Systemic Lupus Erythematosus

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Many reports have suggested that the frequency of exacerbations of systemic lupus erythematosus (SLE) is increased during pregnancy and the postpartum period. There are no convincing data, however, to support this concern. The natural history of the disease is variable, and older series were reported before the effective use of corticosteroids or immunosuppressives. The risk of exacerbations does seem to be minimized in patients who are in complete clinical remission at the time of conception.

A number of factors play a role in the increased frequency of fetal loss, prematurity, and intrauterine growth retardation that occur in SLE. These factors include maternal hypertension and renal disease, namely, proteinuria and decreased creatinine clearance, prior history of fetal death, and the presence of antiphospholipid antibodies. Though initially felt to be directly correlated, lupus activity itself has not been shown to independently affect pregnancy outcome. It has been observed that there is a relationship between fetal heart block and maternal SLE. It appears that maternal anti-Ro (SS-A) or anti-La (SS-B) antibody crosses the placenta and may directly damage fetal cardiac tissue. Only 1% to 5% of the children from mothers with anti-Ro (SS-A) or anti-La (SS-B) antibody develop neonatal lupus, characterized by transient photosensitive skin rash, permanent congenital complete heart block, or both. The absence of these antibodies in maternal serum suggests that a child is unlikely to be affected. The occurrence and severity of neonatal lupus are unrelated to maternal disease activity.

Many patients with SLE demonstrate spontaneous remission and do not require treatment. However, flares do occur. The diagnosis of flare in the gravid patient can be difficult because, in pregnancy, common symptoms suggestive of lupus flare - such as arthralgia, palmar and facial erythema, and proteinuria - often have causes unrelated to SLE. More reliable indicators of active disease during pregnancy include increasing levels of anti-DNA antibody, alternative pathway hypocomplementemia, true arthritis, aphthous ulcers, and lymphadenopathy. Serious flares involving the kidneys or central nervous system reduce fetal survival and pose a serious threat to maternal well-being. These patients require treatment, and corticosteroids are the mainstay of therapy. Treatment should not be deferred because of pregnancy. The management of antiphospholipid antibody syndrome in pregnancy without active SLE includes a regimen of heparin and low-dose aspirin. Some studies advocate the use of prednisone, but this remains controversial.

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