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Systemic lupus erythematosus and the maternal-fetal dyad

Identifieur interne : 003056 ( Main/Exploration ); précédent : 003055; suivant : 003057

Systemic lupus erythematosus and the maternal-fetal dyad

Auteurs : Jill P. Buyon

Source :

RBID : ISTEX:CCF7C7F5ECCE84AEA1E7B10E2E05347695D95F98

English descriptors

Abstract

Summary: Since systemic lupus erythematosus most frequently affects women of childbearing years, the management of patients during pregnancy is an important and common problem facing the clinician. This review concerns the effects of pregnancy on the course of maternal disease and fetal well-being. On the maternal side are the problems of renal disease which may exacerbate and be difficult to differentiate from pre-eclampsia especially when occurring in the third trimester. An active urinary sediment, falling C3 and CH50 and elevated complement split products of the alternative pathway and terminal attack complex may serve as useful parameters of lupus activity. In general, maternal disease is not an imposing threat and prospective studies suggest that the exacerbation rate is not significantly greater in the pregnant lupus patient than in the non-pregnant patient. On the fetal side are the problems of placental insufficiency and in utero attack on developing organs. Maternal antibodies such as those reactive with negatively charged phospholipids are associated with second trimester miscarriages and suggested, but not firmly established, thrombosis of placental vessels. The placental transfer of maternal antibodies against components of the rapidly expanding group of SSA/Ro-SSB/La ribonucleoproteins is strongly implicated in the transient and permanent manifestations of neonatal lupus. Using various techniques for defining the specificity of the antibody response most associated with heart block, the data suggest that mothers whose sera contain antibodies which recognize antigens of SSA/Ro-SSB/La on SDS-immunoblot are at greatest risk. In the absence of antibodies to SSB/La, mothers whose sera contain antibodies reactive only to bovine SSA/Ro by ELISA do not appear to be at high risk. A rational approach to in utero treatment of autoantibody mediated fetal myocarditis includes plasmapheresis and the use of dexamethasone. Finally, the safety of the commonly used medications for the treatment of lupus such as the nonsteroidal anti-inflammatory agents, glucocorticoids and anti-malarials during gestation and breast feeding, is addressed.

Url:
DOI: 10.1016/S0950-3579(05)80245-6


Affiliations:


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Le document en format XML

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<term>Active lupus</term>
<term>Active lupus pregnancies</term>
<term>Alternative pathway</term>
<term>Alternative pathway activation</term>
<term>American journal</term>
<term>Antibodies reactive</term>
<term>Antibody</term>
<term>Antibody response</term>
<term>Anticardiolipin antibodies</term>
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<term>Anticoagulant</term>
<term>Antimalarial drugs</term>
<term>Antiphospholipid antibodies</term>
<term>Antiphospholipid syndrome</term>
<term>Arthritis</term>
<term>Autoantibody</term>
<term>Blood cells</term>
<term>Breast milk</term>
<term>British journal</term>
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<term>Classical pathway activation</term>
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<term>Clinician</term>
<term>Complement activation</term>
<term>Complement components</term>
<term>Complement split products</term>
<term>Congenital</term>
<term>Congenital heart block</term>
<term>Congential heart block</term>
<term>Connective tissue disease</term>
<term>Control group</term>
<term>Control groups</term>
<term>Conventional measurements</term>
<term>Disease activity</term>
<term>Disease flares</term>
<term>Dyad</term>
<term>England journal</term>
<term>Erythematosus</term>
<term>Exacerbation</term>
<term>Exacerbation rate</term>
<term>Fertility rates</term>
<term>Fetal</term>
<term>Fetal circulation</term>
<term>Fetal myocarditis</term>
<term>Fetal side</term>
<term>Fetus</term>
<term>First trimester</term>
<term>Flare</term>
<term>Gestation</term>
<term>Greatest risk</term>
<term>Gynecology</term>
<term>Heart block</term>
<term>Heavy proteinuria</term>
<term>High risk</term>
<term>Human breast milk</term>
<term>Human heart</term>
<term>Human milk</term>
<term>Hypertension</term>
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<term>Maternal</term>
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<term>Maternal antibody response</term>
<term>Maternal autoantibodies</term>
<term>Maternal disease</term>
<term>Menstrual cycle</term>
<term>Metabolic acidosis</term>
<term>Mintz</term>
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<term>Neonatal lupus</term>
<term>Neonatal lupus erythematosus</term>
<term>Nephritis</term>
<term>Normal range</term>
<term>Normal values</term>
<term>Obstetrics</term>
<term>Odds ratio</term>
<term>Partial thromboplastin time</term>
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<term>Placenta</term>
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<term>Pregnancy</term>
<term>Pregnancy complications</term>
<term>Pregnancy loss</term>
<term>Pregnant lupus patient</term>
<term>Pregnant patients</term>
<term>Pregnant women</term>
<term>Protein excretion</term>
<term>Proteinuria</term>
<term>Renal</term>
<term>Renal biopsy</term>
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<term>Renal function</term>
<term>Renal lesion</term>
<term>Retrospective study</term>
<term>Rheumatic diseases</term>
<term>Rheumatoid arthritis</term>
<term>Rheumatology</term>
<term>Russell viper venom time</term>
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<term>Several studies</term>
<term>Slow rate</term>
<term>Small quantities</term>
<term>Steroid</term>
<term>Syndrome</term>
<term>Systemic</term>
<term>Systemic lupus erythematosus</term>
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<term>Third trimester</term>
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<div type="abstract" xml:lang="en">Summary: Since systemic lupus erythematosus most frequently affects women of childbearing years, the management of patients during pregnancy is an important and common problem facing the clinician. This review concerns the effects of pregnancy on the course of maternal disease and fetal well-being. On the maternal side are the problems of renal disease which may exacerbate and be difficult to differentiate from pre-eclampsia especially when occurring in the third trimester. An active urinary sediment, falling C3 and CH50 and elevated complement split products of the alternative pathway and terminal attack complex may serve as useful parameters of lupus activity. In general, maternal disease is not an imposing threat and prospective studies suggest that the exacerbation rate is not significantly greater in the pregnant lupus patient than in the non-pregnant patient. On the fetal side are the problems of placental insufficiency and in utero attack on developing organs. Maternal antibodies such as those reactive with negatively charged phospholipids are associated with second trimester miscarriages and suggested, but not firmly established, thrombosis of placental vessels. The placental transfer of maternal antibodies against components of the rapidly expanding group of SSA/Ro-SSB/La ribonucleoproteins is strongly implicated in the transient and permanent manifestations of neonatal lupus. Using various techniques for defining the specificity of the antibody response most associated with heart block, the data suggest that mothers whose sera contain antibodies which recognize antigens of SSA/Ro-SSB/La on SDS-immunoblot are at greatest risk. In the absence of antibodies to SSB/La, mothers whose sera contain antibodies reactive only to bovine SSA/Ro by ELISA do not appear to be at high risk. A rational approach to in utero treatment of autoantibody mediated fetal myocarditis includes plasmapheresis and the use of dexamethasone. Finally, the safety of the commonly used medications for the treatment of lupus such as the nonsteroidal anti-inflammatory agents, glucocorticoids and anti-malarials during gestation and breast feeding, is addressed.</div>
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