Allergology Clinic, Clinica San Carlo, Paderno Dugnano, Milan, Italy.
Eur Ann Allergy Clin Immunol. 2022 Jul;54(4):189-191. doi: 10.23822/EurAnnACI.1764-1489.227. Epub 2021 Jul 21.
Up to 15% of patients with chronic spontaneous urticaria (CSU) experience severe exacerbations of their baseline cutaneous disease after taking nonsteroidal anti-inflammatory drugs that inhibit cycloxygenase-1 (COX-1) enzyme. These subjects are defined as having a NECD (NSAID-exacerbated cutaneous disease). The way NSAID hypersensitivity correlates with the different pathogenic mechanisms of CSU has not been investigated so far. 235 adults with severe CSU submitted to omalizumab treatment were studied. A rapid omalizumab response was considered as a marker of auto-allergic (Type I) CSU whereas patients showing a slow response or not responding at all were regarded as having a type IIb autoimmune disease. At the first visit medical history of tolerance to aspirin and/or other COX-1 inhibiting NSAID was ascertained. Duration of disease, atopic status, thyroid autoimmunity, CRP, D-dimer plasma levels, and total IgE were assessed appropriately. 23 (10%) were hypersensitive to NSAID. Patients with or without did not differ in any of the variable considered, and a similar proportion in the two groups showed type I or type IIb CSU. The study suggests that in CSU hypersensitivity to NSAID represents a phenomenon that is independent on the pathogenesis of the underlying skin disease.
多达 15%的慢性自发性荨麻疹（CSU）患者在服用抑制环氧化酶-1（COX-1）酶的非甾体抗炎药（NSAID）后，其基础皮肤疾病会出现严重恶化。这些患者被定义为患有 NECD（NSAID 加重的皮肤疾病）。迄今为止，尚未研究 NSAID 过敏与 CSU 不同发病机制之间的相关性。本研究纳入了 235 名接受奥马珠单抗治疗的严重 CSU 成年患者。奥马珠单抗快速应答被视为自身过敏（I 型）CSU 的标志物，而应答缓慢或无应答的患者则被认为患有 IIb 型自身免疫性疾病。在首次就诊时，确定了对阿司匹林和/或其他 COX-1 抑制型 NSAID 的耐受史。适当评估了疾病持续时间、特应性状态、甲状腺自身免疫、CRP、D-二聚体血浆水平和总 IgE。23 名（10%）对 NSAID 过敏。有或没有 NSAID 过敏的患者在考虑的任何变量上均无差异，两组中具有相似比例的患者表现为 I 型或 IIb 型 CSU。该研究表明，在 CSU 中，对 NSAID 的过敏是一种独立于基础皮肤病发病机制的现象。
