Key result
Maternal anti-RNP and Sm antibodies linked to neonatal hypertrophic cardiomyopathy that improves as titers decline.
Why the study?
Neonatal hypertrophic cardiomyopathy associated with transplacental transfer of maternal ribonucleoprotein and Smith autoantibodies is not well characterized compared to cases linked to other maternal autoantibodies.
Case Report (n=1)
Neonatal hypertrophic cardiomyopathy can occur secondary to transplacental transfer of maternal anti-RNP and Sm antibodies and may resolve as antibody titers decline.
Severe asymmetrical hypertrophic cardiomyopathy without heart block accompanied by neuromuscular hypotonia and feeding difficulties was evident shortly after birth in the second child of a mother with systemic lupus erythematosus who had no indication of gestational diabetes. High-level anti-ribonucleoprotein (RNP) and Smoth (Sm) antibodies arising from transplacental transfer of maternal antibodies were detected in the child's serum. The cardiac abnormalities improved with a commensurate decline in antibody titers. Previously reported cases of neonatal cardiomyopathy with endocardial fibroelastosis have been ascribed to the transplacental transfer of maternal Sjogrens Syndrome (SS) A (Ro) and Sjogrens Syndrome (SS) B (La) antibodies and have been more severe and persistent compared with our patient. We advocate close monitoring of all babies of mothers with systemic autoimmunity for changes in heart rate during pregnancy and signs of heart failure and neuromuscular weakness after delivery.
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Shah et al. (2013) conducted a case report in Neonatal hypertrophic cardiomyopathy (n=1). Transplacental transfer of maternal anti-RNP and Sm antibodies was evaluated on Resolution of cardiac abnormalities and antibody titers. Transplacental transfer of maternal anti-RNP and Sm antibodies was associated with neonatal severe asymmetrical hypertrophic cardiomyopathy that improved with a commensurate decline in antibody titers.
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