Preventing congenital neonatal heart block in offspring of mothers with anti-SSA/Ro and SSB/La antibodies: A review of published literature and registered clinical trials

Gleicher, Norbert; Elkayam, Uri

doi:10.1016/j.autrev.2013.04.006

Cited by 51 publications

(27 citation statements)

References 45 publications

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“…As regularly emphasized [21][22][23], the management of CHB remains questionable and controversial, especially regarding the use of fluorinated steroids. In our series, 39.1% of cases received fluorinated steroids versus 38% and 47.8%, respectively, in the European/Brazilian and US registries.…”

Section: Discussionmentioning

confidence: 99%

Description of 214 cases of autoimmune congenital heart block: Results of the French neonatal lupus syndrome

Lévesque

Morel

Maltret

et al. 2015

Autoimmunity Reviews

125

126

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Section: Discussionmentioning

confidence: 99%

Description of 214 cases of autoimmune congenital heart block: Results of the French neonatal lupus syndrome

Lévesque

Morel

Maltret

et al. 2015

Autoimmunity Reviews

125

126

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“…An example is congenital heart block (CHB) that occurs in the fetuses or infants of women with systemic lupus erythrematosus (SLE) or Sjogren’s disease. Although CHB has many possible etiologies (19), a strong candidate is the transplacental transfer of maternal autoAb against the ribonucleoproteins SSA/Ro and SSB/La (20), with SSB/La having a stronger association (21). The maternal autoAb damages the atrioventricular node of the cardiac conduction system by an unknown mechanism.…”

Section: Human Neonatal Autoimmune Disease Induction By Maternal Automentioning

confidence: 99%

The Unique Neonatal NK Cells: A Critical Component Required for Neonatal Autoimmune Disease Induction by Maternal Autoantibody

et al. 2014

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Human maternal autoantibodies can trigger autoimmune diseases such as congenital heart block (CHB) in the progeny of women with lupus or Sjogren’s disease. The pathogenic effect of early autoantibody (autoAb) exposure has been investigated in a murine neonatal autoimmune ovarian disease (nAOD) model triggered by a unique ZP3 antibody. Although immune complexes (IC) are formed in adult and neonatal ovaries, ZP3 antibody triggers severe nAOD only in <7-day-old neonatal mice. Propensity to nAOD is due to the uniquely hyper-responsive neonatal natural killer (NK) cells that lack the inhibitory Ly49C/I receptors. In nAOD, the neonatal NK cells directly mediate ovarian inflammation and oocyte depletion while simultaneously promoting de novo pathogenic ovarian-specific T cell responses. Resistance to nAOD in older mice results from the emergence of the Ly49C/I+ NK cells that regulate effector NK cells and from CD25+ regulatory T cell control. In preliminary studies, FcγRIII+ NK cells as well as the ovarian resident FcγRIII+ macrophages and/or dendritic cells were found to be as indispensable players. Activated by ovarian IC, they migrate to lymphoid organs where NK cell priming occurs. Remarkably, the findings in nAOD are very similar to those reported for neonatal responses to a retrovirus and its cognate antibody that lead to long-lasting immunity. Studies on nAOD therefore provide insights into maternal autoAb-mediated neonatal autoimmunity, including CHB, while simultaneously uncovering new properties of the neonatal innate and adaptive responses, lethality of premature infant infection, and novel neonatal antiviral vaccine design.

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“…Moreover 6/10 displayed also positive ANA at titres ranging from I :80 to I :320 and 2/10 patients showed positive anti-SSA, with no clinical signs of related disease. In these last two patients serial cardiac fetal beat monitoring and echocardiogram during all the pregnancy had been carried out showing no abnormalities (5). An increase of aPL titers during pregnancy was documented in all the patients.…”

mentioning

confidence: 98%

Recurrent Miscarriages in Women Not Fulfilling Classification Criteria for Antiphospholipid Antibody Syndrome

Proietta

Ferrero

Ferri

et al. 2014

Int J Immunopathol Pharmacol

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Obstetric antiphospholipid antibody syndrome (APS), is well defined by classification criteria. It is well known that women with APS should receive prophylactic anticoagulation therapy with subcutaneous low weight heparin all throughout pregnancy and in the first 6 weeks postpartum. However, the optimal treatment for pregnant women having positive anti-phospholipid antibodies, but not fulfilling classification criteria for APS is still unclear. In this retrospective study we report pregnancy outcomes of 10 patients affected by recurrent miscarriages and positive anti-cardiolipin or aβ2GP1 antibodies with titers ranging from 10 to 20 GPL/MPL demonstrated at least twice before pregnancy.

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Preventing congenital neonatal heart block in offspring of mothers with anti-SSA/Ro and SSB/La antibodies: A review of published literature and registered clinical trials

Cited by 51 publications

References 45 publications

Description of 214 cases of autoimmune congenital heart block: Results of the French neonatal lupus syndrome

Description of 214 cases of autoimmune congenital heart block: Results of the French neonatal lupus syndrome

The Unique Neonatal NK Cells: A Critical Component Required for Neonatal Autoimmune Disease Induction by Maternal Autoantibody

Recurrent Miscarriages in Women Not Fulfilling Classification Criteria for Antiphospholipid Antibody Syndrome

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