title: Placental histomorphology in unexplained foetal loss with thrombophilia.
abstract: OBJECTIVE
  Acquired and genetic thrombotic conditions, both organ and non organ specific, are associated with increased foetal wastage. This study was carried out to examine the placenta from women with abnormal pregnancies and a history of unexplained foetal loss, and to associate with maternal thrombophilia status.
  
  
  METHODS
  Placentas from eight women with history of unexplained foetal loss were analyzed for histopathological characteristics. All the women were simultaneously screened for the common acquired and genetic thrombophilia markers i.e., lupus anticoagulants ( LA), IgG / IgM antibodies for anticardiolipin (ACA), beta2 glycoprotein 1 (beta2GPI) and annexin V, protein C (PC), protein S (PS), antithrombin III (AT III), factor V Leiden ( FVL) mutation, prothrombin (PT) gene G20210A, methylene tetrahydrofolate reductase (MTHFR) C 677T, endothelial protein C receptor (EPCR) 23 bp insertion and plasminogen activator inhibitor ( PAI-1 4G/5G) polymorphisms
  
  
  RESULTS
  Six of eight women were positive for one or more thrombophilia markers. The placenta in all the cases except one, showed the characteristic features of infarct fibrin deposition and calcification. Among two women who were negative for thrombophilia, one showed clear evidence of thrombus in the placental sections while the other did not show any characteristic infarcts in the placental sections.
  
  
  CONCLUSIONS
  Our findings showed that the histopathological examination of the placentas confirmed thrombophilia as the aetiological cause of thrombosis in 6 of the 8 women. The presence of thrombus in a negative thrombophilia woman suggests yet unidentified thrombophilia markers or probably non-haemostatic factors causing thrombosis.
authors.affiliation: National Institute of Immunohaematology (ICMR), Mumbai, India.
authors.forename: S
authors.initials: S
authors.lastname: Vora
authors.forename: S
authors.initials: S
authors.lastname: Shetty
authors.forename: M
authors.initials: M
authors.lastname: Khare
authors.forename: K
authors.initials: K
authors.lastname: Ghosh
mesh_terms: D000022:Abortion, Spontaneous / Q000209:etiology*; D017304:Annexin A5 / Q000097:blood; D017153:Antibodies, Anticardiolipin; D015703:Antigens, CD / Q000235:genetics; D000990:Antithrombin III / Q000032:analysis; D015415:Biomarkers; D000074283:Endothelial Protein C Receptor; D004797:Enzyme-Linked Immunosorbent Assay; D005165:Factor V / Q000235:genetics; D005260:Female; D006801:Humans; D016682:Lupus Coagulation Inhibitor / Q000032:analysis; D042965:Methylenetetrahydrofolate Reductase (NADPH2) / Q000235:genetics; D009154:Mutation / Q000235:genetics; D010920:Placenta / Q000098:blood supply / Q000473:pathology*; D017395:Plasminogen Activator Inhibitor 1 / Q000235:genetics; D016133:Polymerase Chain Reaction; D011247:Pregnancy; D011486:Protein C / Q000032:analysis; D017293:Protein S / Q000032:analysis; D011516:Prothrombin / Q000235:genetics; D011956:Receptors, Cell Surface / Q000235:genetics; D019851:Thrombophilia / Q000150:complications / Q000473:pathology*; D053482:beta 2-Glycoprotein I / Q000097:blood
chemical_list: D017304:Annexin A5; D017153:Antibodies, Anticardiolipin; D015703:Antigens, CD; D015415:Biomarkers; D000074283:Endothelial Protein C Receptor; D016682:Lupus Coagulation Inhibitor; C478370:PROCR protein, human; D017395:Plasminogen Activator Inhibitor 1; D011486:Protein C; D017293:Protein S; D011956:Receptors, Cell Surface; D053482:beta 2-Glycoprotein I; C095381:factor V Leiden; D000990:Antithrombin III; D005165:Factor V; D011516:Prothrombin; D042965:Methylenetetrahydrofolate Reductase (NADPH2)