DOI: 10.1111/j.1744-4667.2012.00113.

x 2012;14:167–174
The Obstetrician & Gynaecologist
Review
http://onlinetog.org

Maternal and fetal complications of systemic lupus

erythematosus
a, b
Matthew Cauldwell MBBS BSc, * Catherine Nelson-Piercy FRCP FRCOG
a
Guy’s and St Thomas’ NHS Foundation Trust, Maternity Services, St Thomas’ Hospital, 10th Floor, North Wing, Westminster Bridge Rd, London
SE1 7EH, UK
b
Guy’s and St Thomas’ NHS Foundation Trust, London, UK
*Correspondence: Matthew Cauldwell. Email: matthew.cauldwell@imperial.ac.uk

Key content
 Systemic lupus erythematosus (SLE) is an autoimmune condition
that has multi-organ involvement.
 It is approximately ten times more common in women than in
men and is often diagnosed during the childbearing years.
 SLE is known to increase the risk of spontaneous miscarriage; it
can also cause fetal growth restriction and increased rates of
sudden intrauterine death, pre-eclampsia and preterm delivery.
 Management of women with lupus nephritis can be difficult, as the
disease may mimic and overlap significantly with pre-eclampsia.
 Multidisciplinary management of pregnant women with SLE
ensures optimal surveillance of both mother and fetus.
Learning objectives
 To understand how to manage pregnant women with SLE.
 To understand the importance of pre-pregnancy counselling for
women with SLE.
 To understand the features and associated risk factors which
increase the chance of adverse pregnancy outcome in women with
SLE.
 To understand which therapies for SLE can be used safely in
pregnancy and while breastfeeding.
 To understand the role of the multidisciplinary team in the care of
women with SLE, particularly those with underlying organ
impairment.
Ethical issues
 When should women with SLE be advised against pregnancy?
 At what point should termination of pregnancy be considered if
there is deterioration in maternal health in early pregnancy?
Keywords antiphospholipid syndrome / drug therapy / fetal growth
restriction / perinatal complications / pre-conception counselling /
pre-eclampsia / thromboembolism

Please cite this paper as: Cauldwell M, Nelson-Piercy C. Maternal and fetal complications of systemic lupus erythematosus. The Obstetrician & Gynaecologist
2012;14:167–174.

most frequently, followed by Asian people.3 The mean age of

Introduction
Systemic lupus erythematosus (SLE) is an idiopathic
autoimmune condition which has multi-organ involvement.
Diagnosis is based on both clinical manifestations and
laboratory indices. The disease course can be sporadic and
unpredictable but is typically characterised by periods of
relapse and remission. This article discusses both the
maternal and fetal complications of SLE and management
of the disease during pregnancy.
Incidence
The literature quotes variable rates of SLE, which may be
due to improvements in diagnostic testing.1 The American
Rheumatism Association first devised a framework for SLE in
1971; this has had several subsequent revisions and the most
recent is outlined in Box 1.2 The disease affects women and
men in a ratio of 10:1. In the UK, population-based studies have
shown that the disease tends to affect Afro-Caribbean people
diagnosis also varies in the literature, but most women seem to
be diagnosed during the childbearing years.1 The prevalence of
SLE in women of childbearing years is around 1 in 500.
Pathophysiology
The exact cause of SLE remains unknown, but it has been
proposed that an environmental trigger such as ultraviolet
light or a viral infection; for example, the Epstein–Barr virus,4
combined with a genetic predisposition, forms the basis of
the disease process.5 There is a 25% concordance for SLE
among monozygotic twins.5
The disease is characterised by immune complex
deposition which causes inflammation in vascular beds.
There is polyclonal B-cell activation which is thought to
result in antinuclear antibody production. There is also an
associated impairment of T-cell regulation and deficiencies in
complement which leads to a failure to remove these immune
complexes.

ª 2012 Royal College of Obstetricians and Gynaecologists 167

 Maternal and fetal complications of SLE

Box 1. 1997 update on 1982 American College of Rheumatology classification criteria for systemic lupus
erythematosus2

Criterion Definition

Malar rash Fixed erythema, flat or raised, over the malar eminences, tending to spare the nasolabial folds
Discoid rash Erythematous raised patches with adherent keratotic scaling and follicular plugging; atrophic scarring may occur in older
lesions
Photosensitivity Skin rash as a result of unusual reaction to sunlight, by patient history or physician observation
Oral ulcers Oral or nasopharyngeal ulceration, usually painless, observed by physician
Arthritis Non-erosive arthritis of two or more peripheral joints, with tenderness, swelling or effusion
Pleuritis or pericarditis Pleuritis: convincing history of pleuritic pain or rubbing heard by a physician or evidence of pleural effusion, or
pericarditis: documented by electrocardiogram or rub or evidence of pericardial effusion
Renal disorder Persistent proteinuria >0.5 g per day or > 3 + if quantification not performed, or
cellular casts: may be red cell, haemoglobin, granular, tubular, or mixed
Neurological disorder Seizures: in the absence of offending drugs or known metabolic derangements; e.g. uraemia, ketoacidosis, or electrolyte
imbalance, or
psychosis: in the absence of offending drugs or known metabolic derangements, e.g. uraemia, ketoacidosis, or electrolyte
imbalance
Haematological disorder Haemolytic anaemia: with reticulocytosis, or
leucopenia: <4000/mm3 on  2 occasions, or
lymphopenia: <1500/mm3 on  2 occasions, or
thrombocytopenia: <100 000/mm3 in the absence of offending drugs
Immunological disorder Anti-DNA: antibody to native DNA in abnormal titre, or
anti-Sm: presence of antibody to Sm nuclear antigen, or
positive finding of antiphospholipid antibodies on:
(i) abnormal serum level of IgG or IgM anticardiolipin antibodies
(ii) positive test result for lupus anticoagulant using a standard method, or
(iii) false-positive test result for  6 months confirmed by Treponema pallidum immobilisation or fluorescent
treponemal antibody absorption test

Positive antinuclear An abnormal titre of antinuclear antibody by immunofluorescence or an equivalent assay at any point in time and in the
antibody absence of drugs
Any combination of four or more of 11 criteria, well documented at any time during a woman’s history, makes it likely that she has SLE (specificity
and sensitivity are 95% and 75%, respectively).

system involvement (Box 2). The presence of anti-Ro/La and

Pre-pregnancy counselling
This should form the first part of management for women
with an established diagnosis of SLE, as conception in a
period of quiescence has been shown to reduce the likelihood
of a flare of their disease during pregnancy.6 Fertility is not
thought to be reduced in women with SLE7 unless there is
concurrent ovarian failure associated with the use of high
cumulative dosages of cyclophosphamide, particularly in
older women,8 or unless there is end-stage renal failure
(chronic kidney disease stage 5) associated with lupus
nephritis, which can cause amenorrhoea. Non-steroidal
anti-inflammatory drugs (NSAIDs) can cause infertility by
means of inhibition of cyclooxygenase, which controls
ovulation, known as luteinised unruptured follicle
syndrome.9 Women who have been investigated for
infertility without any obvious cause but who regularly take
NSAIDs should be advised to stop taking these medications
and use alternative analgesia, as fertility may resume.
During the pre-pregnancy consultation the woman should
be assessed for disease activity and the presence of any organ-
antiphospholipid antibodies should also be determined.
These antibodies are associated with congenital heart block
and neonatal cutaneous lupus syndrome.5 Antiphospholipid
antibodies are present in about 30% of women with SLE and
are associated with arterial and venous thrombosis, recurrent
miscarriage, fetal growth restriction, fetal loss and preterm
delivery due to uteroplacental insufficiency; they require
specific management.
Pre-pregnancy counselling should also include a discussion
regarding medications (see Drug therapy in SLE).
Women should be counselled regarding the possible risks
associated with SLE in pregnancy. They can be reassured that
with quiescent disease, without associated antiphospholipid
syndrome (APS), hypertension or renal involvement the risks
of miscarriage/stillbirth and fetal growth restriction are not
significantly increased compared with background rates and
that adverse outcomes are more likely with the above
complications.10 The risk of miscarriage and stillbirth in
pregnancies complicated by lupus varies in the literature
from 6–35% and from 0–22%, respectively.11,12

168 ª 2012 Royal College of Obstetricians and Gynaecologists

 Cauldwell and Nelson-Piercy

Box 2. Investigations for assessment of disease activity in the pre-pregnancy consultation

Organ/system Complication/manifestation/investigation

Cardiac  Pulmonary hypertension, valvular heart disease, cardiomyopathy: assess with echocardiography

Respiratory  Pulmonary fibrosis: may need to consider chest X-ray, CT, lung function tests if there is underlying restrictive respiratory
involvement

Renal  Urine dipstick and protein:creatinine ratio to screen for and to quantify any underlying proteinuria.
 Document and quantify presence of haematuria, hypertension and/or renal impairment (lupus nephritis)
 Renal function tests to assess pre-existing renal dysfunction

Haematology/  Thrombosis: assessment of risk and need for anticoagulation. Full blood count to determine any anaemia, neutropenia or
immunology thrombocytopenia
 Autoantibody profile: antiphospholipid (aPL), anticardiolipin (aCL), lupus anticoagulant (LA), anti-dsDNA and anti-Ro/anti-
La antibodies, complement C3/C4 levels

CT = computed tomography

Obstetric management
Perhaps the most difficult discussions concern when to
It is important to appreciate that not all pregnancies in women
advise women not to conceive or when to terminate a
with SLE need to be considered as high risk. Careful
pregnancy. Of great concern are women with SLE and
identification and stratification should take place to allow
associated pulmonary arterial hypertension who wish to
women to be managed on an individual basis. Women with
conceive: maternal mortality rates have been quoted as being
quiescent skin and/or joint disease who have no other underlying
as high as 40%, but recent data have shown that this rate is
organ impairment and who do not require multidrug therapy or
~33%.13 The point prevalence of pulmonary arterial
an incremental increase in their current drug dosage are very
hypertension in patients with lupus is 4.2%, with most cases
different from those with a history of nephritis/hypertension or
being defined as mild (systolic pulmonary arterial
concurrent APS.
pressure <40 mmHg).14 This was determined for a non-
Pregnant women with active SLE/lupus nephritis or anti-Ro/
pregnant cohort of patients, but the mean age was 41 years,
La/antiphospholipid antibodies shouldbe consideredas a higher
highlighting the importance of selectively screening women for
risk group and managed in centres with appropriate experience.
underlying pulmonary arterial hypertension prior to
Care should be carried out in a multidisciplinary setting where
pregnancy. Women should also be advised not to conceive
obstetricians/midwives and physicians/haematologists work
during a period of active disease, particularly with lupus
closely together to optimise care. It is difficult to recommend
nephritis, because of worse maternal and fetal outcomes.15 In
precisely how often these women should be reviewed, but those
very general terms, women with SLE have two to four-fold
with more active disease need closer monitoring and often
higher rates of complications compared with those without
require hospital admission. For those individuals with stable
the disease: this includes pre-eclampsia, preterm delivery and
disease, 4-weekly reviews of disease activity and regular
fetal growth restriction, all of which are discussed in this
assessment of fetal growth, blood pressure and proteinuria are
article.5,10,16
appropriate. For those at particular risk of fetal growth
Termination of pregnancy or preterm delivery should be
restriction and/or pre-eclampsia because of active disease or
considered in the presence of uncontrolled hypertension and/
previous history, more frequent assessment is indicated.
or worsening renal function despite optimal pharmacological
For those women who are anti-Ro/La positive the fetal
therapy. This may be related to a flare of lupus nephritis
heart rate should be monitored and recorded at each visit and
or severe early-onset pre-eclampsia, particularly if there is
fetal echocardiography assessments made at 18–20 and
associated APS. In active lupus nephritis with worsening
~28 weeks of gestation.
renal function, increasing proteinuria and hypertension,
Careful obstetric management involves an awareness of the
it may be necessary to use such treatments as
possibility of lupus flare and an understanding of how this
cyclophosphamide and mycophenolate mofetil, which are
can overlap with normal pregnancy-related changes and with
associated with congenital malformations if used in the first
pre-eclampsia. Pregnancy and SLE-related changes are
trimester, in which case appropriate counselling should be
summarised in Box 3.
offered.

ª 2012 Royal College of Obstetricians and Gynaecologists 169

 Maternal and fetal complications of SLE
Box 3. Comparison of pregnancy and SLE-related changes
Features Pregnancy-related
Anaemia Physiological haemodilution
Iron deficiency
Proteinuria Pre-eclampsia
Physiological increase of baseline proteinuria
related to pregnancy or withdrawal of ACE inhibitors
Joint swelling/pain Mechanical arthralgia/effusion
Thrombocytopenia Gestational
HELLP syndrome
Pre-eclampsia
Facial rash Melasma
Facial blushing
Seizure Eclampsia
ACE = angiotensin-converting enzyme; HELLP = haemolysis, elevated liver enzymes, low platelet count; APS = antiphospholipid syndrome
Risk of thromboembolism
Women should be individually assessed for risk of
thromboembolism. Ideally, this should be done at the earliest
opportunity: it can be done as part of pre-pregnancy assessment
and counselling. Risk of thromboembolism and the possible
need for thromboprophylaxis should be reassessed in such
circumstances as admission to hospital for a lupus flare.17
Particular care is needed in women with concurrent APS, who
have a higher risk of a thromboembolic event. Women who have
had a previous venous thromboembolism (some of whom may
be on long-term warfarin) should receive thromboprophylaxis
with low molecular weight heparin throughout pregnancy and
for 6 weeks postpartum or until converted back to warfarin.
Management of SLE flares
The risk of an SLE flare in pregnancy is increased with
active disease in the 3–6 months prior to conception, with the
majority of flares occurring in the second half of pregnancy.18
Most flares can be managed expectantly with medical
management and adjustments to drug therapy (see ‘Drug
therapy in SLE’). The blood pressure should be monitored
closely to detect pregnancy-induced hypertension or pre-
eclampsia and the woman should be screened for proteinuria,
which should be quantified with either a urinary protein:
creatinine ratio (PCR) or 24-hour urine collection.
Distinguishing pre-eclampsia from lupus nephritis
This is, perhaps, the most challenging aspect of obstetric
management. The features of lupus nephritis include
hypertension and proteinuria with or without haematuria
and renal impairment. Lupus nephritis is caused by
autoantibodies which produce immune complexes: these are
deposited in the kidneys and they activate the complement
cascade, causing a generalised inflammatory response.19 The
presence of haematuria or red cell casts as well as a rise in anti-
170
Lupus activity
Anaemia of chronic disease
Haemolytic anaemia
Nephritis
Inflammatory synovitis
Immune thrombocytopenia
APS
Malar rash
Neuropsychiatric lupus
Cerebral vein thrombosis (APS)
dsDNA titres or a fall in complement levels help to distinguish
this from pre-eclampsia; in addition, lupus disease activity in
non-renal organ systems suggests that a lupus nephritis flare is
more likely. New-onset lupus nephritis without a previous
history of renal involvement is unusual but not impossible.
Despite these distinguishing features the only definitive and
reliable investigation that can be used to distinguish
pre-eclampsia from lupus nephritis is renal biopsy. This
is not generally undertaken during pregnancy because
complications such as bleeding are greatly increased. It may
be appropriate in the first or second trimester if it is felt that the
result is likely to alter management; for example, if there is
concern about underlying lupus nephritis, for which
appropriate treatment with immunosuppressive agents may
allow prolongation of the pregnancy. In cases of lupus nephritis
that fail to respond to increasing dosages of steroids and
azathioprine, and where there is a deterioration of renal
function and/or hypertension, other immunosuppressive
drugs may be considered, such as mycophenolate mofetil or
tacrolimus. Such management decisions should be undertaken
in consultation with nephrologists and rheumatologists, as
there are associated risks (see Drug therapy in SLE).20
Management of blood pressure in lupus nephritis should
follow the same algorithm as for treatment of pregnancy-
induced hypertension or pre-eclampsia.21 The blood pressure
should ideally be kept below 140/90 mmHg.22
Fetal management
SLE also confers greater risks to the fetus and there needs to
be an awareness of the fetal problems that can develop. It is
generally associated with increased rates of miscarriage,10
although what must be taken into account is that many
women with SLE also have APS.23 However, it is generally
thought that women with SLE without APS have an increased
rate of miscarriage, possibly related to disease activity, and
ª 2012 Royal College of Obstetricians and Gynaecologists

they should be appropriately counselled regarding this in the
pre-pregnancy period.
Scanning and Doppler ultrasound
There is no definitive guide stipulating the absolute timing of
fetal scans and the frequency between scans in pregnancies
complicated with SLE. It is important for the obstetrician to
be aware of the risks of congenital heart block, fetal growth
restriction and increased rates of preterm delivery and
pre-eclampsia.24 These must all be taken into account when
deciding whether increased fetal scanning is indicated.
Scanning at least every 4 weeks to screen for fetal growth
restriction in those women at risk is generally accepted and
fetal echocardiography referral should be arranged for those
with anti-Ro/La antibodies or if any cardiac abnormalities are
detected on ultrasound scan.
Doppler studies can be used to estimate placental function
and can be an aid to predicting outcomes such as pre-eclampsia
and fetal distress. A uterine artery Doppler should be first
carried out at 20 weeks and repeated 4 weeks later if any
abnormality is found. A raised pulsatility index or diastolic
notching are associated with increased risk for developing
pre-eclampsia, as they can indicate underlying placental
dysfunction. Nevertheless, not all women with an abnormal
uterine artery Doppler will develop complications, so it
is important not to treat abnormal Doppler in isolation.
Second trimester Doppler has been shown to predict late
pregnancy outcome in SLE and/or APS in some25,26 but not
all studies.27
Fetal growth restriction
Since this is common in the context of pregnancies
complicated by hypertension, APS and pre-eclampsia, it is
not surprising that pregnant women with SLE are also at risk
of fetal growth restriction. It may affect nearly one in four
pregnancies with maternal SLE and has been reported as
occurring in as many as 35%, particularly with concurrent
lupus nephritis.28
Congenital heart block
This is associated with maternal anti-Ro/La autoantibodies.
Antibodies cross the placenta and destroy the Purkinje
system. The usual presentation is a fixed fetal bradycardia of
60–80 beats per minute on ultrasound scan. It occurs in
2–3% of fetuses of women with the anti-Ro/La antibody and
there is a recurrence rate of 16% in subsequent pregnancies.
It is associated with significant perinatal morbidity and
mortality, with about half of infants requiring pacing by the
first year of life. Congenital heart block develops between 18–
28 weeks of gestation and fetal echocardiography should be
performed around this period to detect it. Hydrops fetalis can
occur in utero and is thought to be due to the degree of
endomyocardial fibrosis and associated myocarditis.
ª 2012 Royal College of Obstetricians and Gynaecologists
Cauldwell and Nelson-Piercy
Neonatal lupus rash
This forms part of the neonatal lupus erythematosus
spectrum, manifesting as annular inflammatory lesions,
which appear much like lesions of subacute cutaneous SLE.
The lesions are most commonly seen on the face and scalp
and appear typically after ultraviolet exposure in the first
2 weeks of life, but up to 3–6 months postpartum. The rash
generally appears spontaneously and can persist for up to
6 months postnatally until the neonate clears the maternal
antibodies. It is rare for neonatal cutaneous lupus and
congenital heart block to occur together in the same
individual.29 Skin biopsy shows histopathology and
immunofluoresence typical of that of cutaneous lupus.
Preterm delivery
This is more common in pregnancies complicated by SLE30
and is often compounded by obstetric intervention and a
tendency to deliver once the fetus is mature. Review of the
literature suggests that the most common indication for
delivery is pre-eclampsia, followed by fetal distress and fetal
growth restriction. Premature rupture of membranes is also
regarded as being more frequent in pregnancies complicated
by SLE; rates vary and are generally quoted as ~20%.31
Interestingly, this risk does not appear to be related to disease
status or serology, although women on steroid treatment
appear to have a greater risk.32
Drug therapy in SLE
Box 4 lists the majority of the pharmacological agentsused in the
treatment of SLE, their mechanism of action, some of the
contraindications to use and safety in pregnancy and
breastfeeding. Drug therapy is an important consideration, as
it is often necessary to manage women with a combination of
different therapies. This is where the experience of clinicians who
treat pregnant women with SLE on a regular basis is invaluable.
Glucocorticoids, mainly in the form of prednisolone, are
frequently but not exclusively used as one of the first-line
treatments in pregnancy. The dosage used does not vary
greatly between pregnant and non-pregnant patients. The risk
of adverse effects of steroids on the fetus is thought to be low,
with little evidence for congenital malformations or neonatal
adrenal suppression. Prednisolone, methylprednisolone and
hydrocortisone are more efficiently metabolised by placental
enzymes than dexamethasone and betamethasone and
therefore cross the placenta in small amounts only. The
adverse effects of steroids on the mother, however, are more
numerous. These include weight gain, immunosuppression
(and therefore increased risk of infections), acne,
gastrointestinal irritation and, probably the most important
adverse effect in pregnancy, increased glucose intolerance.
Women on moderate to high dosages of steroids should
therefore be screened regularly for gestational diabetes.33
171
 Maternal and fetal complications of SLE

Box 4. Pharmacological agents used in the treatment of SLE

Mechanism of Safety in pregnancy and When to stop or

Drug action Placental transfer Effects on fetus breastfeeding to continue

Corticosteroids Anti-inflammatory Betamethasone and Long-term follow-up May breastfeed safely as Continue during
and dexamethasone shows no significant only small amounts pregnancy
immunosuppressive cross placenta neurodevelopmental found in breast milk
readily. delay34
Prednisolone and
hydrocortisone
cross less well
Non-steroidal anti- Inhibit Yes Premature closure of Use with caution in first Ideally, discontinue
inflammatory cyclooxygenase ductus arteriosus if and second trimester. prior to
drugs taken beyond Avoid after 32 weeks of conception
32 weeks gestation.35,36 Safe post-
delivery provided no renal
involvement
Azathioprine Immunosuppressive Crosses placenta but No cases of congenital Safe in pregnancy and Do not stop
agent—prevents fetal liver lacks abnormalities breastfeeding, but use at without
cell proliferation enzyme to convert minimum effective guidance from
and inhibits to active metabolite dose37 rheumatology
lymphocyte staff. Safe to
function continue
Methotrexate Antimetabolite. Does not cross Neural tube defects if Contraindicated in Stop prior to
Inhibits cell- placenta used in early pregnancy. No data on conception
mediated immunity pregnancy effects in breastfeeding
Mycophenolate Inhibitor of purine Crosses placenta and Associated with Avoid in pregnancy and in Stop (change to
mofetil (MMF) synthesis is excreted in breast miscarriage and breastfeeding azathioprine)
milk congenital prior to
malformations36 conception but
seek guidance
from
rheumatology
staff
Cyclophosphamide Alkylating agent Crosses placenta and Teratogenic. Increased Excreted in breast milk, so Stop prior to
is excreted in breast rates of miscarriage should be avoided conception but
milk and congenital altogether in pregnancy in a woman with
abnormalities36 flare consult
rheumatology
staff
Ciclosporin T-cell mediated Crosses placenta and Main problems Treatment used extensively Seek advice from
response prevents found in fetal reported: in transplant patients and rheumatology/
formation of blood prematurity and low autoimmune disease. nephrology staff
interleukin-2 birthweight38 but Breastfeeding probably regarding usage
this may relate to safe
underlying disease
Hydroxychloroquine Disrupts lysosome Does cross placenta No increase in Withdrawal in non- Continue
presentation and congenital pregnant patients may throughout
the processing of abnormalities39 precipitate flare, so safe pregnancy, do
antigens to continue. May not withdraw
breastfeed safely

Other immunosuppressant agents that are frequently
used and are generally considered safe during
pregnancy include azathioprine and hydroxychloroquine.
There is no indication to discontinue them during
pregnancy.
It is also worth noting that several drugs can cause a
lupus-like syndrome. The most common of these are
hydralazine, procainamide, quinidine, isoniazid, diltiazem
and minocycline. The pathophysiology of drug-induced
lupus is not completely understood, but in the case of
hydralazine it is thought to be caused by the formation of
antinuclear antibodies to H1 and the H3–H4 complex
(antihistone). However, these drugs do not cause disease
flare in women with established lupus.

172 ª 2012 Royal College of Obstetricians and Gynaecologists


Postpartum care
This includes:
 ongoing management and treatment of any underlying
pregnancy-induced hypertension
 a risk assessment and prophylaxis regimen for thrombosis,
particularly in women with APS or who have a previous
history of thrombosis or nephrotic syndrome
 advice regarding contraception and on avoiding estrogen-
containing preparations, as these increase the risk of a flare
 vigilance concerning the increased risk of lupus flare in the
postpartum period.
Conclusion
The management of SLE and pregnancy should be
undertaken in a multidisciplinary setting. Labelling all
pregnancies in women with SLE as high risk is not helpful
or appropriate as those with quiescent disease will, in many
cases, have uncomplicated pregnancies. For women who have
active disease in pregnancy, are at risk of neonatal lupus or
who have lupus nephritis or APS and therefore require closer
monitoring because of increased risks of maternal and fetal
adverse outcome, more intensive surveillance by an expert
team is important. The involvement of obstetricians and
physicians with experience of managing SLE in pregnancy
improves the outcome for the mother and fetus.
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ª 2012 Royal College of Obstetricians and Gynaecologists