1985
DOI: 10.1016/s0002-9378(85)80039-9
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Congenital complete heart block and SSA antibodies: Obstetric implications

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Cited by 41 publications
(9 citation statements)
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“…The increased sensitivity for antibodies to SSA52 by LIA is also reported by others using another commercial LIA6 and was apparent in both the sera of SLE patients as well as SSc patients. Although antibodies to SSA are not specific for any of the autoimmune connective tissue diseases, these antibodies may be prognostic for the development of neonatal lupus and/or a congenital heart block 13,14. Interestingly, it has been reported recently that maternal autoantibodies directed to a specific epitope within the leucine zipper amino acid sequence 200–239 (p200) of the SSA52 protein correlate with prolongation of fetal atrioventricular time and heart block 15.…”
Section: Discussionmentioning
confidence: 99%
“…The increased sensitivity for antibodies to SSA52 by LIA is also reported by others using another commercial LIA6 and was apparent in both the sera of SLE patients as well as SSc patients. Although antibodies to SSA are not specific for any of the autoimmune connective tissue diseases, these antibodies may be prognostic for the development of neonatal lupus and/or a congenital heart block 13,14. Interestingly, it has been reported recently that maternal autoantibodies directed to a specific epitope within the leucine zipper amino acid sequence 200–239 (p200) of the SSA52 protein correlate with prolongation of fetal atrioventricular time and heart block 15.…”
Section: Discussionmentioning
confidence: 99%
“…These other antibodies were not measured here. Anti-RoSSA antibodies have been shown to cause fetal heart block [25][26][27], This may have occurred in some of our patients.…”
Section: Discussionmentioning
confidence: 94%
“…The fetal cardiac dysfunction usually appears in the second trimester of pregnancy (Scott et al 1983; Singsen et al 1985) after the heart has completed its main development. The defect is acquired, since normal heart rates and function have been observed before the development of complete heart block (Singsen et al 1985; Buyon et al 1987). The myocardial lesion is, apparently, specific for the fetus, with no evident heart disease in the mother.…”
Section: Discussionmentioning
confidence: 99%
“…Because the heart conduction defects usually develop in the second trimester of pregnancy (Scott et al 1983; Singsen et al 1985), at a time when there is increased transport of maternal antibodies across the placenta, treatment has been directed towards decreasing the quantity of maternal autoantibody, or to suppressing fetal myocarditis and specific inflammation of the conduction system. Plasmapheresis is unsuccessful in reversing established congenital heart block (Herreman & Galezewski 1985; Buyon et al 1987), but may prevent myocarditis and limit cardiac damage.…”
Section: Discussionmentioning
confidence: 99%