Recall Urticaria: Aspirin Also Induces It

Cimbollek, S; Mr, Ávila-Castellano; Labella, M; Baynova, Krasimira; Aramburu, Tomas; Quiralte, Joaquín

doi:10.18176/jiaci.0219

Cited by 6 publications

(9 citation statements)

References 4 publications

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“…At least, three subsets of these patients with NH may have an associated underlying disease: in fact, around 10 percent of patients with chronic rhinosinusitis with nasal polyps and moderate-to-severe asthma and 30 percent of those with chronic urticaria/angioedema may present a nasoocular/asthmatic or urticarial reaction after NSAID exposure at some times in their lives, respectively [6]. Some clinical phenotypes of skin NSAID hypersensitivity are also definitely associated with allergic respiratory disease [3,7].…”

Section: A Working Classification Of Skin Nsaid Hypersensitivity Basementioning

confidence: 99%

“…The skin reactions are the most prevalent clinical phenotypes in patients with NSAID hypersensitivity. We have described at least 5 clinical phenotypes of immediate-type of skin NSAID hypersensitivity: [3,7] NSAID-exacerbated cutaneous disease (NECD), NSAID-induced urticaria/angioedema (NIUA), two clinical phenotypes (NSAID induced isolated periorbital angioedema and NSAID induced recall urticarial) which are present exclusively in patients with respiratory allergy, mainly house dust mites; and a single NSAID induced urticaria/angioedema/ anaphylaxis (SNIUAA) (Table 1). The last mentioned is probably an IgE-mediated allergy.…”

Section: The Skin Clinical Phenotypes Of Nsaid Hypersensitivitymentioning

confidence: 99%

“…This phenomenon might be a new phenotype of skin NSAID hypersensitivity which would appear in those patients with respiratory allergy treated with sq. AIT [7].…”

Section: Nsaid-induced Recall Urticariamentioning

confidence: 99%

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Clinical Phenotypes in NSAID-Induced Urticaria/Angioedema

Quiralte¹,

Ávila²,

Cimbollek³

et al. 2021

Urticaria - Diagnosis and Management

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The skin clinical phenotypes of nonsteroidal anti-inflammatory drug (NSAID) hypersensitivity (NH) are very heterogeneous with several syndromes after NSAID intake, which include different symptoms, different organ involvement and different associated concomitant diseases and possibly different underlying pathophysiology and mechanisms. Making a correct diagnosis in NH is an exciting journey for any allergist. Thus, to classify these diseases properly will be pivotal for appropriate diagnostic and management strategy. Treatment modalities are depending on the clinical phenotypes of NH and they will embrace for each patient: the avoidance of culprit NSAID, the finding of well-tolerated NSAID and in certain cases, desensitization procedures when the NSAID treatment was absolutely needed as well as the control of associated diseases such as spontaneous chronic urticarial or allergic respiratory diseases. This review updates the recent evidence of classification, diagnostic strategies, and management of skin NSAID hypersensitivity reactions.

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Section: A Working Classification Of Skin Nsaid Hypersensitivity Basementioning

confidence: 99%

Section: The Skin Clinical Phenotypes Of Nsaid Hypersensitivitymentioning

confidence: 99%

See 1 more Smart Citation

Clinical Phenotypes in NSAID-Induced Urticaria/Angioedema

Quiralte¹,

Ávila²,

Cimbollek³

et al. 2021

Urticaria - Diagnosis and Management

View full text Add to dashboard Cite

show abstract

“…The most common example is patients who have previously received subcutaneous allergen immunotherapy and experience a local skin reaction at the sites of previous allergen injections when the allergen is administered again at a different site or after significant environmental exposure to the allergen [7]. Other stimuli such as heparin and nonsteroidal anti-inflammatory drugs have also been reported [8].…”

mentioning

confidence: 99%

“…On one hand, the initial symptoms, ie, hives at the previous drug administration sites, favor the idea of anakinra-induced RU. These reactions may be mediated by IgE, T cells, or enzymatic inhibition of the cyclooxygenase type I isoform, which may play a role in the development of this specific reaction [8,9]. In addition, polysorbate, the component that carries both anakinra and canakinumab, has the power to induce mast cell degranulation.…”

mentioning

confidence: 99%