Park S M, Yoo B C, Lee H R, Yoon J H, Cha Y J
Department of Internal Medicine and Clinical Pathology, College of Medicine, Chung-Ang University, Seoul, Korea.
Korean J Intern Med. 1993 Jan;8(1):19-24. doi: 10.3904/kjim.1993.8.1.19.
A randomized prospective study on the response of fasting serum gastrin concentrations in peptic ulcer patients was performed in order to test the hypothesis that H. pylori infection in the gastric antrum increases gastrin release, and to examine whether the high fasting serum gastrin concentrations respond to treatment that eradicates H. pylori.
One hundred and twenty-seven patients with gastric or duodenal ulcer were included in this study. Patients were divided into three groups on the basis of antral H. pylori status and therapeutic modalities. The first group, 58 patients infected by H. pylori, was treated with metronidazole and tripotassium dicitrato bismuthate combined with ranitidine and mylanta. The second group, 40 patients also infected by H. Pylori, was treated with ranitidine and mylanta. The third group, 29 patients, free of H. pylori infection, was designed to evaluate the influence of H2-receptor antagonist on the change of gastrin. When ulcers were completely healed, changes of gastrin concentrations and H. pylori status were re-examined.
H. pylori was eradicated in all patients who have received antibacterial therapy in 4 weeks, and serum gastrin concentrations were significantly decreased after eradication of the organism both in gastric and in duodenal ulcer diseases. (Gastric ulcer: 129.3 +/- 47.0 pg/ml before and 63.7 +/- 21.6 pg/ml after treatment. Duodenal ulcer: 108.3 +/- 35.0 pg/ml and 66.5 +/- 21.9 pg/ml, respectively. Total: 112.7 +/- 38.2 pg/ml vs 66.0 +/- 21.6 pg/ml) (p < 0.01). In contrast, H. pylori-positive patients who have not received antibacterial therapy were still infected at the completion of the study, and serum gastrin concentrations increased even though the difference was not significant. (Gastric ulcer: 118.4 +/- 51.2 pg/ml vs 124.0 +/- 56.5 pg/ml. Duodenal ulcer: 85.4 +/- 35.1 pg/ml vs 104.6 +/- 43.5. Total: 99.5 +/- 45.3 vs 112.9 +/- 48.7 pg/ml.) (p > 0.05). None of the patients who were initially H. pylori-negative has been reinfected during the period of the study, and their serum gastrin concentrations were not changed. (Gastric ulcer: 69.8 +/- 38.0 pg/ml. Total: 63.2 +/- 31.1 pg/ml. Duodenal ulcer: 55.1 +/- 17.6 pg/ml vs 55.8 +/- 13.8 pg/ml. Total: 63.2 +/- 31.1 pg/ml vs 63.4 +/- 30.0 pg/ml). Four- to six-week therapy of H2-receptor antagonist and antacid had no influence on serum gastrin concentrations.
On the basis of the above results, we confirmed that the chronic infection of H. pylori of gastric antrum in peptic ulcer patients causes increased release of serum gastrin, and eradication of the organism results in a significant fall in serum gastrin concentrations.
开展了一项关于消化性溃疡患者空腹血清胃泌素浓度反应的随机前瞻性研究，以检验胃窦幽门螺杆菌感染会增加胃泌素释放这一假设，并研究空腹血清胃泌素浓度升高是否会对根除幽门螺杆菌的治疗产生反应。
本研究纳入了127例胃溃疡或十二指肠溃疡患者。根据胃窦幽门螺杆菌感染状况和治疗方式将患者分为三组。第一组为58例幽门螺杆菌感染患者，采用甲硝唑、枸橼酸铋钾联合雷尼替丁和氢氧化铝治疗。第二组为40例同样感染幽门螺杆菌的患者，采用雷尼替丁和氢氧化铝治疗。第三组为29例未感染幽门螺杆菌的患者，旨在评估H2受体拮抗剂对胃泌素变化的影响。当溃疡完全愈合后，重新检测胃泌素浓度变化和幽门螺杆菌感染状况。
所有接受抗菌治疗4周的患者幽门螺杆菌均被根除，胃溃疡和十二指肠溃疡患者根除该菌后血清胃泌素浓度均显著下降。（胃溃疡：治疗前为129.3±47.0 pg/ml，治疗后为63.7±21.6 pg/ml。十二指肠溃疡：分别为108.3±35.0 pg/ml和66.5±21.9 pg/ml。总体：112.7±38.2 pg/ml对66.0±21.6 pg/ml）（p<0.01）。相比之下，未接受抗菌治疗的幽门螺杆菌阳性患者在研究结束时仍处于感染状态，血清胃泌素浓度虽有升高但差异不显著。（胃溃疡：118.4±51.2 pg/ml对124.0±56.5 pg/ml。十二指肠溃疡：85.4±35.1 pg/ml对104.6±43.5。总体：99.5±45.3对112.9±48.7 pg/ml。）（p>0.05）。最初幽门螺杆菌阴性的患者在研究期间均未再次感染，其血清胃泌素浓度未发生变化。（胃溃疡：69.8±38.0 pg/ml。总体：63.2±31.1 pg/ml。十二指肠溃疡：55.1±17.6 pg/ml对55.8±13.8 pg/ml。总体：63.2±31.1 pg/ml对63.4±30.0 pg/ml）。H2受体拮抗剂和抗酸剂进行4至6周治疗对血清胃泌素浓度无影响。
基于上述结果，我们证实消化性溃疡患者胃窦幽门螺杆菌慢性感染会导致血清胃泌素释放增加，根除该菌会使血清胃泌素浓度显著下降。
