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Urinary leukotriene E 4 and 9α, 11β‐prostaglandin F 2 concentrations in mild, moderate and severe asthma, and in healthy subjects
Author(s) -
Misso N. L. A.,
Aggarwal S.,
Phelps S.,
Beard R.,
Thompson P. J.
Publication year - 2004
Publication title -
clinical and experimental allergy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.462
H-Index - 154
eISSN - 1365-2222
pISSN - 0954-7894
DOI - 10.1111/j.1365-2222.2004.1912.x
Subject(s) - asthma , leukotriene e4 , medicine , urinary system , leukotriene , aspirin , urine , gastroenterology , basal (medicine) , prostaglandin , excretion , eicosanoid , respiratory disease , endocrinology , lung , enzyme , chemistry , arachidonic acid , insulin , biochemistry
Summary Background Airway inflammation in asthma is associated with cysteinyl leukotriene and prostaglandin D 2 production. Measurement of urinary metabolites of these eicosanoids may be useful for monitoring asthma patients. However, the influence of asthma phenotype and severity on basal urinary excretion of these metabolites is unknown. Objective To compare urinary leukotriene (LT)E 4 and 9α, 11β‐prostaglandin (PG)F 2 concentrations in large groups of mild, moderate and severe asthmatic patients and healthy control subjects. Methods Asthma severity, treatment and aspirin sensitivity were assessed by questionnaire in 168 asthmatic patients. Basal LTE 4 and 9α, 11β‐PGF 2 concentrations were measured in urine samples from these patients and from 175 control subjects using enzyme immunoassays. Results Urinary LTE 4 was correlated with 9α, 11β‐PGF 2 in both control subjects and asthmatic patients ( P <0.002). Median LTE 4 and 9α, 11β‐PGF 2 concentrations in patients with severe asthma were significantly reduced compared with mild asthmatic patients ( P <0.05 and <0.001, respectively). Urinary 9α, 11β‐PGF 2 , but not LTE 4 was lower in asthmatic patients using inhaled corticosteroids ( P <0.02). Multiple regression analysis indicated that urinary 9α, 11β‐PGF 2 concentration was negatively correlated with asthma severity ( P =0.003) and also with % predicted FEV 1 (forced expiratory volume in 1 s) ( P =0.005). Conclusions Baseline urinary LTE 4 and 9α, 11β‐PGF 2 concentrations are of limited value in discriminating between patients with different severities of asthma. Reduced urinary LTE 4 and 9α, 11β‐PGF 2 in patients with severe asthma suggest that direct or indirect effects of high‐dose corticosteroid therapy combined with other factors associated with severe asthma may influence eicosanoid production. However, the negative association of urinary 9α, 11β‐PGF 2 with lung function suggests an adverse effect of chronic PGD 2 production on lung function in asthma, irrespective of severity.