Abstract
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.
Highlights
Nonsteroidal anti-inflammatory drugs (NSAID) are one of the most commonly used drugs worldwide
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)
NECD patients seem to have a distinct phenotype compared with NSAID-tolerant CSU patients: the latter have a shorter duration of CSU and less often have angioedema when compared with NECD patients [9]
Summary
Nonsteroidal anti-inflammatory drugs (NSAID) are one of the most commonly used drugs worldwide. Three subsets of these patients with NH may have an associated underlying disease: 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]. The diagnostic approach determines very different clusters of patients [3, 8] Those who present clinical reactivity between different NSAIDs (multiple reactors) versus those who develop a reaction exclusively to a specific NSAID (selective reactors), and secondly, those in whom there is a very defined concomitant associated disease from the clinical and biological point of view. This classification based on clinical phenotypes is a real and practical approach in the daily clinic, which will allow us to make the best appropriate diagnostic and therapeutic decisions
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