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題 名 | Effect of Oral Omeprazole on Active Duodenal Ulcer Reduction, Fasting Serum Gastrin and Pepsinogen I Level=口服Omeprazole對活動性十二指腸潰瘍患者療效的評估及其對空腹時血中胃泌素、胃蛋白酶原I的影響 |
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作 者 | 何愛生; 曹為霖; 葉淳; 謝忠平; 許重得; | 書刊名 | 醫學研究 |
卷 期 | 14:6 1994.05[民83.05] |
頁 次 | 頁389-396 |
分類號 | 418.24 |
關鍵詞 | 胃泌素; 胃蛋白酶原 I; 高胃蛋白酶原血症; Omeprazole; Gastrin; Pepsinogen I; Hyperpepsinogenemia; |
語 文 | 英文(English) |
中文摘要 | Omeprazole是一種新的胃酸分泌抑制劑,藉著阻斷壁細胞内胃酸形成的最後共同路徑-質子幫浦而達到治療消化性潰瘍的作用。本研究乃將15位經由上消化道泛内視鏡檢證實為活動性十二指腸潰瘍的患者給予每人每日口服一次20毫克的Omeprazole兩週,觀察治療前後潰瘍的癒合狀況,血中胃泌素及胃蛋白酶原I的變化情形。結果顯示:十二指腸潰瘍患者在治療前胃蛋白酶原I的血中濃度顯著高於對照組(99.21±8.76及63.48±4.88 ng/ml, p<0.001)15位患者在治療後的胃泌素及胃蛋白酶原I血清濃度亦高出治療前兩倍(p<0.01及p<0.001);停藥兩週後,兩種腸道荷爾蒙回復至治療前濃度(p>0.05),同時癒合率高達87%。因此,本研究除驗證了前人研究的成果,Omeprazole可作用在壁細胞的質子幫浦上達到強效的制酸作用外;且觀察出該藥可能是直接或間接作用於胃G細胞和主細胞上,促使胃泌素及胃蛋白酶原I的生成或釋放,同時亦可增進潰瘍的癒合。然而各腸道荷爾蒙的相互關係或作用機轉仍待進一步的研究。 |
英文摘要 | Omepraole represents a new class of gastric acid secretion inhibitors. It is a clinically useful anti-ulcer agent of the pyridylmethyl-sulfinylbenzimidazole group which blocks the final common pathway of gastric acid secretiong mainly by inhibiting proton pump in the parietal cells. In 15 endoscopically diagnosed duodenal ulcer patients, we measured the fasting serum gastrin and pepsinogen I levels, and ulcer healing status before and after a 20 mg omeprazole capsule per day for 14 days. Our results showed that fasting pepsinogen I level is significantly higher in duodenal ulcer patients, 99.21±8.76 and 63.48±488 ng/ml for duodenal ulcer and control groups respectively (p<0.001). With omeprazole treatment, fasting serum gastrin and pepsinogen I levels increased almost 2 folds from 35.92±3.57 to 68.92±9.10 pg/ml (p<0.01) and from 99.21±8.76 to 223.02±13.27 ng/ml (p<0.001) respectively. They all returned to pretreatment level (p>0.05) 2 weeks following drug discontinuation, which is associated with a high duodenal ulcer healing rate of 87%. In conclusion, the present study suggest that omeprazole not only a strong acid suppressor, which viainhibiting proton pump of parietal cells but also an inducer of hyperpepsinogenemia and hypergastrinemia, which may be due to direct or indirect or indirect effects on G cells and chief cells. The exact mechanism needs further investigation. |
本系統中英文摘要資訊取自各篇刊載內容。