Why the study?
Does smoking increase urinary 11-dehydrothromboxane B2 levels compared to non-smokers?
Does smoking increase urinary 11-dehydrothromboxane B2 levels compared to non-smokers?
Smoking is associated with significantly increased urinary 11-dehydrothromboxane B2 levels, a biomarker of inflammation and cardiovascular risk.
Elevated urinary 11-dehydrothromboxane B2 may mark heightened CV risk in smokers; leaves open its value for risk stratification or cessation monitoring.
Background Thromboxane is a key clinical risk endpoint of smoking-induced inflammation which has been associated in the pathogenesis of cardiovascular disease. The goal of this review is to quantify the effect of smoking and smoking cessation on one of its urinary metabolites, 11-dehydrothromboxane B2 . Methods PubMed and SCOPUS were searched to identify publications which report urinary 11-dehydrothromboxane B2 levels in smokers and non-smokers, as well as articles reporting the effect of smoking cessation on urinary 11-dehydrothromboxane B2 excretion. Results We found ten studies assessing urinary 11-dehydrothroboxane B2 levels in smokers and non-smokers. Four papers reported the amount of urinary 11-dehydrothromboxane B2 excreted in 24 h while six reported the amount excreted adjusted for creatinine. The meta-analyses comparing the excretion of urinary 11-dehydrothromboxane in current smokers to non-smokers report increased levels in current smokers (mean difference = 0.31 μg/24-h [95%CI: 0.27–0.34] and 166.45 pg/mg creatinine [95%CI: 120.51–212.40]). There were not enough publications to perform meta-analyses on the effects of smoking cessation on urinary 11-dehydrothromboxane B2 excretion. Conclusions Urinary 11-dehydrothromboxane B2 levels are increased in cigarette smokers, however, more data are needed to elucidate the effects of smoking cessation on urinary 11-dehydrothromboxane B2 excretion.
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Plas et al. (2018) studied this question.
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