Walters Kristen M, Simon Ronald A, Woessner Katharine M, Wineinger Nathan E, White Andrew A
Scripps Clinic, San Diego, California.
Scripps Clinic, San Diego, California.
Ann Allergy Asthma Immunol. 2017 Jul;119(1):71-76. doi: 10.1016/j.anai.2017.05.003.
Prostaglandin E (PGE) is an anti-inflammatory compound that inhibits 5-lipoxygenase activity. Diminished PGE regulation in aspirin-exacerbated respiratory disease (AERD) leads to respiratory reactions on cyclooxygenase 1 inhibition. In vitro studies have found that exogenous PGE stabilizes inflammatory mediator release.
To examine whether misoprostol (oral prostaglandin E analogue) use during aspirin challenge and desensitization might decrease the severity of aspirin-induced symptoms and make desensitization safer for patients with AERD.
Forty-five patients undergoing aspirin challenge and/or desensitization were randomized to misoprostol (n = 30) or placebo (n = 15) and compared with a group of historical controls (n = 31). Misoprostol (200 μg) was administered at 30 minutes, 90 minutes, and 4 hours after the first dose of nasal ketorolac. Measured end points included change in forced expiratory volume in 1 second (FEV), peak nasal inspiratory flow rate (PNIF), number of treatments received for induced reactions, and adverse gastrointestinal effects.
A difference in FEV and PNIF reduction was detected between misoprostol and placebo (P = .03) and misoprostol and historical controls (P = .01), respectively, during nasal ketorolac challenge. No difference was detected among aspirin reactors. Among all reactors, no difference in magnitude was found for FEV (P = .13) or PNIF (P = .07) reduction across all 3 groups. Total treatment requirement was similar (P = .14). Patients receiving misoprostol were more likely to report adverse gastrointestinal effects (P = .02).
The addition of misoprostol to current aspirin challenge and/or desensitization protocols reveals no protective effect in reducing the intensity of nonsteroidal anti-inflammatory drug-induced symptoms and is not recommended based on the findings in this study.
前列腺素E（PGE）是一种抗炎化合物，可抑制5-脂氧合酶活性。阿司匹林加重性呼吸疾病（AERD）中PGE调节功能减弱会导致环氧化酶1受抑制时出现呼吸反应。体外研究发现，外源性PGE可稳定炎症介质的释放。
探讨在阿司匹林激发试验和脱敏过程中使用米索前列醇（口服前列腺素E类似物）是否可减轻阿司匹林诱发症状的严重程度，并使AERD患者的脱敏过程更安全。
45例接受阿司匹林激发试验和/或脱敏的患者被随机分为米索前列醇组（n = 30）或安慰剂组（n = 15），并与一组历史对照（n = 31）进行比较。在首次给予鼻用酮咯酸后30分钟、90分钟和4小时给予米索前列醇（200μg）。测量的终点指标包括1秒用力呼气量（FEV）的变化、最大鼻吸气流量（PNIF）、因诱发反应而接受的治疗次数以及胃肠道不良反应。
在鼻用酮咯酸激发试验期间，米索前列醇组与安慰剂组（P = 0.03）以及米索前列醇组与历史对照组（P = 0.01）之间，分别检测到FEV和PNIF降低存在差异。阿司匹林反应者之间未检测到差异。在所有反应者中，三组间FEV降低幅度（P = 0.13）或PNIF降低幅度（P = 0.07）均未发现差异。总治疗需求相似（P = 0.14）。接受米索前列醇治疗的患者更有可能报告胃肠道不良反应（P = 0.02）。
在当前的阿司匹林激发试验和/或脱敏方案中添加米索前列醇，在减轻非甾体抗炎药诱发症状的强度方面未显示出保护作用，基于本研究结果不建议使用。
