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273 Aspirin sensitive rhinosinusitis without asthma: The clinical syndrome and effects of aspirin administration
273 ASPIRIN SENSITIVE RHINOSINUSITIS WITHOUT ASTHMA: THE CLINICAL SYNDROMEAND EFFECTS OF ASPIRIN ADMINISTRATION. W.R. Lumry, M.D., J.G. Curd, M.D. R.S. Zeiger, M.D., Ph.D., W.W. Pleskow, M.D., D.D. Stevenson, M.D. La Jolla, California. In a recent prospective study of aspirin(ASA) sensitive asthmatic patients undergoing standard oral ASA challenges, we discovered a spectrum of adverse respiratory tract reactions to ASA that Such a included pure naso-ocular reactions. finding suggested that a subpopulation of ASA sensitive patients manifest their sensitivity to ASA in their naso-ocular tissues alone. From a larger population of adult patients with either perennial rhinosinusitis alone or in combination with asthma, we identified 19 ASA sensitive patients who experienced selective ASA induced naso-ocular responses, without bronchospasm, during standard oral ASA challenges. At that point in time, these 19 patients exhibited all of the characteristics of the ASA triad except asthma. These included: hypertrophic rhinitis with a tendency to develop polyps and sinusitis, nasal eosinophilia, identical ASA provoked responses of the upper airway as those observed in most ASA sensitive asthmatics, and the capacity of the upper airway to be desensitized to ASA; cross-reactivity and/or crossdesensitization of the upper airway to indoAfter desensitization to ASA, 17 methacin. patients ingested ASA 325-2600mg daily for two or more weeks. Thirteen of the 17 (76%)reported improvement in their nasal symptoms during this open therapeutic trial. We propose that this subgroup of patients are a distinct part of the spectrum of ASA respiratory disease and some appear to benefit from ASA treatment.
274
275
C.R. Zeiss, N.D., J.L. halo, M.D., A. Cartier, M.D. and D. Levitz, B.S., Chicago, Illinois and Montreal, Quebec We studied two workers exposed to HDI in spray painting operations; one with hypersensitivity pneumonitis (HP) and late onset asthma reproduced by inhalation challenge and the other with immediate onset asthma. Sera from both workers was tested for total antibody binding of a radiolabeled HDI-human serum albumin conjugate, 1251 HDI-HSA, by an armnonium sulfate assay, and IgG and IgE antibody activity to HDI-HSA by an enzyme linked immunosorbent assay (ELISA). Sera from the first worker with HP and late onset asthma bound 100 ug of HDI-HSA/ml with IgG antibody activity as measured by ELISA at a serum dilution of 1:5000. The IgG antibody was cross reactive with a HSA diphenylmethane diisocyanate (MDI-HSA) conjugate. No IgE antibody activity was detected. There was a marked fall in both measures of antibody activity after removal from exposure. The worker with immediate onset asthma had IgG antibody activity to both HDI-HSA and MDI-HSA at a serum dilution of 1:lOO with IgE antibody activity to both conjugates at a serum dilution of 1:2. HDI inhalation can cause immunologic lung disease in exposed workers with an IgG and IgE antibody response which cross reacts with other isocyanates.
276
JtIDSEWmOCULTH)WITRdSPBMB:m PdBfEiW(llr~MppEARDRATuRINARY~
.
!Bhomas A.E. Platts-Mills. Joan II. LonRbottcmand SusanR. Wilkins, Charlottesville, USAend London UK. In domestic end laboratory animal houseswe have sampledairborne allergens at 17 litres/min using fibreglass filters or a casoadeimpactor. Antigen PI, the major allergen from the mite D.Dts~nYe6inuq, end a rat urinary allergen were measuredusing radioinmunoassays. was never detected (<3ng/m3) in un4Z2XZip' housesbut becameairborne during cleaning in quantities of 5-lOGng/m3. Greater than 90%of the airborne antigen PI was associated with feecal particles which are ZlOpmin diem. and following disturbance 9% of this allergen falls within 5 min. in ret housesallergen was alwaJrs detectable in the air (g-18ng/m3) end 55% was associated with particles of 5-10 m. Animal bedding contains very large quantities of allergen, up to 0.5g/rat box. &eking boxes of aZy bedding produced veq high levels of airborne allergen, 1,80&6,GGoag/m~. Whenthe bedding was dempmuchsmaller quantities were detected in the air. During disturbance 7596 of rat allergen was on particles
>IOpm
of these particles fell
&am.,
however
IMMUNOLOGIC EVALUATION OF LUNG DISEASE IN WORKERS EXPOSED TO HEXAMETHYLENE DIISOCYANATE (HDI).
9896
in 15 min. end at that
time allergen was predominantly on particles of 5-1Opm. Mite allergic asthmatic patients are
exposedin their housesto conoentrated allergen on large particles but only a fewnsnogrems per day would be expeoted to enter the lungs. e contra& in animal houses the qua&i* of airborne allergen on particles
157
--IN VITRO DEMONSTRATION OF SPECIFIC IgE IN A WORKEREXPOSED TO HIMIC ANHYDRIDE. J.S. Gallagher, Ph.D., D.R. Moller, M.D., K.D. Rosenman, M.D., D.I. Bernstein, M.D.,&K. O'Leary, M.S.and M.D. a Cincinnati, OH and Trenton, N.J. Clinical symptoms of rhinorrhea, lacrimation and wheezing occurred in a worker exposed to himic anhydride (HA). Consistent with occupational exposure, all symptoms abated during weekends and vacations. Himic anhydride is a phthalyl compound with a structure similar to phthalic anhydride (PA) except for a CH2 group in the center of the benzene ring. It is used as an ingredient for the production of a brominated fire retardant. Specific IgE to HA was measured by R&T. Positive RAST binding of 12% was realized with an HA human serum albumin (HSA) conjugate while non-exposed controls had neglible binding. RAST inhibition verified the specificity of this reaction. Inhibition of 72% was obtained with the HA-HSA conjugate and the sodium salt of HA (NaHA) inhibited the RAST by 85%. Cross reactivity between HA and other phthalyl compounds was measured by testing HA serum with PA and hexahydrophthalic anhydride (HHPA) albumin conjugates. RAST binding to PA-HSA was 18% while RAST binding to HHPA-HSA was 10%. Thus, another phthalyl ligand, HA, seems to induce IgE mediated industrial sensitivity. The HA sensitive serum demonstrated hapten specificity for HA, since the RAST was inhibited by NaHA, as well as cross reactivity with PA and HHPA.
274
275
C.R. Zeiss, N.D., J.L. halo, M.D., A. Cartier, M.D. and D. Levitz, B.S., Chicago, Illinois and Montreal, Quebec We studied two workers exposed to HDI in spray painting operations; one with hypersensitivity pneumonitis (HP) and late onset asthma reproduced by inhalation challenge and the other with immediate onset asthma. Sera from both workers was tested for total antibody binding of a radiolabeled HDI-human serum albumin conjugate, 1251 HDI-HSA, by an armnonium sulfate assay, and IgG and IgE antibody activity to HDI-HSA by an enzyme linked immunosorbent assay (ELISA). Sera from the first worker with HP and late onset asthma bound 100 ug of HDI-HSA/ml with IgG antibody activity as measured by ELISA at a serum dilution of 1:5000. The IgG antibody was cross reactive with a HSA diphenylmethane diisocyanate (MDI-HSA) conjugate. No IgE antibody activity was detected. There was a marked fall in both measures of antibody activity after removal from exposure. The worker with immediate onset asthma had IgG antibody activity to both HDI-HSA and MDI-HSA at a serum dilution of 1:lOO with IgE antibody activity to both conjugates at a serum dilution of 1:2. HDI inhalation can cause immunologic lung disease in exposed workers with an IgG and IgE antibody response which cross reacts with other isocyanates.
276
JtIDSEWmOCULTH)WITRdSPBMB:m PdBfEiW(llr~MppEARDRATuRINARY~
.
!Bhomas A.E. Platts-Mills. Joan II. LonRbottcmand SusanR. Wilkins, Charlottesville, USAend London UK. In domestic end laboratory animal houseswe have sampledairborne allergens at 17 litres/min using fibreglass filters or a casoadeimpactor. Antigen PI, the major allergen from the mite D.Dts~nYe6inuq, end a rat urinary allergen were measuredusing radioinmunoassays. was never detected (<3ng/m3) in un4Z2XZip' housesbut becameairborne during cleaning in quantities of 5-lOGng/m3. Greater than 90%of the airborne antigen PI was associated with feecal particles which are ZlOpmin diem. and following disturbance 9% of this allergen falls within 5 min. in ret housesallergen was alwaJrs detectable in the air (g-18ng/m3) end 55% was associated with particles of 5-10 m. Animal bedding contains very large quantities of allergen, up to 0.5g/rat box. &eking boxes of aZy bedding produced veq high levels of airborne allergen, 1,80&6,GGoag/m~. Whenthe bedding was dempmuchsmaller quantities were detected in the air. During disturbance 7596 of rat allergen was on particles
>IOpm
of these particles fell
&am.,
however
IMMUNOLOGIC EVALUATION OF LUNG DISEASE IN WORKERS EXPOSED TO HEXAMETHYLENE DIISOCYANATE (HDI).
9896
in 15 min. end at that
time allergen was predominantly on particles of 5-1Opm. Mite allergic asthmatic patients are
exposedin their housesto conoentrated allergen on large particles but only a fewnsnogrems per day would be expeoted to enter the lungs. e contra& in animal houses the qua&i* of airborne allergen on particles
157
--IN VITRO DEMONSTRATION OF SPECIFIC IgE IN A WORKEREXPOSED TO HIMIC ANHYDRIDE. J.S. Gallagher, Ph.D., D.R. Moller, M.D., K.D. Rosenman, M.D., D.I. Bernstein, M.D.,&K. O'Leary, M.S.and M.D. a Cincinnati, OH and Trenton, N.J. Clinical symptoms of rhinorrhea, lacrimation and wheezing occurred in a worker exposed to himic anhydride (HA). Consistent with occupational exposure, all symptoms abated during weekends and vacations. Himic anhydride is a phthalyl compound with a structure similar to phthalic anhydride (PA) except for a CH2 group in the center of the benzene ring. It is used as an ingredient for the production of a brominated fire retardant. Specific IgE to HA was measured by R&T. Positive RAST binding of 12% was realized with an HA human serum albumin (HSA) conjugate while non-exposed controls had neglible binding. RAST inhibition verified the specificity of this reaction. Inhibition of 72% was obtained with the HA-HSA conjugate and the sodium salt of HA (NaHA) inhibited the RAST by 85%. Cross reactivity between HA and other phthalyl compounds was measured by testing HA serum with PA and hexahydrophthalic anhydride (HHPA) albumin conjugates. RAST binding to PA-HSA was 18% while RAST binding to HHPA-HSA was 10%. Thus, another phthalyl ligand, HA, seems to induce IgE mediated industrial sensitivity. The HA sensitive serum demonstrated hapten specificity for HA, since the RAST was inhibited by NaHA, as well as cross reactivity with PA and HHPA.