Inherited thrombophilia and pregnancy loss. Study of an Argentinian cohort.
Trombofilia hereditaria y pérdidas de embarazo. Estudio de una cohorte de Argentina.
Abortion, Habitual
/ genetics
Adult
Antithrombins
/ analysis
Argentina
Case-Control Studies
Cohort Studies
Factor V
/ genetics
Factor XI
/ genetics
Female
Fetal Growth Retardation
/ genetics
Fibrinogens, Abnormal
/ genetics
Genotype
Gestational Age
Humans
Plasminogen Activator Inhibitor 1
/ genetics
Pregnancy
Protein C Deficiency
/ diagnosis
Protein S Deficiency
/ diagnosis
Thrombophilia
/ complications
Factor V Leiden
Factor V de Leiden
Factor XI
Fibrinogen gamma
Fibrinógeno gamma
Foetal growth retardation
Inherited thrombophilia
Pérdidas recurrentes de embarazo
Recurrent pregnancy loss
Retraso del crecimiento fetal
Trombofilia hereditaria
Journal
Medicina clinica
ISSN: 1578-8989
Titre abrégé: Med Clin (Barc)
Pays: Spain
ID NLM: 0376377
Informations de publication
Date de publication:
05 04 2019
05 04 2019
Historique:
received:
29
09
2017
revised:
22
12
2017
accepted:
28
12
2017
pubmed:
11
3
2018
medline:
20
6
2020
entrez:
11
3
2018
Statut:
ppublish
Résumé
Thrombophilia might increase the risk of suffering from obstetric complications by adversely affecting the normal placental vascular function. Our aim was to study the distributions of five thrombosis-associated genetic variants: factor V Leiden, prothrombin G20210A, -675 4G/5G PAI-1, 10034C/T gamma fibrinogen and 7872C/T factor XI and the frequencies of the deficiencies of protein C, S and antithrombin in Argentinian patients with recurrent pregnancy loss (RPL) and, therefore, to analyse their association with the risk and timing of RPL and the risk of suffering other vascular obstetric pathologies. We performed a case-control study that included 247 patients with idiopathic RPL (cases), 107 fertile controls and 224 subjects from general population (reference group). Cases were stratified according to the gestational time of the losses (early RPL, n = 89; late losses, n = 158; foetal losses, n = 107) and according to the type of vascular obstetric pathologies. No differences were found in the distribution of the genetic variants among RPL group vs. control/reference group (p >.05). Similarly, no differences were observed in their distributions when analysing RPL patients stratified according to gestational times or vascular obstetric pathologies (p >.05), except for the factor V Leiden carriage in patients with foetal growth retardation vs. controls (11.8%, 4/34 vs. 1.9%, 2/107; p = .04) (OR = 7.11 [1.24-40.93], p = .03). Factor V Leiden might have a significant impact on certain obstetric pathologies such as foetal growth retardation. The genetic variants, 10034C/T gamma fibrinogen and 7872C/T factor XI, associated with thromboembolic disease, would not have an impact on PRE.
Sections du résumé
BACKGROUND AND OBJECTIVES
Thrombophilia might increase the risk of suffering from obstetric complications by adversely affecting the normal placental vascular function. Our aim was to study the distributions of five thrombosis-associated genetic variants: factor V Leiden, prothrombin G20210A, -675 4G/5G PAI-1, 10034C/T gamma fibrinogen and 7872C/T factor XI and the frequencies of the deficiencies of protein C, S and antithrombin in Argentinian patients with recurrent pregnancy loss (RPL) and, therefore, to analyse their association with the risk and timing of RPL and the risk of suffering other vascular obstetric pathologies.
PATIENTS AND METHODS
We performed a case-control study that included 247 patients with idiopathic RPL (cases), 107 fertile controls and 224 subjects from general population (reference group). Cases were stratified according to the gestational time of the losses (early RPL, n = 89; late losses, n = 158; foetal losses, n = 107) and according to the type of vascular obstetric pathologies.
RESULTS
No differences were found in the distribution of the genetic variants among RPL group vs. control/reference group (p >.05). Similarly, no differences were observed in their distributions when analysing RPL patients stratified according to gestational times or vascular obstetric pathologies (p >.05), except for the factor V Leiden carriage in patients with foetal growth retardation vs. controls (11.8%, 4/34 vs. 1.9%, 2/107; p = .04) (OR = 7.11 [1.24-40.93], p = .03).
CONCLUSIONS
Factor V Leiden might have a significant impact on certain obstetric pathologies such as foetal growth retardation. The genetic variants, 10034C/T gamma fibrinogen and 7872C/T factor XI, associated with thromboembolic disease, would not have an impact on PRE.
Identifiants
pubmed: 29523337
pii: S0025-7753(18)30071-X
doi: 10.1016/j.medcli.2017.12.019
pii:
doi:
Substances chimiques
Antithrombins
0
Fibrinogens, Abnormal
0
Plasminogen Activator Inhibitor 1
0
SERPINE1 protein, human
0
factor V Leiden
0
fibrinogen gamma'
0
Factor V
9001-24-5
Factor XI
9013-55-2
Types de publication
Journal Article
Langues
eng
spa
Sous-ensembles de citation
IM
Pagination
249-254Informations de copyright
Copyright © 2018 Elsevier España, S.L.U. All rights reserved.