Pregnancy and Rheumatic Diseases

M. Gayed; C. Gordon

Disclosures

Rheumatology. 2007;46(11):1634-1640. 

In This Article

Risk of Transmission From Mother to Fetus

SLE and Sjögren's syndrome are the most widely recognized rheumatic diseases in which pathogenic antibodies can pass from mother to infant through the transmission of anti-Ro and/or anti-La across the placenta during pregnancy (see subsequent text).[47] The prevalence of these auto-antibodies in SLE patient is about 35% but transmission of IgG antibodies across the placenta between weeks 16 and 32 gestation occurs in about 5% of mothers.[47,48] Neonatal transmission usually resolves within the first 6 months of life, as maternal antibodies are destroyed in the infant.

Neonatal cutaneous vasculitis has been reported in the infants of mothers with cutaneous PAN due to the transmission of auto-antibodies, but the condition resolved soon after birth.[45] A leucocytoclastic vasculitis has been reported in the newborn following a history of a vasculitis which worsened throughout pregnancy and postpartum in the mother.[14] Finally, neonatal thrombocytopenia is recognized to occur in infants, due to the transmission of anti-platelet antibodies across the placenta in mothers with APS. However, thrombotic complications in the neonate are rare.

Neonatal lupus syndrome occurs due to the transmission of maternal auto antibodies across the placenta from week 16. It may present as transient cutaneous lupus lesions, complete heart block, cytopenia, hepatic and other manifestations, occurring in infants born to mothers with positive anti-Ro or anti-La antibodies.[48] Neonatal lupus rash is the most common manifestation and usually presents within a few weeks of birth and is often induced by exposure to UV light. The lesions are typically annular or elliptical with erythema and scaling, similar to those seen in adults with subacute cutaneous lupus. They usually persist several weeks or even a few months, resolving as the maternal autoantibodies are cleared from the fetal circulation.

The most severe complication of neonatal lupus syndrome is congenital heart block (CHB). Complete CHB is diagnosed when fetal bradycardia is identified usually between 18 and 28 weeks. It is important to closely monitor these pregnancies by serial doppler echocardiography. Measurement of AV time intervals is a suggested surveillance instrument, as incomplete block may progress in utero or post-delivery and carries a 20% mortality rate. Permanent pacemakers are required by 67% of survivors with complete CHB.[48] Dexamethasone or betamethasone may be given to try and reverse heart block, as it is able to cross the placenta unlike prednisolone.[1] First and second degree heart bock and heart failure due to myocarditis may be reversed but there is no evidence for reversal of third degree heart block.[48] Affected fetuses should be referred to a paediatric cardiologist for close monitoring.

It is vital to identify maternal anti Ro/La status prior to conception or in early pregnancy. The mother may or may not have a history of photosensitive rash herself treated with hydroxychloroquine. It is not known if this drug has any influence on the development of neonatal lupus syndrome but it appears to be safe in pregnancy.[49,50] The fetal heart rate should be assessed on a weekly basis from week 16 by the midwife or obstetric unit and close monitoring by ultrasound can be considered from week 16 to week 28.[50] Thus heart block can be identified as early as possible and treatment can be initiated if necessary. It is also important to be aware that approximately half the cases of neonatal lupus will occur in pregnancies where the woman has not been diagnosed with a connective tissue disease. At least half of these women will develop Sjögren's syndrome or lupus over the next 10 yrs.[14,48]

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