Fixed drug eruption (FDE) caused by oxicams is very rare. There are few reports of FDE induced by piroxicam, and this explains why cross-sensitivity among oxicams (piroxicam, tenoxicam, and droxicam) has been studied in only one patient. The patch test on residual lesions has lately been used by some authors in FDE diagnosis with variable results. We describe two cases of piroxicam-caused FDE and demonstrate cross-sensitivity among piroxicam, tenoxicam, and droxicam in both of them. One patient had residual lesions and the patch test was useful for diagnosis and cross-sensitization studies. The second patient had no residual lesions, and the patch test was negative on normal but previously affected skin; therefore, the study was performed by single-blind controlled oral challenge.
We evaluated the usefulness of individual tryptase levels and variations after adverse drug reactions in 64 patients. Our aim was to find a tool for the diagnosis of drug allergy. Thirty-seven subjects were confirmed to have drug allergy, 12 had nonsteroidal anti-inflammatory drug (NSAID) reactions, five had negative controlled drug challenges (NAAR), and 10 had symptoms after placebo intake (PLA). Serum tryptase levels greatly increased after anaphylactic shocks (2242%) and anaphylaxis (710.5%). Patients with allergic urticaria and those with idiosyncratic responses to acetylsalicylic acid (ASA) exhibited a small increase in serum tryptase (49.5% and 38.2%, respectively). In the other two groups (NAAR and PLA), no variation in this serum protease was observed. The time of appearance of the serum tryptase peak differed considerably among patients with similar clinical reactions (from 30 min to 6 h) and was independent of the latent period, severity of symptoms, or the amount of tryptase released. We conclude that serum tryptase determinations are helpful in the diagnosis of anaphylactic shock and anaphylaxis, but serial measurements may be needed to confirm mast-cell participation in milder reactions.
Previously reported allergic reactions to orgotein (superoxide dismutase) injections has assigned responsibility to this molecule, which is obtained from bovine liver. We report an anaphylactic shock probably caused by impurities contained in an orgotein preparation. Prick test to Peroxinorm (orgotein), BSA, and cow liver extract were positive but resulted negative with chymotrypsin, milk, meat and cow epithelium extracts. Tryptase levels determined 3, 24 hours and 15 days after the shock measured 6.32, 0.81 and 0.84 U/L respectively. Detection of specific IgE to Peroxinorm, BSA and chymotrypsin by ELISA was negative and positive to cow liver. Specific IgE to milk and cow epithelium by Pharmacia CAP system was negative. Immunoblotting with Peroxinorm revealed IgE specific bands at an apparent M.W of 67, 51, 56 and 16 kDa; immunoblotting with cow liver revealed bands at 72, 56, 50 and 36 kDa; immunoblotting with BSA and chymotypsin were negative. This case emphasises the role that 20 % of impurities of the pharmaceutical preparation may have in immediate hypersensitivity reactions.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.