The angiotensin-converting enzyme (ACE) insertion/deletion (I/D) polymorphism and the Adducin-1 (ADD1) G460W nonsense single nucleotide polymorphism (SNP) have previously been associated to hypertension, whereas their association with preeclampsia (PE) and gestational hypertension (GH) is still controversial. We genotyped ACE I/D, ADD1 G460W, and ADD1 S586C polymorphisms in 672 unrelated pregnant women: 204 PE (81/204 mild PE), 56 GH, and 412 controls, evaluating both their single and combined effects on these pathologies. The genotype combination of the 3 polymorphisms was not statistically different in cases versus controls, nor were ACE and ADD1 polymorphisms in GH. Nevertheless, the distribution of ACE genotypes was different in PE. This was confirmed in mild PE, whereas no significance was found in severe PE. This could suggest that different factors may lead to mild and severe PE, with ACE polymorphism playing a more important role in the mild form.
Angiotensin-converting enzyme and adducin-1 polymorphisms in women with preeclampsia and gestational hypertension / C., Mandò; P., Antonazzo; S., Tabano; S., Zanutto; P., Pileri; E., Somigliana; F., Colleoni; A., Martinelli; A., Zolin; C., Benedetto; L., Marozio; Neri, Isabella; Facchinetti, Fabio; M., Miozzo; I., Cetin. - In: REPRODUCTIVE SCIENCES. - ISSN 1933-7191. - STAMPA. - 16:9(2009), pp. 819-826. [10.1177/1933719109336612]
Angiotensin-converting enzyme and adducin-1 polymorphisms in women with preeclampsia and gestational hypertension.
NERI, Isabella;FACCHINETTI, Fabio;
2009
Abstract
The angiotensin-converting enzyme (ACE) insertion/deletion (I/D) polymorphism and the Adducin-1 (ADD1) G460W nonsense single nucleotide polymorphism (SNP) have previously been associated to hypertension, whereas their association with preeclampsia (PE) and gestational hypertension (GH) is still controversial. We genotyped ACE I/D, ADD1 G460W, and ADD1 S586C polymorphisms in 672 unrelated pregnant women: 204 PE (81/204 mild PE), 56 GH, and 412 controls, evaluating both their single and combined effects on these pathologies. The genotype combination of the 3 polymorphisms was not statistically different in cases versus controls, nor were ACE and ADD1 polymorphisms in GH. Nevertheless, the distribution of ACE genotypes was different in PE. This was confirmed in mild PE, whereas no significance was found in severe PE. This could suggest that different factors may lead to mild and severe PE, with ACE polymorphism playing a more important role in the mild form.Pubblicazioni consigliate
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