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American Journal of Clinical Nutrition, Vol. 80, No. 5, 1449, November 2004
© 2004 American Society for Clinical Nutrition

LETTERS TO THE EDITOR

Reply to RD Reynolds and JE Leklem

Simonetta Friso, Domenico Girelli and Roberto Corrocher

Department of Clinical and Experimental Medicine
University of Verona School of Medicine
Policlinico "GB Rossi"
P le LA Scuro 10
37134 Verona
Italy
E-mail: simonetta.friso{at}univr.it

Dear Sir:

We are thankful to Reynolds and Leklem for their interest in our work on vitamin B-6 and coronary artery disease (CAD) risk (1). We certainly coincide in the opinion that smoking is a well-documented determinant of pyridoxal-5'-phosphate (PLP) concentrations (2-5), an opinion that we also expressed in our first report suggesting an inverse relation between plasma PLP and C-reactive protein (6). However, in the present study, no difference in PLP concentrations was detected between smokers and nonsmokers either in the whole population study (P = 0.21) or within groups of subjects with or without CAD (P = 0.68 and P = 0.54, respectively). Furthermore, no significant difference in the percentage of smokers across increasing quartiles of PLP concentrations was observed (P = 0.09).

Nevertheless, as affirmed in the article, we conducted multivariate logistic regression analyses to control for, among other factors, smoking status. Because smoking is a well-known risk factor for CAD, it could have been a strong confounder in the estimate of the independent association between low PLP concentrations and CAD risk, and estimation of this association was one of the primary aims of the study. Analysis for potential interactions, moreover, showed that CAD risk, as a result of low PLP, was additive when considered in combination with smoking status. We agree with Reynolds and Leklem that an evaluation of smoking load could be of interest, but such data were not available.

The existence of an inverse relation between plasma PLP concentrations and the activity of alkaline phosphatase is indeed known. In our case-control study for the assessment of CAD risk, however, there was no evident reason to test for alkaline phosphatase, which, we concur with Reynolds and Leklem, could have a stronger effect, particularly in certain diseases (7). We are confident that our report highlights a potentially important role of PLP in CAD, although mechanistic studies are certainly required to clarify the biochemical-molecular basis of this association.

REFERENCES

  1. Friso S, Girelli D, Martinelli N, et al. Low plasma vitamin B-6 concentrations and modulation of coronary artery disease risk. Am J Clin Nutr 2004;79:992-8.[Abstract/Free Full Text]
  2. Manore MM, Vaughan LA, Carroll SS, Leklem JE. Plasma pyridoxal 5'-phosphate concentration and dietary vitamin B-6 intake in free-living, low-income elderly people. Am J Clin Nutr 1989;50:339-45.[Abstract/Free Full Text]
  3. Vermaak WJ, Ubbink JB, Barnard HC, Potgieter GM, van Jaarsveld H, Groenewald AJ. Vitamin B-6 nutrition status and cigarette smoking. Am J Clin Nutr 1990;51:1058-61.[Abstract/Free Full Text]
  4. Pessah-Rasmussen H, Jerntorp P, Stavenow L, et al. Eighty-year-old men without cardiovascular disease in the community of Malmo. Part II. Smoking characteristics and ultrasound findings, with special reference to glutathione transferase and pyridoxal-5-phosphate. J Intern Med 1990;228:17-22.
  5. Serfontein WJ, Ubbink JB, De Villiers LS, Becker PJ. Depressed plasma pyridoxal-5'-phosphate levels in tobacco-smoking men. Atherosclerosis 1986;59:341-6.[Medline]
  6. Friso S, Jacques PF, Wilson PWF, Rosenberg IH, Selhub J. Low circulating vitamin B6 is associated with elevation of the inflammation marker C-reactive protein independently of plasma homocysteine levels. Circulation 2001;103:2788-91.[Abstract/Free Full Text]
  7. Reynolds RD, Lorenc RS, Wieczorek E, Pronicka E. Extremely low serum pyridoxal 5'-phosphate in children with familial hypophosphatemic rickets. Am J Clin Nutr 1991;53:698-701.[Abstract/Free Full Text]




This Article
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