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首页> 外文期刊>The Internet Journal of Asthma, Allergy and Immunology >Intravenous Ibuprofen For Desensitization In Aspirin Exacerbated Respiratory Disease: 2 Case Reports
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Intravenous Ibuprofen For Desensitization In Aspirin Exacerbated Respiratory Disease: 2 Case Reports

机译：静脉使用布洛芬降低阿司匹林致敏性呼吸系统疾病的敏感性：2例报告

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摘要

Ibuprofen is in a category of non-steroidal anti-inflammatory drugs that has nearly complete cross-reactivity with aspirin in terms of ability to provoke symptoms in patients with aspirin exacerbated respiratory disease(AERD)(1,2). While the most widely used desensitization protocols utilize aspirin, these protocols typically involve serial increments of oral aspirin administration over several hours(1,2). Aspirin absorption itself can vary even with the use of rapid release aspirin, with time to peak blood levels ranging from 18 minutes to 2 hours(3). This absorption time could potentially eliminated if intravenous administration were used, and thus could potentially enable a more rapid desensitzation procedure in AERD patients.The contrasting clinical courses of 2 patients desensitized with intravenous ibuprofen are described and the outcomes are discussed in terms of implications for managing AERD patients. Case 1: A 43 year old African American female presented to the office in April 2013 after a reaction to aspirin. She had a history of severe asthma and was using twice daily inhaled fluticasone proprionate/salmeterol in a 500/50 microgram combination formulation, montelukast 10 mg/day, albuterol metered dose inhaler and tiotropium 18 mcg inhaled per day. She had been on multiple courses of systemic prednisone but not in the prior month. She had a history of 3 prior sinus operations which included polypectomies, the most recent of which was in February 2013. Since the sinus operation she had recurrent frontal headaches. She reported having been intubated after taking ibuprofen in 2009, which she developed respiratory distress almost immediately after ingestion. Two days prior to presentation, she had developed pruritus, lip swelling, rash and coughing several hours after ingesting an 81 mg aspirin tablet. She claimed penicillin, egg and shrimp allergy.On physical examination, she had end inspiratory wheezing, no nasal polyps and a body mass index of 30.9 kg/m2. The skin had many less than 1 mm erythematous macules(fig 1). Laboratory tests 3 weeks prior to presentation included a complete blood count which showed an absolute increase in eosinophils(800/uL), elevated specific IgE to egg white, dust mite, and Kentucky Bluegrass, and normal histamine release with lysine acetylsalicylate. The total IgE was 470 IU/mL. No specific IgE to shrimp or penicillin was identified. One month prior, the patient had office spirometry which showed a post-bronchodilator FEV1 of 1.74L, which was noted to be 73% predicted. The patient was treated with fluticasone proprionate nasal spray 100 ugostril/day and cetirizine with improved headache and skin symptoms. In the beginning of May the patient underwent ketorolac nasal challenge with 1.2 mg, 5.2 mg, and 7.8 mg doses separated by 1 hour intervals. She left the office 1 hour after the last nasal spray dose. 30 minutes after leaving the office, she developed asthma and took oral prednisone with resolution of symptoms by the following day.Eight days later, the patient was admitted to the hospital for NSAID desensitization. She had been treated with oral prednisone during the prior 5 days and took 20 mg that morning. The patient had an expiratory peak flow rate of 350 L/min, before the desensitization was started. The first NSAID dose was given in the mid-morning as aqueous ibuprofen 12 mg diluted in 50 ml saline administered intravenously over 10 minutes. The next dose was administered as 24 mg diluted and administered similarly. 2 hours later the patient began to cough and had a decline in expiratory peak flow to 200 L/min. She was treated with 40 mg sodium methylprednisolone and albuterol/ipratropium nebulizations. 5.5 hours after the provoking ibuprofen administration, the patient was administered another 24 mg dose intravenously with no symptoms provoked. The next day in the mid-morning the patient received a 50 mg intravenous dose, which was followed shortly thereafter by itching and rash
机译：布洛芬属于非甾体类抗炎药，在引起阿司匹林加重性呼吸道疾病（AERD）患者的症状方面具有与阿司匹林几乎完全交叉反应的作用（1,2）。尽管使用最广泛的脱敏方案利用阿司匹林，但这些方案通常需要在数小时内连续口服阿司匹林（1,2）。即使使用速释阿司匹林，阿司匹林本身的吸收也会发生变化，使血液水平达到峰值所需的时间为18分钟至2小时（3）。如果使用静脉内给药，吸收时间可能会消除，从而有可能使AERD患者更快地进行脱敏程序。描述了2名接受静脉布洛芬脱敏的患者的对比临床过程，并就治疗的意义讨论了结局AERD患者。案例1：一名43岁的非洲裔美国女性在对阿司匹林反应后于2013年4月来到办公室。她有严重哮喘病史，每天使用两次吸入500/50微克复方制剂丙酸氟替卡松/沙美特罗，孟鲁司特10毫克/天，沙丁胺醇定量吸入器和每天吸入18 mcg噻托溴铵。她曾接受过多次系统性泼尼松治疗，但前一个月没有服用。她有3例先前的鼻窦手术史，其中包括多视镜检查，最近一次是在2013年2月。自鼻窦手术以来，她反复出现额头头痛。她报告说自己在2009年服用布洛芬后就已插管，摄入后几乎立即出现呼吸窘迫。在就诊前两天，摄入81毫克阿司匹林片剂数小时后，她出现瘙痒，嘴唇肿胀，皮疹和咳嗽。她声称自己对青霉素，鸡蛋和虾过敏，经身体检查发现吸气末喘息，没有鼻息肉，体重指数为30.9千克/平方米。皮肤有少于1毫米的红斑（图1）。呈现前3周的实验室检查包括全血细胞计数，显示嗜酸性粒细胞绝对增加（800 / uL），蛋清，尘螨和肯塔基州早熟禾的特异性IgE升高，以及赖氨酸乙酰水杨酸酯的正常组胺释放。总IgE为470 IU / mL。未鉴定出对虾或青霉素的特异性IgE。一个月前，患者进行了办公室肺活量测定，显示支气管扩张剂后FEV1为1.74L，据预测为73％。用丙酸氟替卡松鼻喷雾剂100 ug /鼻孔/天和西替利嗪治疗该患者，头痛和皮肤症状得到改善。在五月初，患者接受了酮咯酸鼻腔刺激，分别间隔1小时，1.2 mg，5.2 mg和7.8 mg。在最后一次鼻喷雾剂给药后一小时，她离开了办公室。离开办公室30分钟后，她患上哮喘，并于次日服用口服泼尼松并缓解了症状。八天后，该患者因非甾体抗炎药脱敏而入院。在之前的5天内，她接受了口服泼尼松的治疗，并于当天早上服用20毫克。在开始脱敏之前，患者的呼气峰值流速为350 L / min。第一个NSAID剂量是在上午中期以布洛芬12 mg水溶液稀释在50 ml生理盐水中稀释10分钟静脉给予的。下一剂以24mg稀释的方式给药，并类似地给药。 2小时后，患者开始咳嗽，呼气峰值流量降至200 L / min。她接受了40 mg甲基强的松龙钠和沙丁胺醇/异丙托溴铵雾化的治疗。激发性布洛芬给药后5.5小时，患者再次静脉注射24 mg剂量，没有引起症状。第二天早上，患者接受了50 mg静脉注射，随后不久出现瘙痒和皮疹

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