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Universidad Central de Venezuela, Caracas, Venezuela University of Houston, Houston, TX
Correspondence to: Alex E. Lechin, MD, FCCP, Department of Clinical Science, University of Houston, 2717 Albans Rd, Houston, TX 77005
To The Editor:
We read with great interest the review article by Boushey (March 2003)1 dealing with new exploratory therapies for asthma. With respect to it, we regret that the author omitted the successful results obtained by our research group, referring to the treatment of bronchial asthma with tianeptine. This drug, a serotonin (5-HT) uptake enhancer, triggers absolute and total disappearance of asthma attacks within 30 to 60 min after oral intake.
Up to the present, we have successfully treated some 20,000 severe asthmatic (children and adults) with this drug, without failures.2 Even more, at the present time we outlined a national program, addressed to eradicate this disease from our country. With respect to the above, we have published many scientific articles dealing with the pathophysiologic mechanisms involved in the infallibility of this therapeutic manipulation.
In 1994, we presented results dealing with the increasing levels of catecholamines and free-serotonin (f-5HT) in plasma during asthma attacks.3 In 1996, we demonstrated that increased levels of f-5HT in plasma, during asthma attacks, were associated with clinical severity and pulmonary function.4 In 1998, we published two research articles showing that tianeptine (a serotonin uptake enhancing drug, which reduces plasma f-5HT) provoked a dramatic and sudden decrease of both clinical rating and f-5HT plasma levels as well as an increase in pulmonary function.5 6 Conversely, buspirone and serotonin-uptake inhibitors (like sertraline, paroxetine, etc), drugs that increase f-5HT in plasma, trigger asthma attacks in asthmatic patients.7 8 9 These undesirable effects were annulled by atropine.10
In 1999, Dupont et al11 demonstrated that serotonin produced frequency- and concentration-dependent facilitation of cholinergic contractions of human airways. This facilitatory effect of 5-HT was mimicked by both 5-HT3 and 5-HT4 agonists. These findings demonstrated that 5-HT facilitates cholinergic contractions in the human airways. In 2000, Cazzola and Matera12 published an article dealing with the role played by 5-HT in asthma and other bronchial disorders. Finally, it has been exhaustively demonstrated that all drugs that increase f-5HT plasma levels trigger not only bronchoconstriction but pulmonary vasoconstriction also, both of which are greatly annulled by tianeptine, a drug that decreases f-5HT plasma level.13 14 15 16 17 18 19 With respect to the latter, it should be remembered that acetylcholine stimulates the release of 5HT from the neuroepithelial autocrine serotonergic cells located at the bronchopulmonary system and, in turn, serotonin triggers acetylcholine release from the parasympathetic terminals.20
References
University of California San Francisco, San Francisco, CA
Correspondence to: Homer A. Boushey, MD, University of California San Francisco, Division of Allergy and Immunology, 505 Parnassus Ave, M-1292, San Francisco, CA 94143
To the Editor:
I have carefully reviewed the letter from Drs. Lechin and van der Dijs and the literature that they cite. Of the citations, only two are to articles describing trials of asthma therapy that were published in peer-reviewed journals (their refs 5 , 6 ). These two articles were published within 4 months of each other, have identical authors, describe findings from the same intervention in the same number of subjects, and have abstracts that read nearly identically. The two articles appear to describe the same study.
Of the remaining references, seven appear not to deal directly with asthma (refs 7 8 9 10 , 14 , 19 , 20 ), seven are letters to the editor (refs 13 14 15 16 17 18 ), one is an abstract (ref 3 ), and one is a book authored by Drs. Lechin and van der Dijs (ref 2 ). I cannot comment on their use of tianeptine in 20,000 patients with severe asthma, nor on its use in a national program to eradicate the disease in their country, for the book that they cite is not yet available to me. I am sure, however, that Drs. Lechin and van der Dijs would want to share with the rest of the medical world a treatment for asthma unfailingly successful. The usual way to share such information is through publishing in peer-reviewed journals large, controlled, prospective, blinded studies demonstrating efficacy. For such a remarkably effective treatment, this should be easy to accomplish. I, for one, would read such reports with the keenest interest.
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