Division of Gastroenterology, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aobaku, Sendai, Miyagi 980-8574, Japan.
J Gastroenterol. 2012 Dec;47(12):1290-7. doi: 10.1007/s00535-012-0598-8. Epub 2012 May 2.
The association of Helicobacter pylori infection with aspirin-induced gastropathy is controversial. H. pylori infection exerts diverse effects on gastric acid secretion. In this study, the interaction between H. pylori infection and aspirin was investigated with reference to the individual gastric acid secretion level in H. pylori-positive subjects.
Ninety-three (81 men, mean age: 70 years) long-term low-dose aspirin takers were prospectively enrolled. H. pylori infection was evaluated by serum IgG antibody determination, and gastrin-stimulated acid output was assessed with the endoscopic gastrin test. H. pylori-positive aspirin-takers were classified into 2 subgroups (hyposecretors and non-hyposecretors). The grade of gastric mucosal injury was assessed endoscopically according to the modified Lanza score; intensive aspirin-induced gastropathy was defined as a modified Lanza score of ≥4. Multiple logistic regression analyses were used to adjust for potential confounders.
With H. pylori-negative patients taken as the reference, H. pylori infection was found to be positively associated with intensive gastropathy among non-hyposecretors, with an odds ratio (OR) (95 % confidence interval [CI]) of 4.2 (1.1-17.1), while the infection was negatively associated with gastropathy among hyposecretors, with an OR (95 % CI) of 0.3 (0.08-0.9). Aspirin-induced gastropathy occurred preferentially in the antrum among H. pylori-positive non-hyposecretors, while it affected the fundus among H. pylori-positive hyposecretors.
The effect of H. pylori infection on the aspirin-induced gastropathy was biphasic depending on the individual gastric acid secretion level. In the presence of sufficient amounts of gastric acid, H. pylori infection and aspirin could synergistically damage gastric mucosal integrity, while in the absence of sufficient amounts of gastric acid, the synergistic effect could be completely counteracted and the infection could even suppress the aspirin-induced gastropathy.
幽门螺杆菌(H. pylori)感染与阿司匹林诱导的胃病之间的关系存在争议。H. pylori 感染对胃酸分泌有多种影响。本研究参考 H. pylori 阳性受试者的个体胃酸分泌水平,探讨了 H. pylori 感染与阿司匹林之间的相互作用。
前瞻性纳入 93 名(81 名男性,平均年龄:70 岁)长期低剂量服用阿司匹林的患者。通过血清 IgG 抗体测定评估 H. pylori 感染,使用内镜胃泌素试验评估胃泌素刺激的胃酸分泌。将 H. pylori 阳性的阿司匹林服用者分为 2 个亚组(低胃酸分泌者和非低胃酸分泌者)。根据改良的 Lanza 评分评估胃黏膜损伤程度;将改良的 Lanza 评分≥4 定义为重度阿司匹林诱导性胃病。采用多变量逻辑回归分析调整潜在混杂因素。
以 H. pylori 阴性患者为参照,在非低胃酸分泌者中,H. pylori 感染与重度胃病呈正相关,比值比(OR)(95 %置信区间 [CI])为 4.2(1.1-17.1),而在低胃酸分泌者中,感染与胃病呈负相关,OR(95 % CI)为 0.3(0.08-0.9)。在 H. pylori 阳性的非低胃酸分泌者中,阿司匹林诱导的胃病主要发生在胃窦,而在 H. pylori 阳性的低胃酸分泌者中,胃病主要发生在胃底。
H. pylori 感染对阿司匹林诱导性胃病的影响呈双相性,取决于个体胃酸分泌水平。在有足够胃酸的情况下,H. pylori 感染和阿司匹林可能协同破坏胃黏膜完整性,而在胃酸不足的情况下,协同作用可完全被抵消,感染甚至可能抑制阿司匹林诱导的胃病。