L A Hefler1, C B Tempfer, A R Gregg. 1. Department of Obstetrics and Gynecology, Baylor College of Medicine, Houston, Texas 77030, USA.
Abstract
OBJECTIVE: To identify associations between polymorphisms within the interleukin-1 beta gene cluster, all of which increase protein expression, and preeclampsia. METHODS: We genotyped a Hispanic population (69 women with preeclampsia and 47 controls) for two polymorphisms of the interleukin-1 beta gene (promoter region and exon 5) and one polymorphism of the interleukin-1 receptor antagonist gene in intron 2. Clinical data were collected from medical records. Values are given as means or medians. Statistical power to identify a difference in occurrence of interleukin-1 beta promoter, interleukin-1 beta exon 5, and interleukin-1 receptor antagonist gene polymorphisms in women with preeclampsia compared with controls was 21%, 15.9%, and 30.9%, respectively. RESULTS: We found no association between any single polymorphism and occurrence of preeclampsia. Among women with preeclampsia, those with polymorphism of interleukin-1 receptor antagonist gene had higher mean systolic blood pressure (BP) at admission (178 +/- 33.4 versus 159 +/- 19.5 mmHg, P =.039). When all three polymorphisms combined were evaluated, women with preeclampsia and at least three mutant alleles (n = 8) had higher mean systolic BP at admission (182 +/- 30 versus 160 +/- 20.5 mmHg, P =.009) and increased alanine aminotransferase (67 [10--1024] versus 20 [3--407] IU/L, P =.04) and aspartate aminotransferase (119 [25--2239] versus 24 [4--489] IU/L, P =.002). At admission, BP in controls was independent of any polymorphism identified. CONCLUSION: Although the power of this study was limited, our data do not support a role for polymorphisms of the interleukin-1 beta and interleukin-1 receptor antagonist genes in the pathogenesis of preeclampsia among Hispanic women. Our findings do suggest that polymorphisms within the gene cluster might influence severity of preeclampsia.
OBJECTIVE: To identify associations between polymorphisms within the interleukin-1 beta gene cluster, all of which increase protein expression, and preeclampsia. METHODS: We genotyped a Hispanic population (69 women with preeclampsia and 47 controls) for two polymorphisms of the interleukin-1 beta gene (promoter region and exon 5) and one polymorphism of the interleukin-1 receptor antagonist gene in intron 2. Clinical data were collected from medical records. Values are given as means or medians. Statistical power to identify a difference in occurrence of interleukin-1 beta promoter, interleukin-1 beta exon 5, and interleukin-1 receptor antagonist gene polymorphisms in women with preeclampsia compared with controls was 21%, 15.9%, and 30.9%, respectively. RESULTS: We found no association between any single polymorphism and occurrence of preeclampsia. Among women with preeclampsia, those with polymorphism of interleukin-1 receptor antagonist gene had higher mean systolic blood pressure (BP) at admission (178 +/- 33.4 versus 159 +/- 19.5 mmHg, P =.039). When all three polymorphisms combined were evaluated, women with preeclampsia and at least three mutant alleles (n = 8) had higher mean systolic BP at admission (182 +/- 30 versus 160 +/- 20.5 mmHg, P =.009) and increased alanine aminotransferase (67 [10--1024] versus 20 [3--407] IU/L, P =.04) and aspartate aminotransferase (119 [25--2239] versus 24 [4--489] IU/L, P =.002). At admission, BP in controls was independent of any polymorphism identified. CONCLUSION: Although the power of this study was limited, our data do not support a role for polymorphisms of the interleukin-1 beta and interleukin-1 receptor antagonist genes in the pathogenesis of preeclampsia among Hispanic women. Our findings do suggest that polymorphisms within the gene cluster might influence severity of preeclampsia.
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