兰索拉唑治疗十二指肠溃疡的临床观察

为验证第二代质子泵抑制剂兰索拉吐治疗十二指肠溃疡的疗效，对经胃镜检查诊断的治疗活动期十二指肠溃疡患者３８例作了观察，并与奥美拉唑组３４例进行了对照。结果两组十二指肠溃疡４周的愈合率分别为９７．４％和９１．２％，有效率分别为１００％与９７．１％（Ｐ＞０．０５）；疼痛消失率两组分别为１００％和９３．５％（Ｐ＞０．０５），而３天内疼痛消失率分别为７４．３％和５１．６％（Ｐ＜０．０５）。兰索拉唑治疗过程中未发现有副作用。提示兰索拉唑是治疗十二指肠溃疡有效的和安全的药物。     

不同胃液中一氧化氮水平变化

目的：研究十二指肠球部溃疡和慢性浅表性胃炎患者胃液的ＮＯ水平，以及胃液ＮＯ水平与幽门螺杆菌（ＨＰ）感染的可能联系。方法：通过胃镜，抽取２３例十二指肠球部溃疡患者、２１例慢性浅表性胃炎患者和１９例正常人的胃液。用Ｇｒｉｅｓ法测胃液中ＮＯ水平。结果：十二指肠球部溃疡患者胃液ＮＯ水平是（３５．５６±６．１５μｍｏｌ／Ｌ），ＨＰ感染者是（３４．１２±８．１０μｍｏｌ／Ｌ）。两者显著高于正常个体（１８．６０±３．０７μｍｏｌ／Ｌ）。慢性浅表性胃炎患者（１９．７３±２．３２μｍｏｌ／Ｌ）和ＨＰ阴性者（２０．２６±３．４４μｏｍｌ／Ｌ）胃液中ＮＯ水平（Ｐ＜０．０１）。结论：结果提示ＮＯ可能是引起十二指肠球部溃疡的一个因素，ＨＰ感染可能是十二指肠球部溃疡患者胃液中ＮＯ增高的原因     

RANITIDINE IN THE TREATMENT OF GASTRIC AND DUODENAL ULCERS ASSOCIATED WITH NON-STEROIDAL ANTI INFLAMMATORY DRUGS

To assess the effect of 4 weeks' therapy with ranitidine 150mg twice daily on the healing of symptomatic NSAID associatedgastric and duodenal ulcers, 149 arthritic patients were randomlyallocated to one of three treatment groups: ranitidine withNSAID continued, ranitidine with NSAID discontinued, and placebowith NSAID discontinued. The healing frequency in patients withgastric ulceration was 67, 68 and 47%, and in those with duodenalulceration 61, 81 and 42%, respectively. Only the differencebetween the duodenal ulcer healing rates for ranitidine withNSAID discontinued and placebo was statistically significant(P=0.02). Healing rates were uninfluenced by gender, age, smokinghabits, alcohol consumption, ulcer frequency or size, arthriticdisease, or participating country. KEY WORDS: Non-steroidal anti-inflammatory drug-associated ulcers, Ulcer healing, Ranitidine     

THE CHOICE OF ULCER HEALING AGENT INFLUENCES DUODENAL ULCER RELAPSE RATE AND LONG-TERM CLINICAL OUTCOME

The mode of pharmacological healing influences subsequent ulcer relapse. Duodenal ulcer relapse following healing and withdrawal of active therapy has been studied in 18 prospectively randomised comparative studies involving cimetidine and alternative healing agents. Most studies (eleven of the 18) showed comparative agents with a lower (> 10%) incidence of relapse than cimetidine while a minority (seven of the 18) showed equal (±10%) relapse. The probability of this distribution occurring by chance is less than 1:1000 (p = 0.0005, sign test).
In three of the 11 published comparative studies the relapse rate was significantly higher in those who had previously received cimetidine (p<0.05, two-sided significance test). This was despite the fact that most of the individual studies were small and required a substantial difference in results for the 5% significance level to be reached.
Paired comparative incidences of relapse at six months were converted to relapse rates (percentage of healed population relapsing monthly), average rates for comparative agents were 8.05±2.7% while those for cimetidine were 16.9±4.4% (x±SEM, n = 5); cimetidine relapse rates derived from non-comparative trials were 17.0 ± 1.9% (x± SEM, n = 7). Higher relapse rates translate into larger numbers of patients at risk and in need of active therapy.
These results are of biological and clinical significance. Differences in relapse must reflect beneficial effects of one group of agents on the ulcer diathesis or adverse effects of the comparator, cimetidine. Each alternative reflects negatively on cimetidine as an antiulcer medication; however, confirmation of adverse effects would force radical review of most current therapy of ulcer disease. Research into ulcer therapeutics must emphasise both the relapse and the healing potential of pharmacological agents. (Aust NZ J Med 1985; 15: 367–374.)