Plasma homocysteine distribution and its association with parental historyof coronary artery disease in black and white children - The Bogalusa Heart Study

Citation
Kj. Greenlund et al., Plasma homocysteine distribution and its association with parental historyof coronary artery disease in black and white children - The Bogalusa Heart Study, CIRCULATION, 99(16), 1999, pp. 2144-2149
Citations number
44
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
CIRCULATION
ISSN journal
00097322 → ACNP
Volume
99
Issue
16
Year of publication
1999
Pages
2144 - 2149
Database
ISI
SICI code
0009-7322(19990427)99:16<2144:PHDAIA>2.0.ZU;2-U
Abstract
Background-Elevated homocysteine is associated with increased risk for coro nary artery disease (CAD) in adults, but ifs distribution in children is no t well documented. We examined the distribution of homocysteine in children and its relation to parental history Of CAD. Methods and Results-A subsample of 1137 children (53% white, 47% black) age d 5 to 17 years in 1992 to 1994 examined in he Bogalusa Heart Study (n = 31 35); including all with a positive parental history of CAD (n = 154), had p lasma homocysteine levels measured. Homocysteine correlated positively with age (r=0.16, P=0.001), No race or sex differences in homocysteine levels w ere observed; geometric mean (GM) levels were 5.8 mu mol/L (95% CI, 5.6 to 6.1) among white males, 5.8 mu mol/L (95% CI, 5.5 to 6.0) among white femal es, 5.6 mu mol/L (95% CI, 5.4 to 5.8) among black males, and 5.6 mu mol/L ( 95% CII 5.4 to 5.9) among black females. Children with a positive parental history of CAD had a significantly greater age-adjusted GM homocysteine lev el (GM, 6.7 mu mol/L: 95% CI, 6.4 to 7.1) than those without a positive his tory (GM, 5.6 mu mol/L; 95% CI, 5.4 to 5.7); this relation was observed in each race-sex group. Conclusions -Higher homocysteine levels were observed among children with a positive family history of CAD. Additional studies should elucidate the co ntribution of genetic, dietary, and other factors to homocysteine levels in children.