在25例幽门螺杆菌感染的消化不良患者中,9例成功根除幽门螺杆菌,其余患者仍为感染状态。在幽门螺杆菌根除治疗前及治疗后4周,对胃窦部活检组织进行生长抑素细胞免疫染色,并检测血浆胃泌素水平。另外10例无幽门螺杆菌感染的消化不良患者作为对照,评估其生长抑素细胞密度。
最初无幽门螺杆菌感染的患者生长抑素细胞密度显著高于最初有幽门螺杆菌感染的患者(中位数分别为57[18 - 83]个/mm与37[6 - 80]个/mm)(P<0.05)。幽门螺杆菌根除后生长抑素细胞密度增加(治疗前中位数为50[15 - 72]个/mm;治疗后为71[39 - 107]个/mm)(P<0.05),但持续幽门螺杆菌感染时细胞密度无变化。幽门螺杆菌根除后血浆胃泌素水平下降(治疗前中位数为70[45 - 100]ng/L;治疗后为30[10 - 100]ng/L)(P<0.05),但持续幽门螺杆菌感染时血浆胃泌素水平无变化。
根除幽门螺杆菌后,生长抑素细胞密度增加,血浆胃泌素水平下降。这支持了幽门螺杆菌感染导致生长抑素细胞密度降低的理论,由于生长抑素细胞是胃泌素细胞的抑制剂,因此导致血浆胃泌素升高。