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Fatima Cintra, MD
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From the Department of Psychobiology, Federal University of São Paulo.

Correspondence to: Fatima Cintra, Federal University of São Paulo-Psychobiology, R. Napoleão de Barros, 925 V. Clementino, São Paulo, São Paulo 04024002, Brazil; e-mail: fatimacintra@interair.com.br


Financial/nonfinancial disclosures: The author has reported to CHEST that no potential conflicts of interest exist with any companies/organizations whose products or services may be discussed in this article.

Reproduction of this article is prohibited without written permission from the American College of Chest Physicians (http://www.chestpubs.org/site/misc/reprints.xhtml).


© 2011 American College of Chest Physicians


Chest. 2011;140(1):268-269. doi:10.1378/chest.11-0738
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To the Editor:

I read with interest the comments of Drs Alrajab, Uysal, and Jenks about our article,1 and I appreciate the contribution on our work. However, I would like to clarify some important points.

First, I agree that tobacco smoking may influence homocysteine and cysteine concentration, which is the reason why smoking was considered an exclusion criterion in this study and is not considered a confounding factor in our results. Moreover, the mechanisms involved in the relationship between smoking and homocysteine/cysteine concentration are still under investigation, and cigarette smoking seems to be a strong determinant of plasma homocysteine level, but the impact on plasma cysteine level should be better demonstrated.2

Second, I also agree that cysteine may be affected by many other conditions, such as arterial hypertension and age, and could be considered a risk factor for atherosclerosis in patients with hyperlipidemia.3 Moreover, obstructive sleep apnea (OSA) may lead to a number of cardiovascular consequences, such as arterial hypertension and atherosclerosis.4 Therefore, it seems to be another “chicken and egg” puzzle. In order to clarify this confusing relationship among cysteine, cardiovascular consequences, and OSA, we performed a longitudinal study with an effective continuous positive airway pressure treatment of 6 months, with a minimum usage of 5.4 h/night. Continuous positive airway pressure significantly decreased plasma cysteine levels after 6 months of treatment, suggesting that OSA directly affected cysteine plasma levels.

Third, the mechanisms explaining the increase in plasma cysteine levels and the corresponding absence of changes in homocysteine concentration and the related vitamin profiles are under investigation, but based on experiments by Perry et al,5 OSA could directly affect cysteine concentration as mentioned in the “Discussion” section of the article. In this study, the combination of sleep deprivation and hypoxia increased cysteine concentration, whereas homocysteine remained unchanged.

Finally, the biomarkers are very important indicators of abnormal biologic processes. A good biomarker should be precise, be reliable, have great potential in predicting chances for diseases, and be affected by the appropriated treatment. OSA is a multifactorial disease with not only cardiovascular consequences but also cognitive, neurologic, and metabolic consequences. A single biomarker that fulfills all the criteria of a good biomarker is unlikely for a multifactorial disease like OSA. I agree that a larger and controlled study is needed, but cysteine could be considered a promising measure that will not replace the need for polysomnography but may help the clinician during follow-up of their patients.

Cintra F, Tufik S, D’Almeida V, et al. Cysteine: a potential biomarker for obstructive sleep apnea. Chest. 2011;1392:246-252. [CrossRef] [PubMed]
 
Sobczak A, Wardas W, Zielinska-Danch W, Pawlicki K. The influence of smoking on plasma homocysteine and cysteine levels in passive and active smokers. Clin Chem Lab Med. 2004;424:408-414. [CrossRef] [PubMed]
 
Jacob N, Bruckert E, Giral P, Foglietti MJ, Turpin G. Cysteine is a cardiovascular risk factor in hyperlipidemic patients. Atherosclerosis. 1999;1461:53-59. [CrossRef] [PubMed]
 
Drager LF, Bortolotto LA, Figueiredo AC, Silva BC, Krieger EM, Lorenzi-Filho G. Obstructive sleep apnea, hypertension, and their interaction on arterial stiffness and heart remodeling. Chest. 2007;1315:1379-1386. [CrossRef] [PubMed]
 
Perry JC, D’Almeida V, Souza FG, Schoorlemmer GH, Colombari E, Tufik S. Consequences of subchronic and chronic exposure to intermittent hypoxia and sleep deprivation on cardiovascular risk factors in rats. Respir Physiol Neurobiol. 2007;1563:250-258. [CrossRef] [PubMed]
 

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References

Cintra F, Tufik S, D’Almeida V, et al. Cysteine: a potential biomarker for obstructive sleep apnea. Chest. 2011;1392:246-252. [CrossRef] [PubMed]
 
Sobczak A, Wardas W, Zielinska-Danch W, Pawlicki K. The influence of smoking on plasma homocysteine and cysteine levels in passive and active smokers. Clin Chem Lab Med. 2004;424:408-414. [CrossRef] [PubMed]
 
Jacob N, Bruckert E, Giral P, Foglietti MJ, Turpin G. Cysteine is a cardiovascular risk factor in hyperlipidemic patients. Atherosclerosis. 1999;1461:53-59. [CrossRef] [PubMed]
 
Drager LF, Bortolotto LA, Figueiredo AC, Silva BC, Krieger EM, Lorenzi-Filho G. Obstructive sleep apnea, hypertension, and their interaction on arterial stiffness and heart remodeling. Chest. 2007;1315:1379-1386. [CrossRef] [PubMed]
 
Perry JC, D’Almeida V, Souza FG, Schoorlemmer GH, Colombari E, Tufik S. Consequences of subchronic and chronic exposure to intermittent hypoxia and sleep deprivation on cardiovascular risk factors in rats. Respir Physiol Neurobiol. 2007;1563:250-258. [CrossRef] [PubMed]
 
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