title: Analysis and modelling of cholesterol and high-density lipoprotein cholesterol changes across the range of C-reactive protein levels in clinical practice as an aid to better understanding of inflammation-lipid interactions.
abstract: OBJECTIVE
  Raised total cholesterol (TC) and reduced high-density lipoprotein (HDL) cholesterol levels are established cardiovascular disease (CVD) risk factors. However, in autoimmune conditions the lipid-CVD association appears paradoxical, with inflammation as a potential confounding factor. We therefore sought to model the relationship between systemic inflammatory illness and lipid levels using C-reactive protein (CRP) as the prototypical marker of inflammation. Our hypothesis was that there would be an inverse association between raised CRP levels and both TC and HDL-cholesterol levels.
  
  
  METHODS
  Results from samples analysed simultaneously for CRP and lipids in a 6-month period were collected retrospectively from a large city hospital laboratory database that collates results from both primary and secondary care. The relationships between CRP and lipids were determined using graphical techniques and empirical, non-parametric, best fit models.
  
  
  RESULTS
  A total of 11 437 blood samples was included. We identified a significant (p<0.001) biphasic relationship between TC and CRP: TC increased within the healthy CRP range of less than 5 mg/l, but decreased with CRP levels above 10 mg/l. The two effects approximately cancelled each other out in the intermediate CRP range of 5-10 mg/l. There was an inverse relationship between HDL-cholesterol and CRP.
  
  
  CONCLUSIONS
  Lipid levels change significantly during inflammatory illness in a population with both acute and chronic conditions. These results provide a strong epidemiological basis for the better understanding of lipid changes in inflammatory conditions and with anti-inflammatory therapies.
authors.affiliation: Department of Biochemistry, Glasgow Royal Infirmary, Glasgow, UK.
authors.forename: Hanna
authors.initials: H
authors.lastname: Johnsson
authors.affiliation: Department of Biochemistry, Glasgow Royal Infirmary, Glasgow, UK.
authors.forename: Maurizio
authors.initials: M
authors.lastname: Panarelli
authors.affiliation: Department of Acute Medicine, Glasgow Royal Infirmary, Glasgow, UK.
authors.forename: Allan
authors.initials: A
authors.lastname: Cameron
authors.affiliation: Institute of Cardiovascular and Medical Sciences, BHF Glasgow Cardiovascular Research Centre, University of Glasgow, Glasgow, UK.
authors.forename: Naveed
authors.initials: N
authors.lastname: Sattar
mesh_terms: D000328:Adult; D000368:Aged; D001172:Arthritis, Rheumatoid / Q000276:immunology / Q000378:metabolism* / Q000401:mortality; D002097:C-Reactive Protein / Q000276:immunology / Q000378:metabolism*; D002318:Cardiovascular Diseases / Q000276:immunology / Q000378:metabolism / Q000401:mortality; D002784:Cholesterol / Q000097:blood* / Q000276:immunology; D008076:Cholesterol, HDL / Q000097:blood* / Q000276:immunology; D005260:Female; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000378:metabolism* / Q000401:mortality; D016018:Least-Squares Analysis; D008297:Male; D008875:Middle Aged; D008954:Models, Biological; D017711:Nonlinear Dynamics; D012189:Retrospective Studies; D012307:Risk Factors; D018709:Statistics, Nonparametric
chemical_list: D008076:Cholesterol, HDL; D002097:C-Reactive Protein; D002784:Cholesterol
keywords: Cardiovascular Disease; Inflammation; Lipids