PURPOSE: We studied whether the CAG (encoding glutamine) repeat length polymorphism in the first exon of the androgen receptor (AR) gene is predictive of preeclampsia. METHODS: Fifty-nine children born after preeclamptic pregnancy (PRE) and 58 control subjects born after normotensive pregnancy (non-PRE) were genotyped for the CAG repeat length of the AR gene. Secondly, the ARCAG repeat lengths of 133 unrelated preeclamptic women and 112 healthy controls were studied. The mean AR gene CAG lengths were compared between the preeclampsia and the control groups. RESULTS: The mean length of the CAG repeat segment among children was significantly shorter in the PRE group compared with the non-PRE group (p = 0.02). Interestingly, the difference between the PRE and the non-PRE boys was even more significant (p = 0.008). Also the distribution of allele frequencies was different, short repeat lengths being overrepresented in the PRE children. However, there were no significant differences in the mean CAG repeat lengths between the unrelated preeclamptic women and their controls, but the shortest CAG repeat lengths were found only in the preeclamptic women. CONCLUSIONS: The AR gene CAG repeat length is not a major determinant in the development of preeclampsia. The association of the shortest CAG repeats with preeclampsia is possible, but a larger study group is needed to confirm this finding.
PURPOSE: We studied whether the CAG (encoding glutamine) repeat length polymorphism in the first exon of the androgen receptor (AR) gene is predictive of preeclampsia. METHODS: Fifty-nine children born after preeclamptic pregnancy (PRE) and 58 control subjects born after normotensive pregnancy (non-PRE) were genotyped for the CAG repeat length of the AR gene. Secondly, the ARCAG repeat lengths of 133 unrelated preeclamptic women and 112 healthy controls were studied. The mean AR gene CAG lengths were compared between the preeclampsia and the control groups. RESULTS: The mean length of the CAG repeat segment among children was significantly shorter in the PRE group compared with the non-PRE group (p = 0.02). Interestingly, the difference between the PRE and the non-PRE boys was even more significant (p = 0.008). Also the distribution of allele frequencies was different, short repeat lengths being overrepresented in the PRE children. However, there were no significant differences in the mean CAG repeat lengths between the unrelated preeclamptic women and their controls, but the shortest CAG repeat lengths were found only in the preeclamptic women. CONCLUSIONS: The AR gene CAG repeat length is not a major determinant in the development of preeclampsia. The association of the shortest CAG repeats with preeclampsia is possible, but a larger study group is needed to confirm this finding.
Authors: Y A Elhaji; B Gottlieb; R Lumbroso; L K Beitel; W D Foulkes; L Pinsky; M A Trifiro Journal: Breast Cancer Res Treat Date: 2001-11 Impact factor: 4.872
Authors: Rosebud O Roberts; Erik J Bergstralh; Julie M Cunningham; Scott J Hebbring; Stephen N Thibodeau; Michael M Lieber; Steven J Jacobsen Journal: Am J Epidemiol Date: 2004-02-01 Impact factor: 4.897