{'fraction_non_alphanumeric': 0.015339663988312637, 'fraction_numerical': 0.0014609203798392988, 'mean_word_length': 6.248677248677248, '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}}
Etiology of anaphylactoid responses. The promise of nonionics.

Though the precise etiology of anaphylactoid contrast media reactions is unknown, recent investigations have contributed important insight into their pathogenesis. Explorations of the complement and coagulation systems, the basophil histamine release system, and antigen-IgE interactions are summarized. Current investigations focusing on the contact system are discussed. Patients with asthma and patients who are contrast material reactors show increased prekallikrein transformation rates indicating increased contact system activity. Increased endogenous heparin-like material was found in asthmatic patients and in 50% of prechallenge citrated plasmas of patients who later developed contrast reactions, suggesting partial explanation of increased incidence of reactions in asthmatics. Elevated heparin-like material may have pathogenic significance; it may potentiate prekallikrein transformation and inhibit adenylate cyclase to induce release of inflammatory mediators and produce bronchospasm. When appropriately administered, glucocorticoids appear to protect against contrast reactions. Incidence of systemic anaphylaxis with nonionic contrast media is unknown but is expected to be less than that with ionic media. Additional experience is needed to assess this potential benefit of nonionics.