Nasal histamine (H), leukotriene C4 (I-LTC4) and SRS-A activity were studied in seven aspirin-(ASA)-intolerant patients (AIR) with rhinitis and in five ASA-tolerant control patients with chronic rhinitis after nasal provocation (NP) with a lysine acetylsalicylate solution. The same parameters were also studied after metabisulfite (MBS) NP in four sulfite-intolerant patients with rhinitis and in six control patients with chronic rhinitis. In six ASA-intolerant subjects and in four controls, we studied the PGD2 levels in nasal washes after ASA NP 0.2 mL of lysine acetylsalicylate solution (10 mg/mL) was sprayed intranasally in ASA-intolerant patients and controls and a 25-mg/mL MBS solution in sulfite intolerant patients and controls. Nasal wash fluids were obtained using 5 mL of 0.15 M saline before and 7 1/2 , 15, 30, and 60 minutes after nasal provocation. The nasal provocation with ASA induced itching and sneezing in four out of seven intolerant subjects. In this subgroup histamine values in nasal wash fluids were significantly higher versus the remaining ASA-intolerant patients at 30 and 60 minutes (P < .05 and P < .01, respectively) and versus controls at 60 minutes (P < .01). We found significantly higher I-LTC4 (P < .01) and SRS-A levels in nasal washes collected from ASA-intolerant subjects versus controls at 60 minutes after nasal provocation. There was no significant increase in the mean PGD2 values in either the ASA-intolerant or control groups. As far as ASA intolerance is concerned, we suggest that the late increase of some anaphylaxis mediators does not support the theory of an IgE-mediated mechanism; however, our data do not exclude a mast cell activation as a secondary amplification factor of an early unknown reaction. In sulfite-intolerant patients, an increase in histamine alone was observed in nasal fluids at 7 1/2 and 60 minutes after nasal provocation. In contrast, a less relevant histamine rise was detected also in the chronic rhinitic control group at 7 1/2 minutes only. This might be due to the irritant properties of the solution employed for nasal provocation.

Study of mediators of anaphylaxis in nasal wash fluids after aspirin and sodium metabisulfite nasal provocation in intolerant rhinitic patients. / C. Ortolani, C. Mirone, A. Fontana, G. Folco, A. Miadonna, N. Montalbetti, M. Rinaldi, A. Sala, A. Tedeschi, D. Valente. - In: ANNALS OF ALLERGY. - ISSN 0003-4738. - 59:5 Pt 2(1987), pp. 106-112.

Study of mediators of anaphylaxis in nasal wash fluids after aspirin and sodium metabisulfite nasal provocation in intolerant rhinitic patients.

G. Folco;A. Sala;A. Tedeschi
Penultimo
;
1987

Abstract

Nasal histamine (H), leukotriene C4 (I-LTC4) and SRS-A activity were studied in seven aspirin-(ASA)-intolerant patients (AIR) with rhinitis and in five ASA-tolerant control patients with chronic rhinitis after nasal provocation (NP) with a lysine acetylsalicylate solution. The same parameters were also studied after metabisulfite (MBS) NP in four sulfite-intolerant patients with rhinitis and in six control patients with chronic rhinitis. In six ASA-intolerant subjects and in four controls, we studied the PGD2 levels in nasal washes after ASA NP 0.2 mL of lysine acetylsalicylate solution (10 mg/mL) was sprayed intranasally in ASA-intolerant patients and controls and a 25-mg/mL MBS solution in sulfite intolerant patients and controls. Nasal wash fluids were obtained using 5 mL of 0.15 M saline before and 7 1/2 , 15, 30, and 60 minutes after nasal provocation. The nasal provocation with ASA induced itching and sneezing in four out of seven intolerant subjects. In this subgroup histamine values in nasal wash fluids were significantly higher versus the remaining ASA-intolerant patients at 30 and 60 minutes (P < .05 and P < .01, respectively) and versus controls at 60 minutes (P < .01). We found significantly higher I-LTC4 (P < .01) and SRS-A levels in nasal washes collected from ASA-intolerant subjects versus controls at 60 minutes after nasal provocation. There was no significant increase in the mean PGD2 values in either the ASA-intolerant or control groups. As far as ASA intolerance is concerned, we suggest that the late increase of some anaphylaxis mediators does not support the theory of an IgE-mediated mechanism; however, our data do not exclude a mast cell activation as a secondary amplification factor of an early unknown reaction. In sulfite-intolerant patients, an increase in histamine alone was observed in nasal fluids at 7 1/2 and 60 minutes after nasal provocation. In contrast, a less relevant histamine rise was detected also in the chronic rhinitic control group at 7 1/2 minutes only. This might be due to the irritant properties of the solution employed for nasal provocation.
Settore BIO/14 - Farmacologia
1987
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/176877
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