Martínek J, Blum A L, Stolte M, Hartmann M, Verdú E F, Lühmann R, Dorta G, Wiesel P
Division of Gastroenterology, CHUV, Lausanne, Switzerland.
Aliment Pharmacol Ther. 1999 Jan;13(1):27-34. doi: 10.1046/j.1365-2036.1999.00440.x.
Omeprazole produces a higher intragastric pH in the presence of Helicobacter pylori infection than after cure.
To investigate whether this effect also occurs with pumaprazole (BY841), a reversible proton pump antagonist which, in contrast to omeprazole, does not require activation in the acid compartment of the parietal cell.
In a randomized, crossover, double-blind study, 24-h intragastric pH was measured in 13 H. pylori-positive subjects before and after a 1-week course of omeprazole (20 mg o.d.) or of pumaprazole (100 mg b.d.). The studies were repeated after the infection was cured.
In the absence of drug administration, the median 24-h pH values before cure (median 2.0, 90% CI: 1.2-3.2) did not differ from those after cure (median 1.5, 90% CI: 1.3-2.2; P = 0.115). The 24-h pH values were higher before cure of the infection than after during both pumaprazole (6.0, 4.8-6.7 vs. 4.3, 2.6-5.7; P = 0.002) and omeprazole (5.8, 4.0-6.2 vs. 3.6, 2.8-5; P = 0.004). Both before and after cure, there were no significant differences between the two drugs with respect to acid inhibition over the 24-h period. The median decrease in acid inhibition after cure of the infection (calculated as the difference in H+ activity in mmol/L) during pumaprazole (median 0.05, 90% CI: 6 x 10-4- 2.3) was no different from that during omeprazole (median 0.2, 90% CI: 3 x 10-3-1.5; P = 0.6).
Both before and after cure of H. pylori infection, pumaprazole raised the intragastric pH over a 24-h period to a similar degree as omeprazole. H. pylori infection similarly augments the pH-increasing effect of both drugs. This effect is related to H. pylori infection and not to an increased activation of acid inhibitory agents in the parietal cell compartment.
在幽门螺杆菌感染存在的情况下，奥美拉唑产生的胃内pH值高于治愈后。
研究对于瑞巴派特（BY841）这种可逆质子泵拮抗剂是否也会出现这种效应，与奥美拉唑不同，瑞巴派特不需要在壁细胞的酸性区室中激活。
在一项随机、交叉、双盲研究中，对13名幽门螺杆菌阳性受试者在接受奥美拉唑（20毫克每日一次）或瑞巴派特（100毫克每日两次）为期1周的疗程前后测量24小时胃内pH值。在感染治愈后重复这些研究。
在未给药时，治愈前24小时pH值中位数（中位数2.0，90%置信区间：1.2 - 3.2）与治愈后（中位数1.5，90%置信区间：1.3 - 2.2；P = 0.115）无差异。在感染治愈前，瑞巴派特（6.0，4.8 - 6.7对比4.3，2.6 - 5.7；P = 0.002）和奥美拉唑（5.8，4.0 - 6.2对比3.6，2.8 - 5；P = 0.004）治疗期间24小时pH值均高于治愈后。在治愈前后，两种药物在24小时期间的抑酸作用均无显著差异。瑞巴派特治疗期间感染治愈后抑酸作用的中位数下降（以毫摩尔/升的H⁺活性差异计算）（中位数0.05，90%置信区间：6×10⁻⁴ - 2.3）与奥美拉唑治疗期间（中位数0.2，90%置信区间：3×10⁻³ - 1.5；P = 0.6）无差异相。
在幽门螺杆菌感染治愈前后，瑞巴派特在24小时内升高胃内pH值的程度与奥美拉唑相似。幽门螺杆菌感染同样增强了两种药物的pH值升高效应。这种效应与幽门螺杆菌感染有关，而与壁细胞区室中酸抑制剂的激活增加无关。
