Stevenson D D, Simon R A
Division of Allergy, Asthma and Immunology, Department of Medicine, Scripps Clinic and The Scripps Research Institute. La Jolla, CA 92037, USA.
J Allergy Clin Immunol. 2001 Jul;108(1):47-51. doi: 10.1067/mai.2001.116290.
Patients with aspirin-sensitive respiratory disease experience cross-reactions to all nonsteroidal anti-inflammatory drugs, which inhibit cyclooxygenase enzymes. With the introduction of antiarthritis drugs, which selectively inhibit cyclooxygenase-2, questions are raised as to whether cross-reactivity occurs between aspirin and these new cyclooxygenase-2 inhibitors.
The goal of this study was to determine whether rofecoxib cross-reacts in aspirin-sensitive patients with asthma.
Sixty patients with asthma underwent doubleblinded, placebo-controlled oral challenges with rofecoxib (12.5 mg, 25 mg, and 2 placebos) over 48 hours in our General Clinical Research Center. The next day, aspirin sensitivity was proven in each of the 60 patients through use of single-blinded oral aspirin challenges.
None of the 60 patients experienced any symptoms, changes in nasal examination findings, or declines in FEV(1) values during their challenges with rofecoxib. All 60 patients experienced typical naso-ocular and asthmatic reactions to aspirin with a mean provoking dose of 61 mg. The exact 1-sided CI for the probability of rofecoxib inducing crossreactions in aspirin-sensitive patients with asthma is calculated to be between 0% and 0.05%.
Given that none of the 60 patients reacted to rofecoxib and given the statistical power of this large sample size, we conclude that cross-reactivity between aspirin and rofecoxib does not occur in patients with aspirin-sensitive respiratory disease. This does not exclude rofecoxib from participating in other types of reactions, including immune recognition after prior treatment with the drug. From the standpoint of the mechanisms involved in aspirin-induced respiratory reactions, this study strongly supports inhibition of cyclooxygenase-1 as the essential initiator of these types of reactions.
对阿司匹林敏感的呼吸道疾病患者会对所有抑制环氧化酶的非甾体抗炎药产生交叉反应。随着选择性抑制环氧化酶-2的抗关节炎药物的问世,人们提出了阿司匹林与这些新型环氧化酶-2抑制剂之间是否会发生交叉反应的问题。
本研究的目的是确定罗非昔布在对阿司匹林敏感的哮喘患者中是否会产生交叉反应。
60例哮喘患者在我们的综合临床研究中心接受了为期48小时的双盲、安慰剂对照口服罗非昔布(12.5毫克、25毫克和2种安慰剂)激发试验。第二天,通过单盲口服阿司匹林激发试验,证实了这60例患者中的每一例对阿司匹林敏感。
60例患者在接受罗非昔布激发试验期间均未出现任何症状、鼻检查结果变化或第一秒用力呼气容积(FEV₁)值下降。所有60例患者对阿司匹林均出现典型的鼻眼和哮喘反应,平均激发剂量为61毫克。计算得出罗非昔布在对阿司匹林敏感的哮喘患者中引发交叉反应的概率的精确单侧置信区间在0%至0.05%之间。
鉴于60例患者中无一例对罗非昔布有反应,且考虑到该大样本量的统计学效力,我们得出结论,阿司匹林与罗非昔布之间在对阿司匹林敏感的呼吸道疾病患者中不会发生交叉反应。这并不排除罗非昔布参与其他类型的反应,包括用药前治疗后的免疫识别反应。从阿司匹林诱导的呼吸道反应所涉及的机制角度来看,本研究有力地支持了环氧化酶-1的抑制是这类反应的关键起始因素。