Eighteen patients with a history of urticaria or asthma, or both, induced by aspirin were studied before and after provocation of symptoms with aspirin. The plasma prostaglandin F, concentration, which was characteristically raised before challenge, fell significantly at the time of adverse reactions. Repeated administration of aspirin up to a dose of 650 mg daily induced tolerance in most of the patients, and several developed bronchodilator responses to aspirin.Although median total IgE concentrations may be raised in patients with aspirin sensitivity, it appears likely that pharmacological rather than immunological mechanisms are chiefly responsible for the phenomena of aspirin sensitivity and desensitisation.
Plasma aspirin esterase activity and cholinesterase activity were reduced in patients with aspirin sensitive asthma and aspirin sensitive urticaria compared to asthmatic and dermatological controls. Phenylacetate (non specific) esterase activities, were however unaltered in these patients. The reason for the lower activity is uncertain but it does not appear to be due to genetically determined lower cholinesterase or due to the avoidance of aspirin by sensitive patients. A low aspirin esterase activity may be a contributory factor in precipitating these aspirin sensitive reactions.
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).
Progressively increasing doses of aspirin (acetylsalicylic acid-ASA) were tolerated by 14 out of 15 patients with confirmed aspirin-sensitive urticaria and in 7 out of 9 patients with aspirin-sensitive asthma. Blood levels ofhistamine and prostaglandin (PG) F2a were significantly raised in these patients before ASA administration. PGF2a levels fell to within the normal range after challenge doses of ASA which were sufficient to cause symptoms. Skin prick testing with histamine and codeine phosphate did not show evidence of abnormal tissue reactivity or mast cell reactivity. A wider spectrum of mediators will need to be considered if the mechanism of symptom production is to be understood.
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