VOLUME 65

NUMBER 4 Correspondence 819

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FIG. 1. Cough score and provocative dose of methacholine causing a fall in FEV, values during captopril challenge and after withdrawal of the drug.

values until therapy was stopped. Both patients demon- strated marked bronchial hyperreactivity in the second week of treatment, as reflected by the provocative concentration of methachcrline causing a 20% fall in FEV, values (Fig. I). Bronchial responses did not become normal until 1 month after Icaptopril withdrawal. Peak expiratory flow rates and the other lung function tests were normal.

Cough is a prominent symptom of bronchial asthma and, indeed, may be the only symptom that is first observed. It is known that cough receptors are functionally different from irritant receptors and also that cough may occur indepen- dently of bronchoconstriction in subjects with asthma. How- ever, cough and bronchoconstriction reflexes are closely related and can potentiate each other. However, neither is entirely dependent on the other for its action. Coughing causes large variations in intrathoracic pressure that deforms the airways. Such deformation will produce a further stim- ulation of the deeper cough receptors, leading to more coughing and bronchoconstriction. This vicious circle ex- plains how coughing may precipitate bronchoconstriction in bronchial-hyperreactive individuals, such as subjects with stable asthma.’ In fact, a characteristic of the patients with cough associated with ACEI compared with the control sub- jects in twcl previous studies’, * was the initial bronchial hyperreactivity of the former group.

It is worth noting that neither of our patients had prior bronchial hyperreactivity; nevertheless, a clear relationship could be established between captopril treatment and the developmen: of both bronchial hyperreactivity and cough.

ACE is identical to kininase II, an enzyme that degradates

bradykinin and other peptides participating in inflammation. Therapy for the inhibition of ACE could potentiate the ef- fects of these substances in airways.“~ I’ Consequently, we hypothesize that ACE-inhibitory therapy causes cough and bronchial hyperreactivity in susceptible patients and that both effects can enhance each other. Moreover, ACE1 could be a powerful pharmacologic probe in the further investi- gations of mechanisms of cough and bronchial hyperreac- tivity.

Miguel Hinojosa, MD Santiago Quirce, MD

Jestis Puyana, MD Department of Allergy

Javier Codina, MD Department of Cardiology

Sergio Garcia Rull, MD Department of Pneumology

Servicio de Alergia Hospital Ram& y Cajal

Carretera Colmenar Km. 9,l 28034 Madrid, Spain

REFERENCES

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Sesoko S, Kaneyo Y. Cough associated with the use of cap- topril. Arch Intern Med 1985;145:1.524. Coulter DM, Edwards lR. Cough associated with captopril and enalapril. Br Med J 1987;294:1521. Semple PF, Herd GW. Cough and wheeze caused by inhibitors of angiotensin-converting enzyme. N Engl J Med 1986;314:61. Fuller RW, Choundry NBC. Increased cough reflex associated with angiotensin-converting enzyme-inhibitor cough. Br Med J 1987;295:1025. Morice AH, Brown MJ, Lowry R, Higenbottam T. Angiotensin-converting enzyme and the cough reflex. Lancet 1987;2:1116. Town GI, Hallwright CP, Mailing T. Angiotensin-converting enzyme inhibitors and cough. N Z Med J 1987;100:161. Bucknall CE, Neilly CB, Carter R, Stevenson RD, Semple PF. Bronchial hyperreactivity in patients who cough after receiving angiotensin-converting enzyme inhibitors. Br Med J 1988; 2%:86. Kaufman J, Casanova JE, Riendl P, Schlueter DP. Bronchial hrperreactivity and cough due to angiotensin-converting en- zyme inhibitors. Chest 1989;95:544. Cough and wheeze in asthma: are they interdependent? Lancet 1988;1:447. Fuller RW, Dixon CMS, Cuss FMC, Barnes PJ. Bradykinin- induced bronchcconsmction in humans. Am Rev Respir Dis 1987;135:176. Femer RE, Simpson JM, Rawlins MD. Effects of intradermal bradykinin after inhibition of angiotensin-converting enzyme. Br Med J 1987;294: 1119-20.

Pollinosis in Brazil: Changing concepts

To the Editor: Soon after I began to practice in Curitiba, Brazil, it be-

came clear that some patients had symptoms of classic sea- sonal allergic rhinitis and conjunctivitis during the spring

820 Correspondence

months (October, November, and December). The results of skin tests in those patients demonstrated markedly pos- itive immediate reactions to different grass-pollen extracts. There was an overlap in positive reactions with different species, but Lolium multtjlorum (Italian ryegrass) caused the most prominent immediate reactions followed by a late reaction in 15% of the patients.’

A search in the literature resulted in the concept that pollinosis was rare in Brazil.2 I then decided to investigate the possibility of a causal relationship between certain grass pollens and the clinical findings.

Since 1978, I have diagnosed grass hay fever in > 100 patients. It was a recent phenomenon (the third season in 72%), and most of these patients had never traveled abroad nor had they lived in a foreign country. Their ages varied between 6 and 65 years. Serum-specific IgE antibodies to Ldium were detected in 32 patients tested by RAST.

The clinical findings were substantiated by the docu- mentation of a grass-pollen season through a year-long, air- pollen survey.’ A search of area fields disclosed L. multi- fIorum as the most p.mvalent grass pollinating in spring that probably would account for the observed peak in pollen counts.

J. ALLERGY CLIN. IMMUNOL. APRIL 1990

In view of this new information in the incidence of pol- linosis in southern Brazil, these findings clearly demonstrate that the preconception must be changed.

It should be realized that during the last few decades, many of our forests have been destroyed and that man has introduced allergenic plants. This is the case with L. mul- tijorum a grass not endemic to Brazil, probably brought in by European immigrants, and now largely cultivated as a forage.

Nelson A. Rosario, MD Associate Professor of Pediatrics

Federal University of Parana Curitiba, Brazil

REFERENCES

Rosario NA. Report of 50 cases of grass pollinosis. Rev Bras Alerg Imunol 1987;10:25-9. Liia AO, Costa PD, Galeno R, Santos PP. Pollinosis in Brazil. Ann Allergy 1946;4:13-32. Rosario NA. Contagem de polens aereos na cidade de Curitiba. Rev Bras Alerg Imunol 1983;6: 12-5.