A Szczeklik, L Mastalerz, E Nizankowska and A Cmiel
Department of Medicine, Jagiellonian University School of Medicine, Cracow, Poland.

We performed a double-blind, two-phase study on protective and bronchodilator effects of prostaglandins E2 and E1 (PGE2, PGE1) and salbutamol in patients with aspirin-induced asthma (AIA). In phase 1 we assessed the effects of pretreatment with PGE2, salbutamol, or the PGE1- analogue, misoprostol, on bronchoconstriction precipitated by inhalation of L-lysine aspirin in 11 patients with AIA. PGE2 and salbutamol were inhaled at equimolar concentrations of 0.25 mumol, 5 min before the aspirin challenge, while 400 micrograms misoprostol was administered orally 1 h before challenge. PGE2 attenuated the bronchoconstrictive reactions in 10 patients, salbutamol in eight, and misoprostol in seven. The mean provocative dose of aspirin causing a 20% fall in FEV1 (PD20) decreased after PGE2 (p = 0.04) and salbutamol (p = 0.06), but only marginally after misoprostol (p = 0.25). There was a positive correlation between magnitude of the protection offered by the three compounds in individual subjects. In phase 2, we examined bronchial response to inhaled PGE2, PGE1, salbutamol, and 2% ethanol in 12 AIA patients compared with 10 aspirin-tolerant patients with asthma. AIA subjects were characterized by less pronounced and shorter bronchodilator responses. There was no correlation between the protective and bronchodilator actions of the compounds used in individual patients. Thus, inhaled PGE2 and salbutamol protect against aspirin-induced attacks of asthma through mechanisms unrelated to their bronchodilator properties. Airways of aspirin-sensitive patients with asthma demonstrate distinct bronchial reactivity.

This article has been cited by other articles:

				L Mastalerz, M Sanak, A Gawlewicz-Mroczka, A Gielicz, A Cmiel, and A Szczeklik Prostaglandin E2 systemic production in patients with asthma with and without aspirin hypersensitivity Thorax, January 1, 2008; 63(1): 27 - 34. [Abstract] [Full Text] [PDF]

				C. Feng, E. M. Beller, S. Bagga, and J. A. Boyce Human mast cells express multiple EP receptors for prostaglandin E2 that differentially modulate activation responses Blood, April 15, 2006; 107(8): 3243 - 3250. [Abstract] [Full Text] [PDF]

				H. Harizi, M. Juzan, J.-F. Moreau, and N. Gualde Prostaglandins Inhibit 5-Lipoxygenase-Activating Protein Expression and Leukotriene B4 Production from Dendritic Cells Via an IL-10-Dependent Mechanism J. Immunol., January 1, 2003; 170(1): 139 - 146. [Abstract] [Full Text] [PDF]

				K. Gomi, F.-G. Zhu, and J. S. Marshall Prostaglandin E2 Selectively Enhances the IgE-Mediated Production of IL-6 and Granulocyte-Macrophage Colony-Stimulating Factor by Mast Cells Through an EP1/EP3-Dependent Mechanism J. Immunol., December 1, 2000; 165(11): 6545 - 6552. [Abstract] [Full Text] [PDF]

				M. L. KOWALSKI, R. PAWLICZAK, J. WOZNIAK, K. SIUDA, M. PONIATOWSKA, J. IWASZKIEWICZ, T. KORNATOWSKI, and M. A. KALINER Differential Metabolism of Arachidonic Acid in Nasal Polyp Epithelial Cells Cultured from Aspirin-sensitive and Aspirin-tolerant Patients Am. J. Respir. Crit. Care Med., February 1, 2000; 161(2): 391 - 398. [Abstract] [Full Text]

				W. Wasiak and M. Szmidt A six week double blind, placebo controlled, crossover study of the effect of misoprostol in the treatment of aspirin sensitive asthma Thorax, October 1, 1999; 54(10): 900 - 904. [Abstract] [Full Text]

				P. J. Barnes, K. F. Chung, and C. P. Page Inflammatory Mediators of Asthma: An Update Pharmacol. Rev., December 1, 1998; 50(4): 515 - 596. [Abstract] [Full Text] [PDF]

				A. SZCZEKLIK, R. DWORSKI, L. MASTALERZ, A. PROKOP, J. R. SHELLER, E. NIZANKOWSKA, A. CMIEL, and J. A. OATES Salmeterol Prevents Aspirin-induced Attacks of Asthma and Interferes with Eicosanoid Metabolism Am. J. Respir. Crit. Care Med., October 1, 1998; 158(4): 1168 - 1172. [Abstract] [Full Text] [PDF]