DÄ internationalArchive12/2008Aspirin Sensitive Asthma: In Reply

Correspondence

Aspirin Sensitive Asthma: In Reply

Dtsch Arztebl Int 2008; 105(12): 220-1. DOI: 10.3238/arztebl.2008.0221

Randerath, W J

LNSLNS We thank the correspondents commenting on our article on aspirin sensitive asthma. Dr Schmidt points out the option of detecting eosinophils in tissues and blood by using histocytochemical testing with the enzyme phenoloxidase. The finding could prove the involvement of eosinophil granulocytes in cytotoxic or antibody forming reactions, also in association with medical drugs. We thank the author for pointing this out. However, thus far the literature does not include reports of immune reactions on a cellular or serological basis in aspirin sensitive asthma. Specific IgE or IgG antibodies have not been found. The pathophysiological factors known so far include polymorphisms of key enzymes in the synthesis of leukotriene and the cysteinyl leukotriene receptors (1). Cyclo-oxygenase inhibition by using non-steroidal anti-inflammatory drugs results in excess production of cysteinyl leukotrienes (2), whose unfavourable effect is particularly pronounced owing to increased sensitivity of the mucosa. An accumulation of eosinophils in the tissue does not only mean increased production of cysteinyl leokotrienes but also of chemotactic factors and a delay in apoptosis, which substantially contributes to polyp formation and recurrence. The eosinophils therefore have a central role in the pathology (3).

Frick's reports on electroacupuncture according to Voll do not currently provide a prompt for us to change the methods described in our article. We have not found any further reports in the literature. A Medline search (19 December 2007, search terms "electroacupuncture" and "asthma") did not yield any articles on aspirin sensitive asthma. The data on the reaction to aspirin sensitive asthma as presented by Frick should be compared with the current diagnostic gold standard (provocation tests). Whether, in addition, destructive interference has an effect that is equal to that of adaptive deactivation will need to be investigated in a prospective study. DOI: 10.3238/arztebl.2008.0221


Prof. Dr. med. Winfried J. Randerath
Institut für Pneumologie an der
Universität Witten/Herdecke
Klinik für Pneumologie und Allergologie
Zentrum für Schlaf- und Beatmungsmedizin
Krankenhaus Bethanien
Aufderhöher Str. 169–175
42699 Solingen, Germany

Conflict of interest statement
As a member of the National Advisory Board-MSD Prof. Randerath receives honoraria for lecturing and reimbursement of travel expenses.
1.
Cowburn AS, Sladek K, Soja J et al.: Overexpression of leukotriene C4 synthase in bronchial biopsies from patients with aspirin-intolerant asthma. J Clin Invest 1998; 101: 834.
2.
Antczak A, Montuschi P, Kharitonov S et al.: Increased exhaled cysteinyl-leukotrienes and 8-isoprostane in aspirin-induced asthma. Am J Respir Crit Care Med 2002; 166: 301.
3.
Szczeklik A: Aspirin-induced asthma: an update and novel findings. In: Dahlén, SE et al. (Hrsg.): Advances in prostaglandin, thromboxane and leukotriene research. New York: Raven Press Ltd 1994; 227–40.
1. Cowburn AS, Sladek K, Soja J et al.: Overexpression of leukotriene C4 synthase in bronchial biopsies from patients with aspirin-intolerant asthma. J Clin Invest 1998; 101: 834.
2. Antczak A, Montuschi P, Kharitonov S et al.: Increased exhaled cysteinyl-leukotrienes and 8-isoprostane in aspirin-induced asthma. Am J Respir Crit Care Med 2002; 166: 301.
3. Szczeklik A: Aspirin-induced asthma: an update and novel findings. In: Dahlén, SE et al. (Hrsg.): Advances in prostaglandin, thromboxane and leukotriene research. New York: Raven Press Ltd 1994; 227–40.

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