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. Author manuscript; available in PMC: 2011 Jan 7.
Published in final edited form as: Nat Genet. 2010 Jul 25;42(8):684–687. doi: 10.1038/ng.628

Table 1.

Baseline clinical attributes of the study sample.

GWAS cohort Resequencing cohort

HTG Controls HTG Controls
Number 463 1197 438 327
Female 30.7% 40.4% 33.2% 50.5%
Diabetes 25.7% 0.4% 28.1% 4.1%
Age (years) 50.9 ± 13.0 47.8 ± 11.1 51.3 ± 13.1 49.9 ± 15.1
Body mass index (kg/m2) 29.9 ± 4.9 26.4 ± 4.6 30.0 ± 4.9 26.8 ± 4.5
Plasma total cholesterol (mmol/L) 8.2 ± 3.9 5.3 ± 1.3 8.7 ± 4.3 4.9 ± 0.8
Plasma HDL cholesterol (mmol/L) 0.9 ± 0.3 1.4 ± 0.4 0.9 ± 0.3 1.3 ± 0.4
Plasma LDL cholesterol (mmol/L) - 3.4 ± 1.2 - 3.2 ± 0.9
Plasma triglycerides (mmol/L) 14.3 ± 19.8 1.1 ± 0.7 14.2 ± 19.0 1.2 ± 0.4

GWAS, genome-wide association study; HDL, high-density lipoprotein; HTG, hypertriglyceridemia; LDL, low-density lipoprotein. There are 346 HTG patients and 205 low triglyceride controls common between both cohorts. Lipid measurements were conducted after a 12-h fasting period. Values are mean ± standard deviation. LDL cholesterol is not accurately calculated using the Friedewald equation for HTG patients when plasma triglyceride concentration exceeds 4.5 mmol/L.

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