{'fraction_non_alphanumeric': 0.020652173913043477, 'fraction_numerical': 0.0, 'mean_word_length': 6.030534351145038, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Mediator assays in aspirin-induced asthma.

It had been postulated from earlier studies that platelets of aspirin-sensitive asthmatics reacted to aspirin and other cyclo-oxygenase inhibitors. Similarly, a generalized abnormality had been suggested in the regulation of arachidonic acid oxidative pathways in blood leukocytes of patients with aspirin-induced asthma. Studies of activation in vitro as well as in vivo assessment of polymorphonuclear leukocytes have not been conclusive of metabolic pathways inducing bronchospasm in aspirin-sensitive asthmatic patients. Serum levels of tryptase, a specific marker of mast cell activation, appear to increase during bronchoconstriction following ingestion of oral aspirin. Eosinophil cationic protein (ECP) levels in serum are concomitantly elevated. Leukotriene antagonists may partially protect individuals with allergen-provoked or aspirin-provoked bronchoconstriction.