Thrombophilic dimension of recurrent fetal loss in Indian patients.
We studied the prevalence of acquired and genetic thrombophilia in 198 women with recurrent fetal loss who were having three or more than three abortions. Seventy-nine women had only early pregnancy losses, that is, first trimester abortions, 30 women had only late pregnancy losses, that is, second and third trimester abortions whereas 89 had both early and late pregnancy losses. The control group included 100 age-matched fertile parous women who did not have any obstetric complications and had at least one normal healthy child. Several genetic and acquired thrombophilia markers were studied. The strongest association was observed with anticardiolipin (odds ratio 22.6, confidence interval 5.7-89, P = 0) followed by lupus anticoagulant, anti-beta2 glycoprotein-1, antiannexin. Association of antiphospholipid antibody syndromes was detected with the time of pregnancy loss in anticardiolipin, lupus anticoagulants, which was significantly associated with early pregnancy loss as compared with second and third trimester loss. In case of beta2 glycoprotein-1, antiannexin it was less significantly associated with early pregnancy loss as compared with second and third trimester loss. The risk of fetal loss with protein S deficiency was the highest risk observed for any heritable thrombophilia, followed by protein C, factor V Leiden, endothelial protein C receptor, antithrombin III deficiency and beta448 fibrinogen polymorphism. Modest risks were also observed with 5,10-methylenetetrahydrofolate reductase, plasminogen activator inhibitor 4G/4G polymorphisms and beta448 fibrinogen polymorphism. A combination of two or more than two genetic risk factors were observed in 55 (27.7%), whereas the genetic and acquired risk factors were observed in 107 (54%) of the cases. Thrombophilia is an important contributing factor for both early and late pregnancy losses; approximately two-thirds of our cases of unexplained fetal losses could be explained by acquired or heritable thrombophilia or both, which is in line with other western studies.
Vora
Sonal
S
National Institute of Immunohaematology (ICMR), KEM Hospital, Parel, Mumbai, India.
Shetty
Shrimati
S
Ghosh
Kanjaksha
K
D000026:Abortion, Habitual / Q000097:blood / Q000209:etiology*; D000293:Adolescent; D000328:Adult; D017304:Annexin A5 / Q000276:immunology; D017153:Antibodies, Anticardiolipin / Q000097:blood; D000918:Antibody Specificity; D016736:Antiphospholipid Syndrome / Q000097:blood / Q000150:complications; D001323:Autoantibodies / Q000097:blood* / Q000276:immunology; D001324:Autoantigens / Q000276:immunology; D025861:Blood Coagulation Disorders, Inherited / Q000097:blood / Q000150:complications*; D020147:Coagulation Protein Disorders / Q000097:blood / Q000150:complications* / Q000235:genetics; D005260:Female; D006801:Humans; D007194:India; D016682:Lupus Coagulation Inhibitor / Q000097:blood; D011247:Pregnancy; D011250:Pregnancy Complications, Hematologic / Q000097:blood* / Q000235:genetics; D011264:Pregnancy Trimesters; D012307:Risk Factors; D019851:Thrombophilia / Q000097:blood / Q000150:complications* / Q000235:genetics; D053482:beta 2-Glycoprotein I / Q000276:immunology
D017304:Annexin A5; D017153:Antibodies, Anticardiolipin; D001323:Autoantibodies; D001324:Autoantigens; D016682:Lupus Coagulation Inhibitor; D053482:beta 2-Glycoprotein I