Baló-Banga József Mátyás, Schweitzer Katalin
Magyar Honvédség Egészségügyi Központ Budapest, Podmaniczky u. 109-111., 1062.
Orv Hetil. 2018 Sep;159(38):1556-1566. doi: 10.1556/650.2018.31170.
According to the present knowledge, the effect of non-steroidal anti-inflammatory drugs (NSAIDs) depends on the inhibitory ratio of cyclooxigenase (COX)-1 to COX-2 in the plasma membranes. In addition to cardiovascular and gastrointestinal side effects, there are adverse symptoms which can be divided into cross-intolerance (non-immune mediated) and single or multiple hypersensitive (immune mediated) reactions. Due to clinical phenotypes and to in vivo aspirin reactivity, adverse effects could be further classified.
The aim of these studies was a comparison of hit ratios obtained by a humoral serum test measuring specific immunglobulin E (IgE) against a rapid cellular test measuring interleukin (IL)-6 release from sensitized mononuclear cells due to various suspect NSAID after symptoms within one year. Retrospective case studies were performed in in- and out-patients of our teaching hospital in Budapest, between 2003 and 2013.
Specific anti-NSAID IgE levels were determined by ELISA in 55 cases. The other matching group of patients consisted of 51 patients and 9 tolerant persons. Their separated cells' supernatants were checked for IL-6 release incubated for 20 minutes by NSAID dilutions including intraassay controls by two-step ELISA assay. Both groups have been stratified according to "new" clinical classification.
Results have disclosed no significant differences among the distribution of clinical symptoms between the two groups. In both groups, 9 non-steroidal anti-inflammatory drugs were tested representing all frequently used compounds with COX-1 inhibitory potential. The overall positivity rate was nearly double (65.4% against 36.9%) within the group using IL-6 release assay against that with specific IgE as the diagnostic tool. In certain cases, non-drug components of commercial preparations prompted IL-6 release as well which was paralleled by in vivo test results. Positive in vitro tests were obtained in both groups with clinically cross-intolerant as well as single or multiple sensitized cases.
The rates of single or multiple sensitized cases exceeded in both groups that of cross-intolerant patients. In some phenotypes belonging to the latter categories, IgE type antibodies against acetylsalicylic acid could be detected as well. IL-6 release assay was the more sensitive test. In addition to pure drugs, other ingredients of medicines could also be responsible for adverse events. Orv Hetil. 2018; 159(38): 1556-1566.
根据目前的认识，非甾体抗炎药（NSAIDs）的作用取决于其对细胞膜中环氧化酶（COX）-1和COX-2的抑制比例。除了心血管和胃肠道副作用外，还有一些不良症状，可分为交叉不耐受（非免疫介导）和单一或多重过敏（免疫介导）反应。根据临床表型和体内阿司匹林反应性，不良反应可进一步分类。
这些研究的目的是比较一年内出现症状后，通过检测针对特定免疫球蛋白E（IgE）的体液血清试验与通过检测致敏单核细胞因各种可疑NSAIDs释放白细胞介素（IL）-6的快速细胞试验所获得的命中率。2003年至2013年期间，在布达佩斯我们教学医院的门诊和住院患者中进行了回顾性病例研究。
采用酶联免疫吸附测定法（ELISA）测定55例患者的特异性抗NSAID IgE水平。另一组匹配的患者包括51例患者和9例耐受者。通过两步ELISA测定法，用NSAID稀释液（包括分析内对照）孵育20分钟后，检测他们分离细胞的上清液中IL-6的释放情况。两组均根据“新的”临床分类进行分层。
结果显示两组临床症状分布无显著差异。在两组中，检测了9种非甾体抗炎药，代表了所有具有COX-1抑制潜力的常用化合物。以IL-6释放试验作为诊断工具的组的总体阳性率几乎是使用特异性IgE作为诊断工具的组的两倍（分别为65.4%和36.9%）。在某些情况下，商业制剂中的非药物成分也会促使IL-6释放，这与体内试验结果一致。两组中临床交叉不耐受以及单一或多重致敏病例的体外试验均呈阳性。
两组中单一或多重致敏病例的发生率均超过交叉不耐受患者。在属于后一类别的某些表型中，也可检测到针对乙酰水杨酸的IgE型抗体。IL-6释放试验是更敏感的检测方法。除了纯药物外，药物的其他成分也可能导致不良事件。《匈牙利医学周报》。2018年；159（38）：1556 - 1566。
