title: C-reactive protein concentrations are very high and more stable over time than the traditional vascular risk factors total cholesterol and systolic blood pressure in an Australian aboriginal cohort.
abstract: BACKGROUND
  Stability of circulating high-sensitivity C-reactive protein (hsCRP) concentrations has implications for its utility in assessing cardiovascular disease (CVD) risk. We sought to determine hsCRP reproducibility in an indigenous Australian cohort with a view to use hsCRP as a marker of future CVD in community-based risk-factor screenings.
  
  
  METHODS
  Seventy people living in a community on the northern coast of Australia participated in 2 risk-factor screenings over a median (interquartile range) follow-up time of 829 (814-1001) days. hsCRP was measured by high-sensitivity nephelometry.
  
  
  RESULTS
  Geometric mean hsCRP concentrations at baseline and follow-up were 4.5 and 5.1 mg/L, respectively (P = 0.220), and Pearson product-moment correlation was 0.775. The proportion of people at high CVD risk (hsCRP >3.0 mg/L) at baseline was 67.1% and remained consistently high (68.6%) at follow-up. Linear regression analysis for follow-up hsCRP as a function of baseline hsCRP, sex, and differences in total and regional body fatness showed that baseline hsCRP was the single predictor in the model, accounting for 63.9% of the total variance in follow-up hsCRP (P(model) < 0.001). Prevalence agreement (95% CI) between baseline and follow-up for the hsCRP >3.0 mg/L category was 84% (73%-92%) (P(McNemar) = not significant), and kappa coefficient was fair (0.64, compared with 0.31 for systolic blood pressure > or =140 mmHg and 0.43 for total cholesterol > or =5.5 mmol/L).
  
  
  CONCLUSIONS
  hsCRP concentrations remained consistently reproducible over time across a wide concentration range in an Aboriginal cohort. Correlations between concentrations over time were better than for other traditional CVD risk factors. hsCRP concentration has potential as a marker of future CVD risk.
authors.affiliation: Menzies School of Health Research, John Mathews Building, Royal Darwin Hospital, Darwin, NT, Australia.
authors.forename: Tomer
authors.initials: T
authors.lastname: Shemesh
authors.forename: Kevin G
authors.initials: KG
authors.lastname: Rowley
authors.forename: Alicia J
authors.initials: AJ
authors.lastname: Jenkins
authors.forename: James D
authors.initials: JD
authors.lastname: Best
authors.forename: Kerin
authors.initials: K
authors.lastname: O'Dea
mesh_terms: D015415:Biomarkers / Q000032:analysis / Q000097:blood; D001794:Blood Pressure / Q000502:physiology*; D002097:C-Reactive Protein / Q000032:analysis*; D002318:Cardiovascular Diseases / Q000097:blood* / Q000208:ethnology / Q000503:physiopathology; D002784:Cholesterol / Q000097:blood*; D015331:Cohort Studies; D005500:Follow-Up Studies; D006801:Humans; D016014:Linear Models; D015876:Northern Territory / Q000453:epidemiology; D011159:Population Surveillance; D012307:Risk Factors
chemical_list: D015415:Biomarkers; D002097:C-Reactive Protein; D002784:Cholesterol