Specific desensitization in ‘aspirin‐sensitive’ urticaria; plasma prostaglandin levels and clinical manifestations

Abstract

Summary Six out of eight patients with a history of aspirin‐provoked urticaria/angioedema responded with adverse reactions, including urticaria and bronchospasm, to provoking doses of oral aspirin from 30‐515 mg. The other two patients did not react to 1.2 g of aspirin on three occasions. Five of the six patients who had reacted became desensitized after their initial aspirin reaction, tolerating 650 mg on the second day. They then took 650 mg day−1 of aspirin for three weeks, during which time the ingestion of foods which had previously caused a variety of moderate or severe reactions caused no symptoms. The resting plasma PGF2α in ten ‘aspirin‐sensitive’ urticaria patients (24.89 + 2‐79 pg m−1) was significantly higher than the levels in ten normal subjects (6.75 + 1‐1 pg ml−1) (P < 0.01). In the patient group the lowest levels of PGF2x were found in the two patients who subsequently did not experience a positive reaction after aspirin provocation. The PGF2α/PGE2 ratio in ‘aspirin‐sensitive’ urticaria patients (1‐83 + 0.026) was significantly higher than that in normal subjects (0‐63 + 0.14) (P < 0.01).

Hypersensitivity reactions to food additives

“…Five of six patients with ASA-provoked urticaria became tolerant to ASA after a single dose of 30-515 mg of ASA (6). These five patients remained free of symptoms during the following weeks when taking 650 mg of ASA daily.…”

Effect of aspirin in "aspirin sensitive" patients.

“…In patients with aspirin intolerance manifested by acute urticaria, angioedema, or bronchospasm within two hours of ingestion there is evidence that tolerance to aspirin may be induced by repeated administration over 24-48 hours of doses up to 650 mg a day.1 2 The time course for both the induction and the loss of tolerance to aspirin and the known effect of aspirin as a cyclooxygenase inhibitor suggest that the mechanisms may be pharmacological rather than allergic, acting through an effect on prostaglandin production. A purely pharmacological effect would not, however, explain the apparent association of aspirin intolerance with other allergic features.…”

Μοριακοί Και Κυτταρικοί Ανοσολογικοί Μηχανισμοί Κατά Τις Αντιδράσεις Υπερευαισθησίας Στα Μη Στερεοειδή Αντιφλεγμονώδη Φάρμακα

“…Τα παραπάνω αποτελούν μια πιθανή εξήγηση για τις διαφορές στα αναφερόμενα επίπεδα εικοσανοειδών και μεταβολιτών της ισταμίνης σε άτομα με αντιδράσεις υπερευαισθησίας σε ΜΣΑΦ (Asad et al, 1983• Asad et al, 1984• Mita et al, 2001• Mastalerz et al, 2004• Gaber et al, 2008• Doña et al, 2019. Ωστόσο, τα μαστοκύτταρα παρουσιάζουν ετερογένεια και διαφορές τόσο μεταξύ όσο και εντός των ειδών (Kakavas et al, 2006).…”