© 2007 American Thoracic Society
Racemic = R Enantiomer: A Dual CitationTo the Editor:Like any author, I was delighted to see my article on enantiomeric forms of albuterol cited in the recent Pro-Con Editorial debate in the AJRCCM (1, 2), but I am nonetheless perplexed over why the data were used to support both sides of the argument. As the first author and corresponding author of our article (3)—which includes the name and contribution of a senior Sepracor scientist—I can categorically say that the statements suggesting that our work supports the notion that R enantiomer suppresses proinflammatory activity in eosinophils are misleading (1). The implication is that R enantiomer behaves differently than the racemic form, because there is no mention at this point that we found the two to be equivalent (3). Our study, which utilized 26 subjects, both atopic and nonatopic, categorically showed that there was no difference between R- and R,S-(racemic) albuterol in blocking degranulation of freshly isolated human eosinophils. Both R- and R,S-albuterol blocked equivalently secretion of eosinophil peroxidase (EPO) caused by formyl-met-leu-phe (FMLP). Later in their argument, Pro side proponents Drs. Ameredes and Calhoun indicate that "some effects of R-albuterol and racemate were statistically indistinct," again referencing our article. The lack of statistical significance should have accompanied the first statement, as should the mention that no data taken from this article showed any difference in the inhibitory ability of R-albuterol over the racemic mixture. It also has been suggested (fortunately not in this argument) that our study showed that the S enantiomer augmented secretion of EPO in isolated human eosinophils activated by FMLP. The small difference in secretion was swamped by a standard error that was greater than twice the "augmented" difference in secretion in both atopic and nonatopic subjects. The large size of the samples for a study of this sort makes a type II error highly unlikely, given the obvious and equivalent differences in inhibition caused by R- and R,S-albuterol. However, even if there were a statistically significant difference, the magnitude of difference would be physiologically irrelevant. Professor Barnes, in his Con argument (2), succinctly and accurately summarizes the data from this study: "... S albuterol was without effect," as did we in the final sentence of our abstract: "Our data demonstrate that both R and R,S-albuterol are equivalently effective in inhibiting stimulated secretion of EPO in both normal and allergic subjects and that there is no paradoxical augmenting effect of S-albuterol in stimulated eosinophil secretion." We found R-albuterol to be equivalent to R,S-albuterol in preventing eosinophil degranulation and that S-albuterol had no proinflammatory effect.
The University of Chicago, Chicago, Illinois FOOTNOTES Conflict of Interest Statement: A.R.L. has received basic research grants from GlaxoSmithKline ($1,760,000 in the past 3 years) and a prior research grant for approximately $75,000 from Sepracor more than 5 years previously. REFERENCES
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