American Journal of Epidemiology Advance Access originally published online on November 9, 2006
American Journal of Epidemiology 2006 164(12):1253-1254; doi:10.1093/aje/kwk094
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LETTERS TO THE EDITOR |
THREE AUTHORS REPLY
1 Department of Epidemiology, Harvard School of Public Health, Boston, MA 02115
2 Boston Collaborative Drug Surveillance Program, Boston University, Lexington, MA 02421
(e-mail: aalogut{at}alumni.unav.es)
We thank Parratt et al. (1) for their interest in our study (2), in which we found a 50 percent reduction in the risk of multiple sclerosis among penicillin users (at least 3 weeks of use) compared with nonusers during the 3 years before the onset of the disease. Our study findings did not support our original hypothesis that use of antibiotics effective against Chlamydophila pneumoniae was associated with a lower risk of multiple sclerosis. However, this lack of evidence cannot be construed as proof of the absence of an association between chronic infection by C. pneumoniae and multiple sclerosis, as Parratt et al. point out in their letter (1), and as we acknowledge in our paper (2). For example, if the microorganism increases multiple sclerosis risk through chronic stimulation of the immune system, our study design may be unable to find an association, because it is known that short-term treatment for acute respiratory illness (the usual clinical manifestation of C. pneumoniae infection) does not suffice to eliminate this organism in patients with chronic infection (3). Similar arguments have been repeatedly raised to explain the lack of effect of antichlamydial antibiotics in the secondary prevention of cardiovascular outcomes (4).
Another issue raised by Parratt et al. (1) is the lack of consistency in results from epidemiologic studies on C. pneumoniae and multiple sclerosis risk. Because a clinical trial may be unfeasible or extremely costly if the effect of C. pneumoniae on the risk of multiple sclerosis were evident only after a very long incubation period (5), truly prospective observational studies with repeated measures of the serologic status of C. pneumoniae infection before the onset of multiple sclerosis are needed. This prospective approach, with quantitative assessment of antibodies against the infective agent, has provided valuable insight into the potential link between Epstein-Barr virus and the risk of multiple sclerosis (6).
In summary, our paper did not provide evidence for the involvement, or lack of it, of C. pneumoniae in multiple sclerosis pathogenesis. However, our findings regarding penicillin use and multiple sclerosis risk require further attention and, probably, confirmation in other populations.
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ACKNOWLEDGMENTS |
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Conflict of interest: none declared.
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References |
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 TOP References |
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- Parratt JDE, O'Riordan JI, Swingler RJ, et al. (2006) Re: "Antibiotic use and risk of multiple sclerosis." (Letter). Am J Epidemiol 164:1253.
[Free Full Text] - Alonso A, Jick SS, Jick H, et al. (2006) Antibiotic use and risk of multiple sclerosis. Am J Epidemiol 163:997–1002.
[Abstract/Free Full Text] - Kutlin A, Roblin PM, Hammerschlag MR. (2002) Effect of prolonged treatment with azithromycin, clarithromycin, or levofloxacin on Chlamydia pneumoniae in a continuous-infection model. Antimicrob Agents Chemother 46:409–12.
[Abstract/Free Full Text] - Grayston JT. (2003) Antibiotic treatment of atherosclerotic cardiovascular disease. Circulation 107:1228–30.
- Munger KL, DeLorenze GN, Levin LI, et al. (2004) A prospective study of Chlamydia pneumoniae infection and risk of MS in two cohorts. Neurology 62:1799–803.
[Abstract/Free Full Text] - Levin LI, Munger KL, Rubertone MV, et al. (2005) Temporal relationship between elevation of Epstein-Barr virus antibody titers and initial onset of neurological symptoms in multiple sclerosis. JAMA 293:2496–500.
[Abstract/Free Full Text]
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