(Circulation. 1999;100:e146.)
© 1999 American Heart Association, Inc.
Circulation Electronic Pages |
Nuclear Cardiology and Nuclear Medicine Centre de Médecine Nucléaire de lArtois (CMNA), Arras, France
| Introduction |
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The review by Fishman1 seems to bring simple answers to a rather complex problem that deserves a more exhaustive analysis. This article establishes a link between an aminorex epidemic of pulmonary hypertension between 1965 and 1972 and the recent fenfluramine affair. By deductive reasoning, the author suggests that all of the complications attributed to fen-phen or fenfluramine alone (ie, pulmonary hypertension and cardiac valvular abnormalities) might simply be explained from a pathogenetic point of view within the framework of dietary pulmonary hypertension. The weakness of this argument must be underlined, because it completely ignores the epidemiological dimensions of the fenfluramine affair.
Fenfluramine was launched in France in 1963, 2 years before aminorex
was introduced in Switzerland, Austria, and Germany.2 A
few cases of pulmonary hypertension associated with
fenfluramine curiously appeared in the European literature in 1981,
although the drug had been prescribed for >500 000 patients. Between
1963 and 1996, fenfluramine was prescribed mainly in Europe in >50
million patients,2 and the prevalence of pulmonary
hypertension associated with fenfluramine was estimated at
2 cases
per million treated patients. International Primary Pulmonary
Hypertension Study (IPPHS) was a case-control study,3 and
its results, which are hypothetical, were not confirmed by other
studies or approaches. In science as in medicine, the results of only 1
study are largely insufficient to firmly establish facts or causality.
This is an inescapable scientific rule that is more important than the
biological credibility of any hypothesis or theory. Thus, there was no
fenfluramine epidemic
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