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Possible involvement of mast-cell activation in aspirin provocation of aspirin-induced asthma.
Allergy. 2001 Nov; 56(11):1061-7.A

Abstract

BACKGROUND

Although there is increasing evidence of the importance of cysteinyl leukotrienes (LT) as mediators of aspirin-induced bronchoconstriction in aspirin-sensitive asthma, the cellular origin of the LT is not yet clear.

METHODS

Urinary concentrations of leukotriene E4 (LTE4), 11-dehydrothromboxane B2, 9alpha,11beta-prostaglandin F2, and Ntau-methylhistamine were measured during the 24 h following cumulative intravenous administration of increasing doses of lysine aspirin to asthmatic patients. In addition, the urinary concentrations of these metabolites were measured on 5 consecutive days in a patient who suffered an asthma attack after percutaneous administration of nonsteroidal anti-inflammatory drugs.

RESULTS

In aspirin-induced asthma patients (AIA, n=10), the basal concentration of urinary LTE4, but not the other metabolites, was significantly higher than that in aspirin-tolerant asthma patients (ATA, n=10). After intravenous aspirin provocation, the AIA group showed a 13.1-fold (geometric mean) increase in excretion of LTE4 during the first 3 h, and 9alpha,11beta-prostaglandin F2 also increased in the AIA group during the first 0-3 h and the 3-6 h collection period. Ntau-methylhistamine excretion was also increased, but to a lesser degree. Administration of aspirin caused significant suppression of 11-dehydrothromboxane B2 excretion in both the AIA and ATA groups. When the percentage of maximum increase of each metabolite from the baseline concentrations was compared between the AIA group and the ATA group, a significantly higher increase in excretion of LTE4, 9alpha,11beta-prostaglandin F2, and Ntau-methylhistamine was observed in the AIA group than the ATA group. An increased excretion of LTE4 and 9alpha,11beta-prostaglandin F2 has been detected in a patient who suffered an asthma attack after percutaneous administration of nonsteroidal anti-inflammatory drugs.

CONCLUSIONS

Considering that human lung mast cells are capable of producing LTC4, prostaglandin D2, and histamine, our present results support the concept that mast cells, at least, may participate in the development of aspirin-induced asthma.

Authors+Show Affiliations

Clinical Research Center, National Sagamihara Hospital, Japan.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Evaluation Study
Journal Article

Language

eng

PubMed ID

11703219

Citation

Mita, H, et al. "Possible Involvement of Mast-cell Activation in Aspirin Provocation of Aspirin-induced Asthma." Allergy, vol. 56, no. 11, 2001, pp. 1061-7.
Mita H, Endoh S, Kudoh M, et al. Possible involvement of mast-cell activation in aspirin provocation of aspirin-induced asthma. Allergy. 2001;56(11):1061-7.
Mita, H., Endoh, S., Kudoh, M., Kawagishi, Y., Kobayashi, M., Taniguchi, M., & Akiyama, K. (2001). Possible involvement of mast-cell activation in aspirin provocation of aspirin-induced asthma. Allergy, 56(11), 1061-7.
Mita H, et al. Possible Involvement of Mast-cell Activation in Aspirin Provocation of Aspirin-induced Asthma. Allergy. 2001;56(11):1061-7. PubMed PMID: 11703219.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Possible involvement of mast-cell activation in aspirin provocation of aspirin-induced asthma. AU - Mita,H, AU - Endoh,S, AU - Kudoh,M, AU - Kawagishi,Y, AU - Kobayashi,M, AU - Taniguchi,M, AU - Akiyama,K, PY - 2001/11/13/pubmed PY - 2002/1/30/medline PY - 2001/11/13/entrez SP - 1061 EP - 7 JF - Allergy JO - Allergy VL - 56 IS - 11 N2 - BACKGROUND: Although there is increasing evidence of the importance of cysteinyl leukotrienes (LT) as mediators of aspirin-induced bronchoconstriction in aspirin-sensitive asthma, the cellular origin of the LT is not yet clear. METHODS: Urinary concentrations of leukotriene E4 (LTE4), 11-dehydrothromboxane B2, 9alpha,11beta-prostaglandin F2, and Ntau-methylhistamine were measured during the 24 h following cumulative intravenous administration of increasing doses of lysine aspirin to asthmatic patients. In addition, the urinary concentrations of these metabolites were measured on 5 consecutive days in a patient who suffered an asthma attack after percutaneous administration of nonsteroidal anti-inflammatory drugs. RESULTS: In aspirin-induced asthma patients (AIA, n=10), the basal concentration of urinary LTE4, but not the other metabolites, was significantly higher than that in aspirin-tolerant asthma patients (ATA, n=10). After intravenous aspirin provocation, the AIA group showed a 13.1-fold (geometric mean) increase in excretion of LTE4 during the first 3 h, and 9alpha,11beta-prostaglandin F2 also increased in the AIA group during the first 0-3 h and the 3-6 h collection period. Ntau-methylhistamine excretion was also increased, but to a lesser degree. Administration of aspirin caused significant suppression of 11-dehydrothromboxane B2 excretion in both the AIA and ATA groups. When the percentage of maximum increase of each metabolite from the baseline concentrations was compared between the AIA group and the ATA group, a significantly higher increase in excretion of LTE4, 9alpha,11beta-prostaglandin F2, and Ntau-methylhistamine was observed in the AIA group than the ATA group. An increased excretion of LTE4 and 9alpha,11beta-prostaglandin F2 has been detected in a patient who suffered an asthma attack after percutaneous administration of nonsteroidal anti-inflammatory drugs. CONCLUSIONS: Considering that human lung mast cells are capable of producing LTC4, prostaglandin D2, and histamine, our present results support the concept that mast cells, at least, may participate in the development of aspirin-induced asthma. SN - 0105-4538 UR - https://www.unboundmedicine.com/medline/citation/11703219/Possible_involvement_of_mast_cell_activation_in_aspirin_provocation_of_aspirin_induced_asthma_ L2 - https://onlinelibrary.wiley.com/resolve/openurl?genre=article&sid=nlm:pubmed&issn=0105-4538&date=2001&volume=56&issue=11&spage=1061 DB - PRIME DP - Unbound Medicine ER -