title: Polymorphism rs7023923 and monocyte count in blood donors and coronary artery disease patients.
abstract: BACKGROUND
  The importance of the role of monocytes in coronary artery disease (CAD) is well documented. An increased number of circulating monocytes is associated with higher incidence of CAD. Both environmental and genetic factors influence monocytosis. The latter have been extensively studied since the development of high-throughput genome-wide association studies. Several associations between polymorphisms and monocytosis were found among healthy individuals; the first example was rs7023923. The magnitude of the association of studied polymorphisms with the trait of interest is often confounded by environmental factors and may therefore differ between patient and healthy populations. It is very important to determine the magnitude of the association among patients to predict outcome of the disease, e.g. myocardial infarction.
  
  
  OBJECTIVE
  To determine whether the magnitude of association of rs7023923 with monocytosis, previously reported among healthy volunteers, is similar in patients in whom diagnosis of CAD was determined during elective coronarography.
  
  
  RESULTS
  Leucocytosis and neutrophilocytosis were higher among patients with CAD, while thrombocytosis was lower. Monocyte count did not differ among the studied groups (p = 0.25). We confirmed the association of rs7023923 with monocytosis among healthy blood donors (p = 0.0156) but not among patients admitted for elective coronarography (p = 0.61). Inclusion of the age and sex of patients in the statistical model did not modify the results.
  
  
  CONCLUSIONS
  Our data suggest that translation of the results of genetic association with the studied traits from healthy to patient population should be implemented with caution. It is possible that numerous environmental factors, which discriminate healthy volunteers from CAD patients, confound the magnitude of genetic associations and make interpretation of the data in patients less clear.
authors.forename: Jarosław Szymon
authors.initials: JS
authors.lastname: Świrta
authors.forename: Marzena
authors.initials: M
authors.lastname: Krzemień-Grandys
authors.forename: Justyna
authors.initials: J
authors.lastname: Totoń-Żurańska
authors.forename: Katarzyna
authors.initials: K
authors.lastname: Kuś
authors.forename: Rafał
authors.initials: R
authors.lastname: Olszanecki
authors.forename: Jacek
authors.initials: J
authors.lastname: Jawień
authors.forename: Marcin
authors.initials: M
authors.lastname: Wnuk
authors.forename: Agnieszka
authors.initials: A
authors.lastname: Słowik
authors.forename: Jacek
authors.initials: J
authors.lastname: Godlewski
authors.forename: Krzysztof
authors.initials: K
authors.lastname: Żmudka
authors.forename: Ryszard
authors.initials: R
authors.lastname: Korbut
authors.affiliation: Uniwersytet Jagielloński Collegium Medicum. Pawel.Wolkow@uj.edu.pl.
authors.forename: Paweł Piotr
authors.initials: PP
authors.lastname: Wołkow
mesh_terms: D000368:Aged; D003324:Coronary Artery Disease / Q000209:etiology / Q000235:genetics*; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D007958:Leukocyte Count; D007964:Leukocytosis / Q000150:complications / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D009000:Monocytes; D020641:Polymorphism, Single Nucleotide