ABSTRACT
Avoidance is the key treatment of anaphylaxis if an allergen exists; thus, we have evaluated 102 patients with the initial diagnosis of idiopathic anaphylaxis with a battery of 79 food-antigen skin prick tests selected to include foods reported or suspected of provoking anaphylaxis. Only those patients whose episodes consisted of at least two of the following were included in the study: angioedema with or without hives, laryngeal edema leading to severe dyspnea, hypotension, or loss of consciousness. Detailed history, physical examination, and conventional laboratory tests ruled out known causes of anaphylaxis. Thirty-two patients (31%) had positive tests to one or more food antigens. In five of these patients, subsequently eating a food that elicited a positive test provoked an anaphylactic reaction. Two patients eliminated the foods completely, stopped having reactions, and refused challenge. In these seven patients, 10 different antigens provoked anaphylaxis: aniseed, cashew nut, celery, flaxseed, hops, mustard, mushroom, shrimp, sunflower, and walnut. We conclude that a battery of selected food-antigen skin prick tests provided a useful method for identifying an offending antigen in these patients and that some (7% in our series) cases of "idiopathic" anaphylaxis by history are not truly idiopathic.
Subject(s)
Anaphylaxis/etiology , Food Hypersensitivity/complications , Adolescent , Adult , Aged , Antigens/administration & dosage , Child , Female , Food Hypersensitivity/immunology , Humans , Male , Middle Aged , Skin TestsABSTRACT
Incubation of chrysotile and anthophyllite asbestos fibers with normal human peripheral blood monocytes resulted in significant suppression of monocyte metabolic activity as measured by chemiluminescence. Both fiber types were cytotoxic to monocytes and depressed monocyte phagocytosis of latex beads. We conclude that asbestos-induced monocyte cytotoxicity could result in release of lysosomal enzymes and/or degradation products which contribute to fibrosis in asbestosis. The depression of phagocytosis and microbicidal function may contribute to the increased incidence of carcinogenesis observed in asbestosis.
