BACKGROUND: Elevated plasma concentrations of C-reactive protein (CRP) and total sialic acid (TSA) have been associated with increased cardiovascular risk. Additionally, levels of both CRP and TSA have been reported to be significantly elevated in smokers. However, it is not clear if the raised TSA and CRP levels noted in smokers are directly attributable to the smoking experience, or if they may be elevated due to a secondary mechanism(s), such as smoking-induced tissue inflammation. SUBJECTS AND METHODS: We measured the plasma concentration of CRP and TSA in a group of smokers at baseline and following one year of validated smoking cessation (n = 30) and in a control group of tobacco users who continued to smoke over the year (n = 30). RESULTS: The baseline concentration of TSA and CRP was 67.2 mg dL(-1) and 1.91 mg L(-1), respectively (n = 60). No significant dose-dependent relationship was noted between baseline CRP or TSA concentration and either plasma cotinine, expired-air CO or daily cigarette consumption. There was no difference in the mean change in CRP level in the quitters over one year (- 0.2 mg L(-1)) compared to the continuing smokers (+ 0.5 mg L(-1)), P = 0.80, or in the change in concentration of TSA in the quitters (- 2.7 mg dL(-1)) compared to the continuing smokers (+ 0.4 mg dL(-1)), P = 0.26. CONCLUSIONS: As the circulating concentrations of both CRP and TSA remain unchanged following one year of smoking cessation, these results would suggest that the elevated levels noted in smokers are not directly attributable to tobacco use and are more likely to be elevated due to a secondary process that is yet to be established.
BACKGROUND: Elevated plasma concentrations of C-reactive protein (CRP) and total sialic acid (TSA) have been associated with increased cardiovascular risk. Additionally, levels of both CRP and TSA have been reported to be significantly elevated in smokers. However, it is not clear if the raised TSA and CRP levels noted in smokers are directly attributable to the smoking experience, or if they may be elevated due to a secondary mechanism(s), such as smoking-induced tissue inflammation. SUBJECTS AND METHODS: We measured the plasma concentration of CRP and TSA in a group of smokers at baseline and following one year of validated smoking cessation (n = 30) and in a control group of tobacco users who continued to smoke over the year (n = 30). RESULTS: The baseline concentration of TSA and CRP was 67.2 mg dL(-1) and 1.91 mg L(-1), respectively (n = 60). No significant dose-dependent relationship was noted between baseline CRP or TSA concentration and either plasma cotinine, expired-air CO or daily cigarette consumption. There was no difference in the mean change in CRP level in the quitters over one year (- 0.2 mg L(-1)) compared to the continuing smokers (+ 0.5 mg L(-1)), P = 0.80, or in the change in concentration of TSA in the quitters (- 2.7 mg dL(-1)) compared to the continuing smokers (+ 0.4 mg dL(-1)), P = 0.26. CONCLUSIONS: As the circulating concentrations of both CRP and TSA remain unchanged following one year of smoking cessation, these results would suggest that the elevated levels noted in smokers are not directly attributable to tobacco use and are more likely to be elevated due to a secondary process that is yet to be established.
Authors: Stephan J L Bakker; Ron T Gansevoort; Erik M Stuveling; Rijk O B Gans; Dick de Zeeuw Journal: Curr Hypertens Rep Date: 2005-10 Impact factor: 5.369
Authors: D E Laaksonen; L Niskanen; K Nyyssönen; K Punnonen; T-P Tuomainen; V-P Valkonen; R Salonen; J T Salonen Journal: Diabetologia Date: 2004-07-28 Impact factor: 10.122