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非甾体抗炎药在健康受试者中引起的严重胃黏膜损伤与幽门螺杆菌感染及高血清胃蛋白酶原水平有关。

Severe gastric mucosal damage induced by NSAIDs in healthy subjects is associated with Helicobacter pylori infection and high levels of serum pepsinogens.

作者信息

Santucci L, Fiorucci S, Patoia L, Di Matteo F M, Brunori P M, Morelli A

机构信息

Istituto di Gastroenterologia ed Endoscopia Digestiva, Università degli Studi di Perugia, Italy.

出版信息

Dig Dis Sci. 1995 Sep;40(9):2074-80. doi: 10.1007/BF02208681.

Abstract

Helicobacter pylori infection and NSAIDs are considered the two most important exogenous factors in ulcer disease. The interrelation between the two factors is not, however, clear. Moreover, serum pepsinogen has been suggested as a risk marker for the development of NSAID-induced gastrointestinal lesions. Fifty-one healthy volunteers, enrolled in a prospective, double-blind study carried out to evaluate gastrointestinal side effects of meloxicam and piroxicam, were analyzed to determine whether: (1) the prevalence of H. pylori correlates with the occurrence and severity of NSAID-induced gastrointestinal lesions, and (2) serum pepsinogen A and C levels could be used as markers of NSAID-induced mucosal damage. Upper endoscopy was performed by the same investigator before and after 28 days of treatment with placebo, meloxicam (7.5 mg/day and 15 mg/day), or piroxicam (20 mg/day). NSAID-induced damage was graded separately for hemorrhages and erosion ulcers according to Lanza's scale. There were no statistically significant differences in the prevalence of H. pylori in subjects with and without NSAID-induced mucosal lesions. However, there was a positive association between H. pylori infection and the severity of mucosal damage: total mean endoscopic score was 2.9 +/- 0.3 in H. pylori-positive subjects versus 1.6 +/- 0.5 in H. pylori-negative subjects (P < 0.05). Pepsinogen A and C levels increased from 55.3 +/- 3 to 149.4 +/- 15 and from 6.3 +/- 0.5 to 11.5 +/- 2.2, respectively (P < 0.05) in subjects who developed severe endoscopic injury.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

幽门螺杆菌感染和非甾体抗炎药(NSAIDs)被认为是溃疡病中两个最重要的外部因素。然而,这两个因素之间的相互关系尚不清楚。此外,血清胃蛋白酶原已被提议作为非甾体抗炎药引起的胃肠道病变发生的风险标志物。对51名健康志愿者进行了分析,这些志愿者参与了一项前瞻性、双盲研究,以评估美洛昔康和吡罗昔康的胃肠道副作用,目的是确定:(1)幽门螺杆菌的患病率是否与非甾体抗炎药引起的胃肠道病变的发生和严重程度相关,以及(2)血清胃蛋白酶原A和C水平是否可作为非甾体抗炎药引起的黏膜损伤的标志物。在使用安慰剂、美洛昔康(7.5毫克/天和15毫克/天)或吡罗昔康(20毫克/天)治疗28天之前和之后,由同一位研究者进行上消化道内镜检查。根据兰扎量表,分别对出血和糜烂性溃疡的非甾体抗炎药引起的损伤进行分级。在有和没有非甾体抗炎药引起的黏膜病变的受试者中,幽门螺杆菌的患病率没有统计学上的显著差异。然而,幽门螺杆菌感染与黏膜损伤的严重程度之间存在正相关:幽门螺杆菌阳性受试者的内镜总平均评分为2.9±0.3,而幽门螺杆菌阴性受试者为1.6±0.5(P<0.05)。在出现严重内镜损伤的受试者中,胃蛋白酶原A和C水平分别从55.3±3升高到149.4±15,从6.3±0.5升高到11.5±2.2(P<0.05)。(摘要截断于250字)

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