Seventeen patients with aspirin-induced asthma were studied, the majority being intolerant to more than one analgesic. In addition to asthma, eleven patients had sinusitis and eight had nasal polyps. Serum IgE levels were normal with a mean of 295 iu/ml. However, some patients had positive cutaneous and PK tests against inhalants and non-analgesic drugs.Spirometry showed the bronchial obstruction to be mild. However, all patients were hyper-reactive to acetylcholine. Oral provocation tests with aspirin alone and also with the prior administration of sodium cromoglycate (SCG) by inhalation were performed and the results assessed by spirometry and clinical examination.The results suggest that the obstruction is probably due to oedema of the bronchial mucosa together with pulmonary congestion rather than a simple spasm of the bronchi.SCG was found to prevent significantly the ventilatory obstruction induced by aspirin.It is suggested that non-immunological factors are responsible for the asthma and that SCG may have an effect on the altered receptors protecting them from the action of aspirin on kinins.

Summary Serum samples from eighty‐one patients with suspected penicillin allergy were investigated with Phadebas RAST using the penicillin derivatives Benzylpenicilloyl‐human serum albumin (PBO‐HSA) and Phenoxymethylpenicilloyl‐human serum albumin (PMPO‐HSA) and the results were compared with skin test results and clinical data. Of the sixty‐one patients who had anaphylactic shock and/or urticaria as a possible consequence of penicillin administration, reagins against PBO‐HSA and PMPO‐HSA could be detected in thirty‐four cases (56%). Five per cent of these patients, with positive RAST results, showed negative skin tests; in the other 95% both RAST and skin tests were positive. All, except eight, of the RAST‐negative patients had had their adverse reactions at least 2 years prior to the blood sampling and in some of these cases skin tests were also negative. RAST and provocation test results agreed in 80% of the cases where exposition was performed. It is concluded that the RAST technique is a valuable diagnostic tool for the detection of immediate type hypersensitivity to penicillin.

In a study of the incidence of respiratory reaction to tartrazine, challenge tests were made with doses of 5, 25, 50, 100 and 200 mg of tartrazine and with a placebo, on forty-seven patients with asthma associated with intolerance to analgesics (ASA-Triad). The patient's clinical and spirographic condition was satisfactory when the test was made, and the administration of bronchodilators had been stopped 24 hr previously.In a total of 141 tests with tartrazine on forty-seven patients, only five tests were positive and occurred in only four patients. In three patients the test gave a negative result when repeated with an identical or larger dose of tartrazine. Only one patient had a respiratory reaction with 5 mg of tartrazine on two successive occasions, and this result is considered doubtful bearing in mind that the variation in FEV| was at its limit. All the tests with placebo were negative except one.The clinical lability of the ASA-Triad patients could be the cause of some of the respiratory reactions attributed to tartrazine in some studies. The lability could, above all, be dependent on the suppression of the symptomatic treatment.The inconvenience associated with a colour-free diet and the small incidence of proven reactions to tartrazine, tend to invalidate the practice of recommending such diets unless evidence is available of a positive challenge test on at least two occasions. Even so, the risks induced are minimal.

The case of a woman with a serious anaphylactic pattern during menstruation is described. The patient had a clinical picture of urticaria, angioedema and shock at each menstruation for a period of 2 years until hysterectomy was performed. The studies showed no hormonal or immunological change. The only relevant finding was the extraordinarily strong vasodilating action of the menstrual fluid in the patient, and not in the controls. The results of the study suggest the possibility of two mechanisms: 1) an IgE-mediated mechanism causing hypersensitivity to some metabolic substance in the menstrual fluid and 2) an excessive pharmacological vasodilatory action produced by the prostacyclin in the fluid itself.

In a patient with a past history of allergy to penicillin and requiring treatment, skin tests with penicillin and penicilloyl-polylysine (PPL) were positive, and a penicilloyl RAST was strongly positive, although the Prausnitz-Kustner test to penicillin and PPL were negative. The hapten BPO-Flys was administered together with penicillin to try to prevent reactions. An anaphylactic reaction occurred on the fifth day, and treatment was stopped. Serum total IgE values increased markedly after the reaction and PK titres to penicillin and PPL reached values of 1/256. The skin test reaction to PPL was negative the day after the clinical reaction, but became strongly positive again a few days later. The penicilloyl RAST remained strongly positive throughout. The authors consider that there was hypersensitivity to a penicillin metabolite other than the penicilloyl group, e.g. to minor determinants, and for this reason the hapten inhibitor failed.