84.- Pregnancy and systemic lupus erythematosus
Patients with SLE have traditionally been advised against becoming pregnant. This was based on the description of SLE in the pre-steroid era, when patients with this disease did poorly, particularly with the added stress of pregnancy. Our concepts of SLE in general have evolved over the past one to two decades, and so has our understanding of the relationship between lupus and pregnancy.
Effect of sle on pregnancy
While there has been concern about the effect of lupus pregnancy itself, it has been noted that the disease does not interface with conception. Indeed, fertility rates in patients with SLE have been reported to be the same as in the general population. In one study failed contraception was noted.
Spontaneous abortions, prematurity and still births
Whereas a patient with lupus may conceive normally, her chances of maintaining the pregnancy are reduced. The incidence of fetal wastage has been shown to be increased among patients with SLE.
This results from a greater incidence of prematurity, spontaneous abortion, and intrauterine death. Several factors have been pro posed as possible mechanisms in the increased fetal loss in SLE, including: The presence of active SLE resulting in decidual vasculitis, compromising placental blood supply and consequent deprivation of the fetus;
The presence or trophoblast-reactive lymphocytotoxic anti bodies; Anti-Ro/SSA and anti-LA/SSB antibodies have been associated with destruction of the fetal cardiac conducive system and may lead intra-uterine death; The presence of the lupus anticoagulant and anti bodies to cardiolipin predisposes to thrombosis in the placenta.
Effect of pregnancy on lupus
Early studies of SLE and pregnancy in the steroid era have perpetuated the idea that pregnancy had an adverse effect on the control of SLE. However, it was noted that not all patients did poorly. The rule of three was often quoted: a third of the patients got better, a third got worse and a third remained unchanged.
Recent studies suggest that there in no increased frequency of flared in SLE during pregnancy. A case control prospective study performed by Lockshin and colleagues from New York, comparing pregnant and non-pregnant SLE patients matched for age, race, organ system involvement and disease severity. These investigators found no difference in the frequency of flares occurring either during or after pregnancy between the two groups of patients. A study by Mintz and Coworkers from Mexico City, showed frequent exacerbations among pregnant SLE patients, but the frequency of exacerbations did not differ from that noted in a group of non pregnant SLE patients. Our own studies have shown that there may actually be a protective effect of pregnancy on disease activity in lupus. Thus the premise that pregnancy exacerbates lupus in seriously questioned. Nonetheless, it is clear that if the lupus is active, the chances of it being aggravated by pregnancy are higher, and the chances of successful pregnancy are reduced. Indeed, the study by Mintz et al, which was a prospective study of 102 lupus patient during pregnancy, showed that patients who started the pregnancy during episodes of active lupus had a poorer outcome than other lupus patients.
Exacerbations of lupus nephritis have been a particular worry in SLE patients during pregnancy. Several studies have now shown that if the disease was well control led at conception, SLE was not adversely affected by the pregnancy, nor would permanent renal damage result. The development of edema and hypertension in a pregnant patient with SLE raises the differential diagnosis of pre-eclampsia and a 11 are of SLE with nephritis. Other symptoms and signs of active SLE, or the presence of serologic abnormalities such as elevated anti-DNA antibody or depressed serum complement would favor the diagnosis of a flare of SLE.
Since earlier studies suggested that lupus tended to flare in pregnancy, it was suggested to patients with lupus that they terminate their pregnancies. However, it has subsequently been shown that flared of lupus may occur following therapeutic abortions, and therefore the practice of recommending therapeutic abortions to patients with SLE has stopped. At present there appear to be very few indications for abortion in patients with SLE. Although most studies of SLE in pregnancy include cases which resulted in therapeutic abortions, their indications are primarily psychological.
Management of sle during pregnancy
The best time for a patient with SLE to contemplate pregnancy is when the disease is under good control, and on the lowest dose of mediation. Therefore, whenever possible lupus patients should consult both the obstetrician and the rheumatologist before becoming pregnant. Antibodies to Ro/SSA. La/SSB, anticardioliping antibodies and lupus anticoagulant should be ought, in order to identity any risk factors for the fetus. Once pregnant, patients with SLE should be followed closely by both the obstetrician and the internist/rheumatologist.
There is no information regarding the effect of breast feeding on lupus. There is no indication to suggest that the hormonal changes that result from suckling have and adverse effect on the disease. However, breast feeding may demand tome and energy of the mother, and if the disease is not under good control, breast feeding may not be advisable. Although the is little evidence supporting the transmission of drugs in human milk, animal studies suggest that cortisone may be transmited through mother’s milk. Therefore, it is suggested that lupus patient taking large doses of corticosteroids and/or cytotoxic drugs should be discouraged from breast feeding.
Until recently, lupus patients were advised that if their pregnancies went to term, their newborns were at no increased risk of developing congenital abnormalities. However, a number of neonates born to mothers with SLE have been found to have transient serologic abnormalities, skin lesions and congenital heart block.
The neonatal lupus syndrome has been characterized by the presence of a dermatitis, as well as a variety of systemic and haematologic abnormalities, including hepatitis, isolated congenital heart block, hemolytic anemia and thrombocytopenia. It is thought to result from maternal transfer an IgG antibody, since it usually resolves within nine months of birth. As already mentioned, antibodies to Ro/SSA and La/SSB are considered markers for the development of congenital heat block, as well as other features of t he neonatal lupus syndrome.
These antibodies arc of the IgG type, and thus cross the placenta. While there is no treatment for the newborn with fixed congenital heart block, aside from a pacemaker where necessary, it may very well be that identifying the problem in utero may all ow for early treatment, with high dose steroids or plasmapheresis, and prevention of the development of heart block■
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