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bradykinin and other peptides participating in inflammation. Therapy for the inhibition of ACE could potentiate the effects 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 investigations of mechanisms of cough and bronchial hyperreactivity. Miguel Hinojosa, MD Santiago Quirce, MD Jestis Puyana, MD Department of Allergy Javier Codina, MD Department of Cardiology

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Sergio Garcia Rull, MD Department of Pneumology Servicio de Alergia Hospital Ram& y Cajal Carretera Colmenar Km. 9,l 28034 Madrid, Spain

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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.

REFERENCES I. SesokoS, Kaneyo Y. Cough associatedwith the use of cap-

topril. Arch Intern Med 1985;145:1.524. 2. Coulter DM, EdwardslR. Cough associatedwith captopril and

values until therapy was stopped. Both patients demonstrated 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 independently of bronchoconstriction in subjects with asthma. However, 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 stimulation of the deeper cough receptors, leading to more coughing and bronchoconstriction. This vicious circle explains 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 subjects 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

enalapril. Br Med J 1987;294:1521. 3. SemplePF, Herd GW. Cough and wheezecausedby inhibitors

of angiotensin-convertingenzyme. N Engl J Med 1986;314:61. 4. Fuller RW, Choundry NBC. Increasedcough reflex associated

with angiotensin-convertingenzyme-inhibitor cough. Br Med J 1987;295:1025. 5. Morice AH, Brown MJ, Lowry R, Higenbottam T. Angiotensin-converting enzyme and the cough reflex. Lancet 1987;2:1116. 6. Town GI, Hallwright CP, Mailing T. Angiotensin-converting enzyme inhibitors and cough. N Z Med J 1987;100:161. I. Bucknall CE, Neilly CB, Carter R, StevensonRD, SemplePF. Bronchial hyperreactivity in patientswho cough after receiving angiotensin-converting enzyme inhibitors. Br Med J 1988; 2%:86. 8. Kaufman J, CasanovaJE, Riendl P, Schlueter DP. Bronchial

hrperreactivity and cough due to angiotensin-convertingenzyme inhibitors. Chest 1989;95:544. 9. Cough and wheezein asthma:are they interdependent?Lancet 1988;1:447. 10. Fuller RW, Dixon CMS, Cuss FMC, Barnes PJ. Bradykinininduced bronchcconsmctionin humans. Am Rev Respir Dis 1987;135:176. II. Femer RE, SimpsonJM, Rawlins MD. Effects of intradermal bradykinin after inhibition of angiotensin-convertingenzyme. 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 became clear that some patients had symptoms of classic seasonal allergic rhinitis and conjunctivitis during the spring

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Correspondence

months (October, November, and December). The results of skin tests in those patients demonstratedmarkedly positive immediatereactions to different grass-pollenextracts. 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 causalrelationship betweencertain grass pollens and the clinical findings. Since 1978, I have diagnosedgrass hay fever in > 100 patients. It was a recent phenomenon(the third seasonin 72%), and most of thesepatients had never traveled abroad nor had they lived in a foreign country. Their ages varied between 6 and 65 years. Serum-specificIgE antibodies to Ldium were detectedin 32 patients tested by RAST. The clinical findings were substantiatedby the documentation of a grass-pollenseasonthrough a year-long, airpollen survey.’ A searchof area fields disclosed L. multifIorum as the most p.mvalentgrasspollinating 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 pollinosis in southernBrazil, thesefindings clearly demonstrate that the preconceptionmust be changed. It should be realized that during the last few decades, many of our forests have been destroyedand that man has introduced allergenic plants. This is the casewith L. multijorum a grassnot 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

RosarioNA. Reportof 50 casesof grasspollinosis.RevBras Alerg Imunol 1987;10:25-9. Liia AO, CostaPD,GalenoR, SantosPP.Pollinosisin Brazil. Ann Allergy 1946;4:13-32. RosarioNA. Contagem depolensaereosnacidadedeCuritiba. RevBrasAlerg Imunol 1983;6:12-5.

Pollinosis in Brazil: changing concepts.

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