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Titolo:
Lipoprotein lipase gene mutations and the genetic susceptibility of preeclampsia
Autore:
Kim, YJ; Williamson, RA; Chen, K; Smith, JL; Murray, JC; Merrill, DC;
Indirizzi:
Wake Forest Univ, Sch Med, Dept Obstet & Gynecol, Winston Salem, NC 27157 USA Wake Forest Univ Winston Salem NC USA 27157 , Winston Salem, NC 27157 USA Ewha Womans Univ, Dept Obstet & Gynecol, Seoul 120750, South Korea Ewha Womans Univ Seoul South Korea 120750 col, Seoul 120750, South Korea Univ Iowa, Dept Pediat, Iowa City, IA USA Univ Iowa Iowa City IA USAUniv Iowa, Dept Pediat, Iowa City, IA USA
Titolo Testata:
HYPERTENSION
fascicolo: 5, volume: 38, anno: 2001,
pagine: 992 - 996
SICI:
0194-911X(200111)38:5<992:LLGMAT>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
FREE FATTY-ACIDS; WOMEN; HYPERTENSION; DEFICIENCY; PREGNANCY; DISEASE; SERA; RISK;
Keywords:
preeclampsia; lipoprotein lipase; mutations; genetic susceptibility;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
16
Recensione:
Indirizzi per estratti:
Indirizzo: Merrill, DC Wake Forest Univ, Sch Med, Dept Obstet & Gynecol, Med Ctr Blvd, Winston Salem, NC 27157 USA Wake Forest Univ Med Ctr Blvd Winston Salem NC USA 27157 7 USA
Citazione:
Y.J. Kim et al., "Lipoprotein lipase gene mutations and the genetic susceptibility of preeclampsia", HYPERTENSIO, 38(5), 2001, pp. 992-996

Abstract

In the pathogenesis of preeclampsia, endothelial cell activation or dysfunction is a central theme, and marked dyslipidemia may contribute to endothelial cell dysfunction. The objective of this study was to evaluate the association between preeclampsia and mutations within the lipoprotein lipase (LPL) gene. DNA was extracted from whole blood or cheek swabs of 250 preeclamptic patients, 265 control subjects, and 106 offspring of preeclamptic patients (all white). Control subjects were women who had undergone greater than or equal to2 term pregnancies unaffected by preeclampsia. All samples were genotyped for 3 LPL polymorphisms with the use of polymerase chain reaction of known allelic variants. The 3 mutations studied were the following: (1) Asp9Asn substitution in exon 2, (2) T-to-G substitution at position -93 of the proximal promotor region (-93T/G), and (3) Asn291Ser substitution inexon 6. Results were analyzed with an chi (2) contingency table. The prevalences of the Asp9Asn mutation, -93T/G promotor mutation, and Asn291Ser mutation were not significantly different among the preeclamptic patients and control subjects (Asp9Asn: patients, 2.8%; control subjects, 4.0%, -93T/G: patients, 4.5%; control subjects, 5.5%; Asn291Ser: patients, 4.0%; control subject, 3.0%). In addition, there was no difference in the frequency of any of the mutations in the offspring of preeclamptic women compared with that observed in the control population. Between a small group of patients with nulliparous HELLP syndrome (a variant of severe preeclampsia: hemolysis, elevated liver enzyme, low platelets) patients (n=12) and control subjects,there was a significant difference in the prevalence of the Asn291Ser mutation (16.7% versus 3.0%, P = 0.01). In this large white population, the Asp9Asn mutation. - 93T/G promotor mutation, and Asn291Ser mutation were not associated with an increased risk for preeclampsia. In a small subgroup of patients, the Asn291Ser mutation was associated with an increased risk for nulliparous HELLP syndrome.

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Documento generato il 02/04/20 alle ore 10:50:00