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McFadden and Gilbert,
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We question the authors' statements about the role of interleukin-2 in allergic asthma. None of the cited papers have in fact reported that interleukin-2 prolongs the survival of eosinophils. Furthermore, interleukin-2 is not a feature of allergic asthma4. Activated, interleukin-2 receptor-positive T lymphocytes have been observed in allergic as well as in intrinsic asthma. Persons with intrinsic asthma were the only group with asthma that had increased levels of interleukin-2 in bronchoalveolar-lavage fluid3. Although fluid from both persons with extrinsic asthma and those with intrinsic asthma has been shown to contain interleukin-5 (the most specific cytokine to prolong eosinophil survival), interleukin-4 was elevated only in those with allergic asthma3.
These data suggest that the clinically defined syndrome of asthma includes two independent pathogenetic pathways with different profiles of cytokines. Allergic asthma involves an acute immunologic activation with the classic IgE-dependent and mast-cell-mediated response. Nonatopic asthma has many features of a chronic cell-mediated disease that may occur independently of antibody(IgE)-mediated immune mechanisms. Hence, intrinsic asthma may be related to an as yet unidentified antigen (or autoantigen)-mediated T-lymphocyte activation, possibly triggered by a respiratory tract infection. Both immunologic mechanisms, however, may have a common final pathway -- an eosinophil-dominated reaction of the bronchial tissue that results in the clinical expression of asthma.
Claus Kroegel, M.D., Ph.D.
J.-Christian Virchow, Jr., M.D.
University Medical Clinic
D-7800 Freiburg, Germany
Christoph Walker
Swiss Institute of Allergy and Asthma Research
CH-7270 Davos, Switzerland
References
Albin Leong, M.D.
6600 Bruceville Rd.
Sacramento, CA 95823
References
In Table 2 of the article, if the percentage predicted for the forced vital capacity (FVC) before bronchodilation is correct, the corresponding figure for an FVC of 100 percent after bronchodilation should be 5.18 rather than 5.78. Is this a transcriptional error?
None of the values for the FVC or the maximal forced expiratory flow (FEFmax) in Table 2 correspond to those in Figure 1 according to visual inspection. Were data for another patient inadvertently substituted?
The values for the FVC and vital capacity (VC), after correction for the (presumed) transcriptional error noted above, are identical. Although not stated, the FVC rather than the VC thus appears to have been used to compute the total lung capacity (TLC)1,2.
Jerome Reich, M.D.
Bess Kaiser Medical Center
Portland, OR 97227
References
To the Editor: We are grateful to Dr. Reich for bringing to our attention the inconsistencies between Figure 1 and Table 2. These data were obtained in the same patient but at different times. Instead of providing the spirographic and lung-volume measurements associated with the flow-volume curves in Figure 1, as we intended, we inadvertently substituted a set of observations in Table 2 that were obtained after a period of treatment. The typographic error was introduced when the data were transcribed (i.e., 5.18 was miswritten as 5.78). We regret the confusion that our oversight caused. Fortunately, the patterns of physiologic derangements that we wished to demonstrate were not affected. In Table 2, the TLC was calculated according to standard procedures that incorporate the slow VC. In this particular instance, the FVC and the VC were equal.
Dr. Leong appears to have placed far more weight on our statements concerning the use of combined therapy with cromolyn and inhaled steroids than we intended. We carefully summarized the relative advantages and disadvantages of both drugs and developed some theoretical considerations about possible positive interactions between cromolyn and steroids. If appropriately controlled trials show otherwise, so be it. Unfortunately, to our knowledge, such data are not yet available. Although the studies cited by Dr. Leong in support of his position are provocative, their impact is limited by such issues as study design, numbers of patients, and the end points chosen to demonstrate efficacy.
We agree with Dr. Kroegel and associates that not all asthma is related to atopy. However, before addressing their concern, we wish to point out that we incorrectly cited the work of Sears et al.1 linking asthma with elevated serum IgE levels in children. The population in this study was not preselected, as we had indicated, and it appears that in children, asthma and elevated IgE levels are strongly associated. Kroegel et al. are correct in their statements that there are no data relating the presence of interleukin-2 to allergic asthma or to eosinophil survival in a direct fashion. Our discussion of interleukin-2 was colored by its capacity to influence other cytokine-producing systems that have profound effects on eosinophils. We should have been more specific. We also took the finding of the expression of messenger RNA for interleukin-2 in various cells or tissues in atopic asthma2,3 as evidence that interleukin-2 was physically present. Of course, this need not be the case. We did not become aware of the interesting and important observations of Walker and colleagues4 on the differences in cytokine production between allergic and nonallergic asthma in time to include them in our review.
E.R. McFadden, Jr., M.D.
Ileen A. Gilbert, M.D.
University Hospitals of Cleveland
Cleveland, OH 44106
References
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