title: Prevention of severe premenstrual asthma attacks by leukotriene receptor antagonist.
abstract: BACKGROUND
  The etiology and treatment of premenstrual exacerbations of asthma (PMA) remain uncertain.
  
  
  OBJECTIVE
  We investigated the role of cellular mediators released from inflammatory cells in the airflow limitation during PMA.
  
  
  METHODS
  Serum levels of leukotriene (LT) B(4), LTC(4), platelet- activating factor, histamine, IL-1beta, IL-4, IL-5, IL-6, and GM-CSF were measured at different time points, first just before or during menstruation when the peak expiratory flow rate (PEFR) began to decrease precipitously and second during the menstrual midcycle week (days 10-16) when the PEFR returned to baseline values in patients with PMA and in age-matched asthma patients without PMA at the same intervals.
  
  
  RESULTS
  Serum levels of LTC(4) were significantly higher during exacerbations of asthma than after recovery (69.0 +/- 16.0 pg/mL vs 24.0 +/- 9.5 pg/mL, P <.05), whereas those of IL-1beta, IL-4, IL-5, IL-6, GM-CSF, histamine, LTB(4), and platelet-activating factor did not differ between 2 periods in 5 patients with PMA. In contrast, in 5 asthmatic patients without PMA serum levels of cellular mediators did not differ between corresponding periods. Oral administration of pranlukast, an LT receptor antagonist (225 mg twice daily), significantly reduced decreases in PEFR from the baseline values (110 +/- 21 L/min with pranlukast vs 233 +/- 20 L/min without pranlukast, P <.01) in association with an improvement of asthma symptom scores (6.5 +/- 1. 1 with pranlukast vs 9.8 +/- 0.7 without pranlukast, P <0.05) in 5 patients with PMA.
  
  
  CONCLUSIONS
  LTs are partly involved in the pathogenesis of PMA, and LT receptor antagonists may be useful for preventing airflow obstruction in patients with PMA.
authors.affiliation: Department of Geriatric Medicine and the First Department of Internal Medicine, Tohoku University School of Medicine, Sendai, Japan.
authors.forename: H
authors.initials: H
authors.lastname: Nakasato
authors.forename: T
authors.initials: T
authors.lastname: Ohrui
authors.forename: K
authors.initials: K
authors.lastname: Sekizawa
authors.forename: T
authors.initials: T
authors.lastname: Matsui
authors.forename: M
authors.initials: M
authors.lastname: Yamaya
authors.forename: G
authors.initials: G
authors.lastname: Tamura
authors.forename: H
authors.initials: H
authors.lastname: Sasaki
mesh_terms: D000293:Adolescent; D000328:Adult; D018927:Anti-Asthmatic Agents / Q000627:therapeutic use*; D001249:Asthma / Q000097:blood / Q000188:drug therapy / Q000503:physiopathology / Q000517:prevention & control*; D002867:Chromones / Q000627:therapeutic use*; D016207:Cytokines / Q000097:blood; D005260:Female; D006632:Histamine / Q000097:blood; D006801:Humans; D020024:Leukotriene Antagonists / Q000627:therapeutic use*; D007975:Leukotriene B4 / Q000097:blood; D017997:Leukotriene C4 / Q000097:blood; D008407:Mast Cells / Q000378:metabolism; D008598:Menstruation; D010366:Peak Expiratory Flow Rate / Q000502:physiology; D013601:T-Lymphocytes / Q000378:metabolism
chemical_list: D018927:Anti-Asthmatic Agents; D002867:Chromones; D016207:Cytokines; D020024:Leukotriene Antagonists; D007975:Leukotriene B4; D017997:Leukotriene C4; D006632:Histamine; C047681:pranlukast