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Increased Risk of Complete Congenital Heart Block in Infants Born to Women with Hypothyroidism and Anti-Ro and/or Anti-La Antibodies

DAWN SPENCE, LISA HORNBERGER, ROBERT HAMILTON, and EARL D. SILVERMAN

ABSTRACT.

Objective.
To determine whether the presence of hypothyroidism is associated with an increased incidence of neonatal lupus erythematosus (NLE) in infants of mothers with anti-Ro autoantibodies.

Methods. The cohort consisted of 87 women with anti-Ro antibodies who delivered 102 infants. All infants had a full history and physical examination within 12 weeks of birth, electrocardiogram (echocardiogram when clinically indicated), complete blood cell count with differential, liver function tests, and autoantibody profile. Nine women had hypothyroidism and 78 had normal thyroid function.

Results. At least one manifestation of NLE was seen in 7/9 (78%) infants born to mothers with hypothyroidism and 45/78 (58%) infants born to mothers with normal thyroid function. Complete congenital heart block (CCHB) was seen in 5/9 (55%) in the hypothyroid group and 10/78 (13%) of the normal thyroid function group (p < 0.005). Mothers with hypothyroidism had a 9-fold increased risk over women with normal thyroid function of having a child with CCHB (odds ratio 8.63). Twenty-seven (31%) of the women were healthy: 4/9 of the hypothyroid and 23/78 of the normal thyroid function group. Of the 23 infants born to healthy mothers with normal thyroid function, 15/23 (65%) had NLE and 8/23 (35%) of these had CCHB.

Conclusion. Women with hypothyroidism and anti-Ro antibodies were at increased risk for delivering a child with CCHB compared to women with antibodies alone, irrespective of maternal health. This study indicates that women with hypothyroidism should be tested for anti-Ro antibodies, as they may be at risk to deliver a child with CCHB. (J Rheumatol 2006; 33:167-70; First Release: Nov 15, 2005)

Key Indexing Terms:

NEONATAL LUPUS ERYTHEMATOSUS
HYPOTHYROIDISM
ANTI-La
COMPLETE CONGENITAL HEART BLOCK
AUTOANTIBODIES
ANTI-Ro


From the Divisions of Rheumatology and Cardiology, Departments of Pediatrics and Immunology, Hospital for Sick Children, Hospital for Sick Children Research Institute, University of Toronto, Toronto, Ontario, Canada.

Supported in part by a grant from the March of Dimes Foundation of America.

D. Spence, RN, MSN, PNP, Division of Rheumatology; L. Hornberger, MD, FRCPC, Division of Cardiology, Department of Pediatrics (currently Division of Cardiology, Department of Pediatrics, University of California at San Franscico); R. Hamilton, MD, FRCPC, Division of Cardiology, Department of Pediatrics; E.D. Silverman, MD, FRCPC, Division of Rheumatology, Departments of Pediatrics and Immunology.

Address reprint requests to D. Spence, Division of Rheumatology, Hospital for Sick Children, 555 University Avenue, Toronto, Ontario M5G 1X8. E-mail: Dawn.Spence@sickkids.ca

Accepted for publication August 15, 2005.




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