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Histamine levels following adenosine monophosphate challenge
ARTICLE IN PRESS Respiratory Medicine (2005) 99, 516
LETTER TO THE EDITOR Histamine levels following adenosine monophosphate challenge In commenting the results of our study on cysteinylleukotrienes and histamine following metacholine and AMP bronchial challenge Lee et al. are correct in pointing out that our findings do not rule out involvement of histamine in mediating the response following adenosine monophosphate (APM) challenge. The failure to detect increases in histamine following AMP challenge is probably due to the sensitivity of the assay or factors that may reduce the concentration of histamine in exhaled breath condensate. We agree that the failure to identify histamine in exhaled breath condensate certainly does not exclude a role for histamine release from mast cells activated by AMP. Recently, Crummy and collegues investigated the response to endobronchial AMP challenge in normal, atopic nonasthmatic and asthmatic subjects and found that histamine, tryptase, protein, and PGD2 concentrations all increased significantly after endobronchial AMP challenge in healthy subjects. However, the response in asthmatic and atopic nonasthmatic subjects was variable with no overall significant increase in mediator levels.1 Our
study is the first on post challenge histamine detection in exhaled breath condensate, and we agree with Dr. Lee and colleagues that further studies, both with invasive and noninvasive techniques, are necessary to understand which mediators are involved in responses to bronchial challenge.
Reference 1. Crummy F, Livingston M, Ennis M, Heaney LG. Mast cell mediator release in nonasthmatic subjects after endobronchial adenosine challenge. J Allergy Clin Immunol 2004;114:34–9.
Enrica Bucchioni, Luigi Allegra Department of Respiratory Medicine, Ospedale Policlinico, IRCCS, University of Milan, Milan, Italy E-mail address: [email protected] Peter J. Barnes, Zsuzsanne Csoma, Sergei A. Kharitonov Department of Thoracic Medicine, National Heart and Lung Institute, Imperial College, London, UK E-mail address: [email protected]
DOI of original article 10.1016/j.rmed.2004.09.004 0954-6111/$ - see front matter & 2004 Elsevier Ltd. All rights reserved. doi:10.1016/j.rmed.2004.09.003
LETTER TO THE EDITOR Histamine levels following adenosine monophosphate challenge In commenting the results of our study on cysteinylleukotrienes and histamine following metacholine and AMP bronchial challenge Lee et al. are correct in pointing out that our findings do not rule out involvement of histamine in mediating the response following adenosine monophosphate (APM) challenge. The failure to detect increases in histamine following AMP challenge is probably due to the sensitivity of the assay or factors that may reduce the concentration of histamine in exhaled breath condensate. We agree that the failure to identify histamine in exhaled breath condensate certainly does not exclude a role for histamine release from mast cells activated by AMP. Recently, Crummy and collegues investigated the response to endobronchial AMP challenge in normal, atopic nonasthmatic and asthmatic subjects and found that histamine, tryptase, protein, and PGD2 concentrations all increased significantly after endobronchial AMP challenge in healthy subjects. However, the response in asthmatic and atopic nonasthmatic subjects was variable with no overall significant increase in mediator levels.1 Our
study is the first on post challenge histamine detection in exhaled breath condensate, and we agree with Dr. Lee and colleagues that further studies, both with invasive and noninvasive techniques, are necessary to understand which mediators are involved in responses to bronchial challenge.
Reference 1. Crummy F, Livingston M, Ennis M, Heaney LG. Mast cell mediator release in nonasthmatic subjects after endobronchial adenosine challenge. J Allergy Clin Immunol 2004;114:34–9.
Enrica Bucchioni, Luigi Allegra Department of Respiratory Medicine, Ospedale Policlinico, IRCCS, University of Milan, Milan, Italy E-mail address: [email protected] Peter J. Barnes, Zsuzsanne Csoma, Sergei A. Kharitonov Department of Thoracic Medicine, National Heart and Lung Institute, Imperial College, London, UK E-mail address: [email protected]
DOI of original article 10.1016/j.rmed.2004.09.004 0954-6111/$ - see front matter & 2004 Elsevier Ltd. All rights reserved. doi:10.1016/j.rmed.2004.09.003