Maconi G, Lazzaroni M, Sangaletti O, Bargiggia S, Vago L, Bianchi Porro G
Gastrointestinal Unit, L. Sacco University Hospital, Milan, Italy.
Am J Gastroenterol. 1997 Oct;92(10):1844-8.
The evolution of gastritis and the behavior of basal and meal-stimulated gastrin release, pepsinogen levels, and gastric emptying of solids were studied in a series of consecutive patients with Helicobacter pylori-positive, uncomplicated, non-NSAID-related type I gastric ulcer over a follow-up period of 3 months after eradication therapy was begun.
Before starting treatment (consisting of omeprazole 40 mg a day for 1 month and amoxycillin 1 g three times daily for 14 days), and for 3 months after ulcer healing, 16 patients had a series of functional examinations, including basal and meal-stimulated serum gastrin concentration, serum pepsinogen I levels, evaluation of gastric emptying of solids by means of serial ultrasonographic measurement of the gastric antrum area, and histological assessment of antral and corpus gastritis.
Double therapy resulted in the successful eradication of H. pylori in eight of 16 evaluable patients. In the group of H. pylori-eradicated patients, the mean scores of gastritis activity and inflammation in the antrum and corpus had fallen, 3 months after eradication. No significant changes in mean gastritis scores were observed in the case and control group with regard to intestinal metaplasia and atrophy in the antrum and corpus. In H. pylori-eradicated patients, the integrated gastrin response to meal, but not fasting gastrin concentration, fell significantly during follow-up, and serum pepsinogen I levels significantly decreased, compared with baseline. In contrast, the fasting and maximal antral area and the gastric emptying of solids remained unchanged over time. In the control group (but not the H. pylori-eradicated group), no significant modifications of any of the above-mentioned parameters were observed during follow-up.
Our findings suggest that in non-NSAID-related type I gastric ulcers, the eradication of H. pylori significantly reduces gastritis activity and inflammatory scores, but not atrophy and intestinal metaplasia, and modifies gastrin and pepsinogen I release in a short follow-up period. In contrast, H.pylori eradication does not significantly affect gastric emptying of solids, at least within a period of 3 months from therapy.
在一系列连续的幽门螺杆菌阳性、无并发症、非非甾体抗炎药相关的Ⅰ型胃溃疡患者中,研究根除治疗开始后3个月随访期内胃炎的演变以及基础和进餐刺激后胃泌素释放、胃蛋白酶原水平和固体食物胃排空的情况。
在开始治疗前(包括每天服用40mg奥美拉唑1个月和每日3次每次1g阿莫西林共14天)以及溃疡愈合后的3个月内,16例患者进行了一系列功能检查,包括基础和进餐刺激后的血清胃泌素浓度、血清胃蛋白酶原I水平、通过连续超声测量胃窦面积评估固体食物胃排空,以及胃窦和胃体胃炎的组织学评估。
在16例可评估患者中,8例通过双重治疗成功根除幽门螺杆菌。在根除幽门螺杆菌的患者组中,根除后3个月,胃窦和胃体胃炎活动度和炎症的平均评分下降。在病例组和对照组中,胃窦和胃体的肠化生和萎缩方面,胃炎平均评分未观察到显著变化。在根除幽门螺杆菌的患者中,随访期间进餐刺激后胃泌素的综合反应显著下降,但空腹胃泌素浓度未下降,与基线相比,血清胃蛋白酶原I水平显著降低。相比之下,空腹和最大胃窦面积以及固体食物胃排空随时间保持不变。在对照组(而非根除幽门螺杆菌组)中,随访期间上述任何参数均未观察到显著变化。
我们的研究结果表明,在非非甾体抗炎药相关的Ⅰ型胃溃疡中,根除幽门螺杆菌可显著降低胃炎活动度和炎症评分,但不能改善萎缩和肠化生,且在短时间随访期内可改变胃泌素和胃蛋白酶原I的释放。相比之下,根除幽门螺杆菌至少在治疗后3个月内对固体食物胃排空无显著影响。