BackgroundWe aimed to compare the associations of smoking exposure as assessed by self‐reports and urine cotinine with cardiovascular disease (CVD) risk and determine the potential utility of cotinine for CVD risk prediction.Methods and ResultsSmoking status by self‐reports and urine cotinine were assessed at baseline in 4737 participants (mean age, 53 years) of the PREVEND (Prevention of Renal and Vascular End‐Stage Disease) prospective study. Participants were classified as never, former, light current (≤10 cigarettes/day), and heavy current smokers (>10 cigarettes/day) according to self‐reports and analogous cutoffs for urine cotinine. During a median follow‐up of 8.5 years, 296 first CVD events were recorded. Compared with self‐reported never smokers, the hazard ratios (95% confidence interval) of CVD for former, light current, and heavy current smokers were 0.86 (0.64–1.17), 1.28 (0.83–1.97), and 1.80 (1.27–2.57) in multivariate analysis. Compared with urine cotinine–assessed never smokers, the corresponding hazard ratios of CVD for urine cotinine–assessed former, light current, and heavy current smokers were 1.70 (1.03–2.81), 1.62 (1.15–2.28), and 1.95 (1.39–2.73) respectively. The C‐index change on adding urine cotinine–assessed smoking status to a standard CVD risk prediction model (without self‐reported smoking status) was 0.0098 (0.0031–0.0164; P=0.004). The corresponding C‐index change for self‐reported smoking status was 0.0111 (0.0042–0.0179; P=0.002).ConclusionsSmoking status as assessed by self‐reports and urine cotinine is associated with CVD risk; however, the nature of the association of urine cotinine with CVD is consistent with a dose‐response relationship. The ability of urine cotinine to improve CVD risk assessment is similar to that of self‐reported smoking status.
Objective: To investigate whether there is an association between HLA class II and distal interphalangeal osteoarthritis (DIP OA). Methods: The study group consisted of consecutive patients with and without DIP OA aged between 40 and 70 years. DIP OA was diagnosed by radiology. These patients were referred to an "Early Arthritis Clinic" (EAC) with different types of arthritis at an early stage. Patients with rheumatoid arthritis, systemic lupus erythematosus, spondyloarthropathies, and psoriatic arthritis were excluded for the purpose of this study. DNA typing for HLA-DR and x ray examination of the hands were performed at enrolment in the EAC. To establish whether the study group was representative of the Dutch population, a population based study in Zoetermeer (n=3243) for the prevalence of DIP OA and blood donors in the Leiden area (n=2400) for the HLA-DR antigen frequencies were used as references. Results: Fifty five patients (33%) of the total study group (n=166) had DIP OA. The prevalence of DIP OA and frequency of the HLA-DR alleles were similar to those of the two reference groups. Within the study group an association between DIP OA and HLA-DR2 and DR4 with respectively odds ratios of 2.4 (95% confidence interval (CI) 1.1 to 5.0) and 0.3 (95% CI 0.1 to 0.7) was found. No association was found between other HLA-DR alleles and DIP OA. Conclusion:The study group is a representative sample of the Dutch population. The HLA-DR2 allele was more common in patients with DIP OA. Furthermore, an inverse relation was observed between DIP OA and HLA-DR4. The results confirm findings from other investigations implicating HLA-DR2 as a risk factor in the development of DIP OA.
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