Clinical course and urinary eicosanoids in patients with aspirin-induced urticaria followed up for 4 years

Abstract

Aspirin hypersensitivity manifesting as urticaria/angioedema remains present after 4 years in about two thirds of patients. Aspirin-precipitated skin reactions associate with increased excretion of LTE(4) and PGD(2).

Hypersensitivity to nonsteroidal anti-inflammatory drugs (NSAIDs) - classification, diagnosis and management: review of the EAACI/ENDA# and GA2LEN/HANNA*

“…According to this hypothesis, inhibition of cyclooxygenase by NSAIDs may lead to a decrease in protective prostaglandins production, leading to activation of mediator release from inflammatory cells in the skin. This hypothesis was further supported by observations that skin eruptions after oral aspirin challenge were accompanied by the release of eicosanoids similarly to patients with AERD (49,50).…”

“…Skin eruptions usually subside within few hours but may persist for several days. The degree of sensitivity to NSAIDs may show temporary fluctuations related to activity of underlying chronic disease and may even disappear in some patients (50). A certain proportion of patients with cutaneous adverse reactions may also develop respiratory symptoms.…”

Update in drug allergy: novel drugs with novel reaction patterns

“…Setkowicz et al [53] studied patients with chronic idiopathic urticaria and aspirin hypersensitivity. They followed patients for 4 years, performing aspirin provocations and measuring urinary levels of leukotriene E4 (LTE4) and the main prostaglandin (PGD2) metabolite (9a11bPGF2) at the beginning and at the end of the period.…”

Copy number variation in ALOX5 and PTGER1 is associated with NSAIDs-induced urticaria and/or angioedema

“…NERD and NECD are considered to be caused by a nonspecific immunological mechanism whereby NSAIDs inhibit COX enzymes, leading to a dysregulation of leukotriene homeostasis [7]. Since Szczeklik associated the capacity of NSAIDs to block the COX-1 enzyme with asthma exacerbations [10], many studies on the basis of this hypothesis have been published [11][12][13][14][15][16][17][18][19][20]. However, despite considerable study, there is a lack of evidence to support this hypothesis for NIUA [7].…”

“…For example, it has been shown that these patients have higher basal LTs levels that are augmented after drug intake [13][14][15]20] and related to the severity of symptoms [25]. This dysregulation is not only found for NERD patients; in fact, NECD patients also show high levels of LTs [17,19]. However, little evidence exists for NIUA [20].…”