title: Placental pathologic conditions in anticardiolipin antibody positive women whose infants had congenital heart defects.
abstract: Anticardiolipin antibodies (ACLA) are present in 10% of women with recurrent pregnancy loss. Other associations with ACLA are arterial and venous thrombosis, cerebral infarction, pulmonary hypertension, preterm delivery, and fetal growth retardation. A previous prospective study of infants of mothers with positive ACLA identified an increased incidence of congenital heart disease in this population. As a follow-up, the placentas of the initial 40 ACLA-positive patients were studied to determine whether there was an increased incidence of infarct or thrombosis compared with that in control subjects matched for maternal age and gestational age within the same 2-year period. The age of ACLA-positive mothers was 30 +/- 5 years versus 29 +/- 5 years in the ACLA-negative mothers. Gestational age was 37 +/- 2 weeks in both groups; placental weight was 553 +/- 169 gm in the ACLA-positive group versus 593 +/- 117 gm in the ACLA-negative group. The birth weight was 2972 +/- 709 gm in infants of ACLA-positive mothers and 2920 +/- 674 gm in infants of ACLA-negative mothers. There was no statistically significant difference between the two groups in gestational age, maternal disease, placental histologic findings, placental weight, type of delivery, or type of ACLA. Twenty-seven ACLA-positive women were receiving prednisone. Chi square analysis showed the ACLA-positive mothers to have more spontaneous abortions (p = 0.02) and to have more children with congenital heart disease (5 ventricular septal defects and 2 atrial septal defects) (p = 0.006). In summary, infants born with congenital heart defects in women positive for ACLA did not have significant placental pathologic conditions when compared with control infants.
authors.affiliation: Department of Pathology, Loyola University Medical Center, Maywood, Ill 60153, USA.
authors.forename: A
authors.initials: A
authors.lastname: Kowal-Vern
authors.forename: S G
authors.initials: SG
authors.lastname: Fisher
authors.forename: J
authors.initials: J
authors.lastname: Muraskas
authors.forename: M A
authors.initials: MA
authors.lastname: Jandreski
authors.forename: J G
authors.initials: JG
authors.lastname: Gianopoulos
authors.forename: A
authors.initials: A
authors.lastname: Husain
mesh_terms: D000328:Adult; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use; D017153:Antibodies, Anticardiolipin / Q000032:analysis*; D016009:Chi-Square Distribution; D005260:Female; D005315:Fetal Diseases / Q000209:etiology*; D006330:Heart Defects, Congenital / Q000453:epidemiology* / Q000209:etiology; D006801:Humans; D015994:Incidence; D007231:Infant, Newborn; D016015:Logistic Models; D010927:Placental Insufficiency / Q000150:complications / Q000188:drug therapy / Q000276:immunology*; D011241:Prednisone / Q000627:therapeutic use; D011247:Pregnancy; D011248:Pregnancy Complications / Q000503:physiopathology*; D011256:Pregnancy Outcome; D011295:Prenatal Care; D012189:Retrospective Studies; D012307:Risk Factors
chemical_list: D000893:Anti-Inflammatory Agents; D017153:Antibodies, Anticardiolipin; D011241:Prednisone