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Background Although the mechanism that underlies aspirin hypersensitivity is not completely understood, an IgE-mediated response was reported for a patient with aspirin-intolerant chronic urticaria (AICU). Objective We investigated whether genetic polymorphisms on the α-chain of the high-affinity IgE receptor (FcɛRIα) gene were associated with the AICU phenotype. Methods We genotyped 2 promoter polymorphisms (−344C>T and −95T>C) of FcɛRIα gene in the Korean population, and the functional effect of the −344C>T polymorphism was analyzed by using a luciferase reporter assay and an electrophoretic mobility shift assay. Results The rare allele frequency of the −344C>T polymorphism was significantly higher in the patients with AICU compared with the other subjects ( P = .008 for AICU vs aspirin-tolerant chronic urticaria; P = .03 for AICU vs controls). This polymorphism was also significantly associated with total serum IgE concentrations and a higher rate of atopy in the patients with AICU ( P = .01 and .05, respectively). The reporter plasmid that carried the −344T allele exhibited significantly higher promoter activity in a rat mast cell line (RBL-2H3) compared with the promoter activity of the −344C allele ( P T polymorphism exhibited greater anti-IgE–mediated histamine release compared with those with the homozygous CC genotype. Conclusion These results suggest that the −344C>T polymorphism of the FcɛRIα promoter may be associated with increased expression of FcɛRIα on mast cells and enhanced release of histamine. Clinical implications The FcɛRIα −344C>T polymorphism may contribute to the development of AICU.

Toluene diisocyanate (TDI), a widely used aromatic diisocyanate with the potential to cause asthma, reacts with albumin in the airway fluid, which acts as a carrier protein for chemical presentation to the immune system. Structural elucidation of TDI-albumin conjugates is crucial to understanding the human immune response to TDI exposure.Investigate the dependence of TDI's antigenicity on the biophysics of exposure and its association with TDI asthma.Toluene diisocyanate-albumin conjugates were generated by exposing albumin to TDI in liquid or vapor phase (liquid or vapor TDI-albumin, respectively). Conjugates were characterized by native gel electrophoresis and matrix-assisted laser desorption/ionization-mass spectrometry, and used as antigens in ELISA assays for serum specific-IgE and IgG.The physical phase of TDI (vapor vs liquid) affects the formation of TDI-albumin conjugates, with measurable differences in the amount of TDI per albumin molecule, migration in native gels, matrix-assisted laser desorption/ionization-mass spectrometry mass/charge spectra, and antigenicity. Vapor TDI-albumin conjugates were recognized by IgE from 44% of subjects with TDI asthma, whereas liquid TDI-albumin conjugates are recognized by IgE from only 17% of these patients. A significant (P.05) association between TDI exposure and vapor TDI-albumin specific serum IgG was also observed.Biophysics of TDI exposure substantially affects formation of TDI-albumin conjugates recognized by the immune system in association with exposure and asthma.The data suggest that serology may help identify TDI asthmatics and exposed workers if the appropriate form of TDI is used as the antigenic basis for analysis.

S A T U R D A Y 145 Hypersensitivity To Nitrile As A Contact Allergen S. Kumar, J. Moallem, R. Joks; Virginia Commonwealth University, RICHMOND, VA, SUNY Downstate Medical Center, BROOKLYN, NY. RATIONALE: Sensitization and clinical allergy to latex is common. Nitrile products are replacing latex products due to allergic sensitization, especially in hospitals. Clinical allergy to nitrile products is not recognized among health care workers and others routinely exposed to nitrile. We devised a modified skin prick test methodology to test for nitrile hypersensitivity. METHOD: Adults (n5 3), either health care workers or dialysis patients, with a history of cutaneous hypersensitivity reaction to nitrile glove underwent a modified skin prick challenge through nitrile glove material to assess immediate hypersensitivity, as well as Finn chamber patch testing for delayed hypersensitivity. RESULTS:All patients in the studywith history consistent with type-1 hypersensitivity reaction to nitrile glove tested positive with a wheal and flare reaction similar to histamine control; none had positive patch test reactivity. CONCLUSIONS: Nitrile contact allergy is an unrecognized problem in health care. This modified skin test methodology is a new tool in the diagnosis of nitrile allergy.

Background: Digestive drugs, including pancreatic extracts, have been widely prescribed in this country. There have been several reports of occupational asthma and rhinitis caused by digestive enzymes in workers in pharmaceutical industries; however, there has been no epidemiologic study among the medical personnel. Objective: We evaluated the prevalence of occupational allergy and sensitization rates to digestive drugs in medical personnel and its pathogenic mechanisms. Method: Eighteen pharmacists, 135 nurses and 123 non atopic normal controls were enrolled. Skin prick tests with 12 common aeroallergens and 5 commonly exposed drugs and its ingredients were performed. Serum specific IgE, IgG1 and IgG4 to α-amylase were measured by ELISA. SDS-PAGE followed by IgE and IgG4 immunoblot analysis was performed. Result: Work-related allergy symptoms were observed in 27.8% of pharmacists and 27.4% of nurses. IgE immunoblot analysis demonstrated 3 components which of 19 and 24 kDa were more frequently identified in sera from symptomatic subjects. IgG4 immunoblot analysis demonstrated 2 components of which 19 kDa was more frequently identified in sera from asymptomatic subjects. Conclusion: Digestive drug powders could induce IgEmediated respiratory allergy symptoms in the medical personnel. Two major allergenic components of α-amylase (19, 24 kDa) were identified. Specific IgG4 response to 19 kDa might have a role for preventing the development of workrelated allergy symptoms after exposure to α-amylase powder. (Korean J Asthma Allergy Clin Immunol 2007; 27:10-19)