Systemic lupus erythematosus (SLE) is a multisystem connective tissue disease characterized by multi-organ involvement; characteristic inflammatory lesions of the skin, joints, serous membranes, kidneys and CNS; and its association with high titres of autoantibodies to an array of autoantigens. Its clinical course is often one of the disease flares followed by variable periods of remission. Approximately 90 % of the affected population are young women in their second or third decades of life. Therefore, SLE is the commonest connective tissue disorder encountered during pregnancy, and it has been widely studied by researchers across the globe. Evidence shows the foetal and maternal outcomes are adversely affected by the disease.

A multidisciplinary team comprising of obstetrician with experience in high-risk care, rheumatologist, nephrologists and haematologist is essential for monitoring and managing women with SLE during pregnancy and puerperium [1].

The prevalence of the disease shows wide variation in relation to geographical and racial background.

A point prevalence of 3/100,000 population was observed by researchers in India [2]. This was much lower than data available from the western countries (12.5/100,000 in England [2a], 39/100,000 in Finland [2b], 124/100,000 in the USA [2c]).

Evidence suggests that SLE is more common in African American and Hispanic groups than in Caucasians. The incidence of lupus is much higher in women than in men. During the childbearing years, the female-to-male ratio is about 12:1.

Twenty to 30% of women with SLE develop gestational hypertension or pre-eclampsia during pregnancy [10]. Women with lupus nephropathy develop this complication more frequently. SLE associated with chronic hypertension, antiphospholipid syndrome and long-term steroid use are also vulnerable to develop pre-eclampsia.

Women with SLE who have antiphospholipid antibodies (anticardiolipin antibody and lupus anticoagulant) carry additional risk of thrombosis during pregnancy and especially during puerperium.

Women with SLE have higher rates of miscarriages and intrauterine foetal death than the general healthy obstetric population. In a meta-analysis of various prospective studies on foetal outcome of women with SLE, it was found that 8–23 % (median 14 %) had miscarriages, 2–12 % (median 5 %) had foetal deaths, and 15–34 % (median 24 %) had overall pregnancy losses. Women with nephropathy and antiphospholipid syndrome were found to have higher rates of pregnancy loss [9].

The cause of miscarriages and foetal death is uncertain. Inflammation and altered compliment regulation, poor placentation and placental infarction are some of the possible causes.

Although the preterm birth rate in women with SLE and in healthy controls were compared in a few studies, available evidence shows a higher incidence of preterm birth in women with SLE, more so in women with active disease [11]. It may be attributed to higher incidence of pre-eclampsia and foetal growth restriction needing premature termination.

Co-morbidities as hypertension and renal disease and also steroid therapy lead to high incidence of foetal growth restriction in women with SLE.

Neonatal lupus is the occurrence of SLE symptoms in an infant born from a mother with SLE, most commonly presenting with a rash resembling discoid lupus erythematosus, and sometimes with systemic abnormalities such as heart block or hepatosplenomegaly or haematological complications as haemolytic anaemia, leucopenia and thrombocytopenia. Cause of neonatal lupus may be due to transplacental passage of antibodies from mother. Neonatal lupus is highly associated with maternal anti-Ro/SSA (usually also with anti-La/SSB) antibodies, although the rash may occur with anti-ribonucleoprotein (RNP) antibodies.

Revised American Rheumatism Association (1997) [12] criteria have been widely used for diagnosis of SLE. According to it, the women should have at least four of the following features, either simultaneously or serially.