**10. Conclusion**

*Lupus - Need to Know*

hypertension, obesity or smoking.

**9.2 Newborn complications of SLE**

women with severe pre-eclampsia [43]. Catastrophic antiphospholipid syndrome (CAPS), characterized by acute thrombotic micro-angiopathy, was also recorded in the postpartum period [76]. These syndromes are more frequent in patients with

The postpartum period demands a rigorous monitoring for maternal complications, as SLE flare [75]. Although no increased risk of lupus flares between 2 and 6 months postpartum, compared to during pregnancy, was found, which rate is about 24%, flares can reach almost every patient in the first 6 months after delivery [39]. The treatment for these situations is similar for non-pregnant SLE patients, but the risks of breastfeeding under aggressive therapy should be outweighed. LMHW should be continued for 6 weeks after delivery, due to the increased risk of venous thromboembolism (VTE) during puerperium. Contraception should be encouraged, but estrogen-containing pills must not be used by women with aPL antibodies or APS, moderate to severe SLE and other conditions, as previous VTE,

In general, SLE in pregnancy is associated with a higher incidence of stillbirths, a greater occurrence of great premature babies, with a greater number of newborns admitted to neonatal intensive care units, an APGAR score below 7 within 1 and

Neonatal SLE (0 to 27 days after delivery) is an autoimmune disease that results from passive transfer of autoantibodies from a mother with SLE to the fetus, resulting in fetal and neo-natal disease. It occurs in about 3.5–8% of theses pregnancies and is associated with the presence of maternal anti-Ro/SSA and anti-La/SSB autoantibodies [20, 79]. Main manifestations involve cutaneous and cardiac systems, but it can affect and cause other organ dysfunctions (including thrombocytopenia, hepatitis, and myocarditis) [71]. The presence of anti-Ro/SSA antibodies may be associated with clinical manifestations, but does not appear to have a negative

The most frequent manifestation of SLE in the neonate, with a prevalence of 10 to 20%, is a transient cutaneous rash with annular or elliptical erythematous plaques, which develops in the weeks following delivery [80]. It involves predominantly the face and scalp, is generally photosensitive and resolves spontaneously in the first 6 to 8 months of life, which coincides with the clearance of maternal

The most serious complication of neonatal SLE is a CHB, which can be diagnosed in-utero, on the date of birth or in the neonatal period. This occurs in about 2% of the fetuses of women with anti-Ro/SSA antibodies with a recurrence rate of 20% in the following pregnancies [76, 81, 82]. CHB can be of any degree and can be accompanied by extra-nodal disease, with valve involvement, endocardial (endocardial fibroelastosis) or structural changes, including dilated cardiomyopathy. About 60% of CHB babies will require a pacemaker; 10% of those will develop cardiomyopathy after birth [12]. The 10-year mortality rate ranges 20–35%. The use of HCQ during pregnancy seems to reduce in 65% the risk of cardiac manifestations of neonatal lupus in women with anti-Ro/SSA and anti-La/SSB autoantibodies [83, 84]. Despite immunoglobulin can reduce transplacental transfer of

Management of SLE pregnancy includes serial fetal echocardiography surveillance between 16 and 28 weeks of gestation [22]. If CHB is detected, it is usually no longer reversible. However, corticosteroids that are transplacental, as dexamethasone, can be administrated in order to reduce the resultant cardiomyopathy.

anti-Ro/SSA antibodies, a clinical trial failed to prove its efficacy [22].

5 minutes and a significantly higher number of birth defects [33, 77, 78].

impact on other SLE-related events during pregnancy [80].

autoantibodies from the circulation [71].

SLE, thus increasing the risk of complications in this population.

**100**

The improvement in disease management and pregnancy monitoring have resulted in a significant decrease in maternal and fetal complications in the last few decades. This has been mainly contributed by 3 pillars: 1) new technologies – which have permitted a better understanding of the immunopathogenesis of the disease, enabling substantial data on SLE patients and focusing on the area of genetics, such as genetic predisposition, epigenetics contribution and how these contribute in developing irreversible loss of immunologic self-tolerance; 2) access to healthcare – has permitted SLE patients to better hospital care through the course of their disease; and most importantly: 3) multidisciplinary management – this is essential to achieve successful maternal and fetal outcomes. This is made by a multidisciplinary team of experienced and dedicated physicians that define a strategic plan, such as preconception counseling, pregnancy planning and increased availability of safe drugs in pregnancy and puerperium, to improve both maternal and fetal outcomes. It is crucial to make the correct choice of therapy for women with SLE preconceptionally, during pregnancy and lactation. Medications must be reviewed and adjusted to minimize the effect on the fetus, while maintaining the disease under control.

In this way, even if SLE keeps being a severe risk factor for pregnancy, a healthy outcome for both mother and child has become a more frequent reality.
