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Cardiac Septal Defects More Common In SLE Offspring

  • RheumatologyNetwork Staff
Nov 16, 2013
  • ACR 2013, Lupus, Women's Health And Rheumatology

Children born to women with systemic lupus erythematosus (SLE) may be at greater risk of atrial septal heart defects (ASD) and ventricular septal defects (VSD), a study from Canada suggests.
Researchers found a more than tripled risk of ASDs and VSDs in children born to SLE mothers compared to those of women without SLE, in a study reported at the recent 2013 annual meeting of the American College of Rheumatology (ACR) in San Diego.

“Previous studies do suggest a greater prevalence of congenital heart defects among children born to women with SLE,” lead investigator Evelyne Vinet MD, an assistant professor in the Department of Rheumatology at McGill University in Montreal said in an interview.

Those uncontrolled studies by Jill Buyon MD at the NYU Langone Hospital for Joint Diseases in New York found that more than 10% of children born to SLE moms in a cohort with anti-rho antibodies had congenital heart defects , Vinet noted. Buyon also found those children had manifestations of congenital heart block.

In the current study, the McGill researchers analyzed data from the population-based Offspring of Systemic Lupus Erythematosus mothers Registry (OSLER), looking for ASD and VSD diagnoses among 719 children born to 509 mothers with lupus, comparing them to 8,493 children of 5,824 randomly selected women without SLE  followed for over nine years.

ASD and VSD diagnoses were based on records of  more than one hospitalization or physician visit with a relevant diagnostic code within the first year of life.

The McGill team found that, compared to controls, children born to women with SLE had substantially more ASDs (2.9% vs 0.8%) and VSDs (1.7% vs 0.7%).

A multivariate analysis, taking into account the sex and birth order of children and maternal co-morbidities, showed children born to women with SLE had a substantially increased risk of both ASDs and VSDs and of undergoing a cardiac septal defect repair.

Even after accounting for possible detection bias by excluding children with more than one fetal echocardiography (n=331), adjusted effect estimates were similar to the primary multivariate analysis results for both ASDs and VSDs.

In a further subsample analysis of children with maternal public drug coverage throughout pregnancy adjusted for relevant maternal medications, the trend appeared independent of medication exposures.

“Dr. Buyon’s work also suggests that anti-phospholipid antibodies may also be involved in cardiac defects. So perhaps exposure to anti-rho, other antibodies, or even cytokines, may cause fibrosis that prevents septal closures,” says Vinet. “It may not be detected before birth because some atrial septal defects regress spontaneously during fetal life and manifest later on.”

The OSLER registry includes all Canadian women with one or more hospitalizations for childbirth after an SLE diagnosis, identified through universal health care databases between 1989 and 2009.

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