0
Communications to the Editor |

Methimazole-Induced Asthma? FREE TO VIEW

Mehmet Polatli, MD
Author and Funding Information

Affiliations: Adnan Menderes University Aydin, Turkey,  University of Catanzaro Catanzaro, Italy

Correspondence to: Mehmet Polatli, MD, Assistant Professor, ADU Tip Fak., Gogus Hastalıkları AD, 09010, Aydin, Turkey; e-mail: mpolatli@ttnet.net.tr



Chest. 2002;121(1):305-306. doi:10.1378/chest.121.1.305
Text Size: A A A
Published online

To the Editor:

I read with great interest the case report of Grembiale et al (May 2001).1 I have some questions to the authors about the clinical course of this patient. Although the patient received a diagnosis of bronchial asthma, I haven’t seen any ratio of FEV1 to FVC that is important for obstruction criteria of the airways. Moreover, if a patient has a multinodular goiter, inspiratory flow limitation must also be taken account. I haven’t seen any mention of it in the article. Do the authors suggest that there is no upper-airway obstruction in this patient? The authors also claimed that neither parasites nor other causes of systemic eosinophilic diseases were found. What were they… ie, vasculitis or others?

Although the patient has a diagnosis of asthma, I couldn’t understand why treatment with corticosteroids was discontinued instead of increasing the dosage. The benefits of corticosteroid drugs in the treatment of asthma have been documented previously. Knowing that the mortality of asthma is usually due to undertreatment with corticosteroids, osteoporosis or lack of response to treatment should not be a reason for discontinuing treatment with corticosteroids in this patient.

There are > 6 weeks from the onset of the symptoms after initial treatment with methimazole. Is it correct to use the phrase,“ methimazole-induced asthma”? What were the exclusion criteria of drug-induced eosinophilic lung disease?

Does the increasing eosinophil count in serum and sputum cause asthma, as the authors mentioned? If it is true, why was it resistant to corticosteroid treatment?

References

Grembiale, RD, Naty, S, Iorio, C, et al (2001) Bronchial asthma induced by an antithyroid drug.Chest119,1598-1599. [PubMed] [CrossRef]
 
To the Editor:

We are pleased to answer the questions about our report (May 2001)1 asked by Dr. Polatli, who allows us to give additional information about this case of methimazole-induced asthma. The presence of an obstructive ventilatory defect was undoubtable, as shown by the typical aspect of the flow-volume curve, characterized by a progressive reduction of forced expiratory flows: FVC, 56% predicted; FEV1, 48% predicted; FEV1/FVC ratio, 71%; mean expiratory flow (MEF) at 75% of FVC, 42% predicted; MEF at 50% of FVC, 14% predicted; and MEF at 25% of FVC, 10% predicted. The diagnosis of asthma was also confirmed by the prompt reversibility of airway obstruction obtained after the inhalation of a short-actingβ 2-adrenoceptor agonist (30% increase in FEV1). Since inspiratory flows were normal, it could be argued that the multinodular goiter did not produce any laryngeal or tracheal compression. Furthermore, classical, perinuclear, and atypical antineutrophil cytoplasmic antibodies were not detectable, thus probably ruling out the presence of a vasculitis.

Increased eosinophil levels, in both blood and bronchial submucosa, are often associated with atopic as well as nonatopic asthma.2 Indeed, the eosinophil represents one of the main cellular targets for the antiasthma action of corticosteroids, which effectively inhibit eosinophil mediator release and reduce, rather than completely suppressing, the increase in circulating eosinophil number.3 Consistently with these widely known effects, the blood eosinophil count decreased under systemic corticosteroid treatment in our patient (from 27.7 to 17%), who, therefore, was not resistant to corticosteroids, though no clinically significant benefit was detected. For this reason, methylprednisolone was stopped whereas inhaled steroid therapy was, of course, continued. However, we think that the main goal of a physician should be to find the causal factor of a pathologic event, thus trying whenever possible to eliminate it, rather than simply increasing the dosage of powerful drugs such as corticosteroids.

Finally, the apparently quite long period (approximately 7 weeks) elapsed from the beginning of methimazole administration to the onset of asthma exacerbation might have been due to underestimation of asthma symptoms, which could also have been partially masked by corticosteroid treatment. Anyway, some time is needed for eosinophil-induced tissue damage to reach the threshold of clinical significance. Hoping to have provided satisfactory answers to Dr. Polatli’s remarks, we look forward to welcoming further questions and comments about this interesting case of methimazole-induced asthma.

References
Grembiale, RD, Naty, S, Iorio, C, et al Bronchial asthma induced by an antithyroid drug.Chest2001;119,1598-1599. [PubMed] [CrossRef]
 
Humbert, M, Menz, G, Ying, S, et al The immunopathology of extrinsic (atopic) and intrinsic (non-atopic) asthma: more similarities than differences.Immunol Today1999;20,528-533. [PubMed]
 
Barnes, PJ, Pedersen, S, Busse, WW Efficacy and safety of inhaled corticosteroids: new developments.Am J Respir Crit Care Med1998;157,S1-S53. [PubMed]
 

Figures

Tables

References

Grembiale, RD, Naty, S, Iorio, C, et al (2001) Bronchial asthma induced by an antithyroid drug.Chest119,1598-1599. [PubMed] [CrossRef]
 
Grembiale, RD, Naty, S, Iorio, C, et al Bronchial asthma induced by an antithyroid drug.Chest2001;119,1598-1599. [PubMed] [CrossRef]
 
Humbert, M, Menz, G, Ying, S, et al The immunopathology of extrinsic (atopic) and intrinsic (non-atopic) asthma: more similarities than differences.Immunol Today1999;20,528-533. [PubMed]
 
Barnes, PJ, Pedersen, S, Busse, WW Efficacy and safety of inhaled corticosteroids: new developments.Am J Respir Crit Care Med1998;157,S1-S53. [PubMed]
 
NOTE:
Citing articles are presented as examples only. In non-demo SCM6 implementation, integration with CrossRef’s "Cited By" API will populate this tab (http://www.crossref.org/citedby.html).

Some tools below are only available to our subscribers or users with an online account.

Related Content

Customize your page view by dragging & repositioning the boxes below.

  • CHEST Journal
    Print ISSN: 0012-3692
    Online ISSN: 1931-3543