Rheumatic disease in pregnancy and breastfeeding

01Purpose and principlesWhat the treatment does and how it fits into care.

Pregnancy planning is a disease-control intervention. Active lupus nephritis, pulmonary hypertension, severe interstitial lung disease, recent vasculitis or uncontrolled inflammatory arthritis can harm fertility, placental function, preterm birth and maternal organs. The safest conception usually follows at least six months of stable low activity on medicines that can continue, with renal, cardiac, respiratory, obstetric and thrombosis risks explicitly reviewed.

At preconception assessment record prior pregnancy outcomes, venous or arterial thrombosis, nephritis, hypertension, pulmonary or cardiac disease, diabetes, infection and vaccination. Measure FBC, renal and liver profiles, blood pressure, urinalysis and protein quantification. In lupus or related disease, check complement and anti-dsDNA, anti-Ro and anti-La and the full antiphospholipid profile when not already established. Review cervical screening and live vaccines before immunosuppression.

TNF inhibitors have the strongest biologic pregnancy evidence. BSR considers infliximab, adalimumab, etanercept, certolizumab and golimumab compatible. Certolizumab lacks an Fc region and has minimal placental transfer. To permit a normal infant live-vaccine schedule, Fc-containing treatment can sometimes stop at a drug-specific gestation when maternal disease allows; if continued later or throughout, defer rotavirus, BCG and other live vaccines until six months according to the exact exposure.

Antiphospholipid syndrome needs shared obstetric-haematology-rheumatology ownership. A woman with persistent aPL but no thrombosis has a different plan from obstetric APS or thrombotic APS. Low-dose aspirin 75–150 mg daily and prophylactic or treatment-dose low-molecular-weight heparin are used according to the precise phenotype and prior outcome. Medicine compatibility is considered here, while the APS disease pathway owns diagnostic criteria, anticoagulant intensity and postnatal duration.

Anti-Ro and anti-La antibodies cross the placenta and can cause neonatal lupus and congenital heart block, most often between 16 and 26 weeks. Arrange fetal-medicine surveillance according to local protocol and previous affected pregnancy. Hydroxychloroquine should continue. Routine maternal dexamethasone for isolated first-degree change is not an automatic standard; management depends on confirmed fetal rhythm and tertiary expertise.

Distinguishing lupus nephritis from pre-eclampsia requires trends and obstetric context. Active sediment, falling complement and rising anti-dsDNA support lupus activity; hypertension, elevated placental markers and later gestation support pre-eclampsia, but both can coexist. Kidney biopsy can be considered when the result will materially change treatment and procedural risk is acceptable. Maternal stabilisation and delivery timing require renal, rheumatology and fetal-medicine decisions together.

Key points

Aim for stable low disease activity for about six months before conception, using medicines that can continue through pregnancy; active disease is itself a maternal and fetal exposure.
At preconception review define renal, cardiac, pulmonary and thrombotic risk, check blood pressure and urine, and test anti-Ro, anti-La and antiphospholipid antibodies when relevant.
Hydroxychloroquine, sulfasalazine with folic acid 5 mg daily, azathioprine, tacrolimus, ciclosporin, prednisolone, colchicine and TNF inhibitors can be compatible when clinically indicated.
Methotrexate is incompatible: stop at least one month before maternal conception. Mycophenolate requires at least six weeks, and leflunomide requires accelerated elimination with verified teriflunomide levels.
Use NSAIDs cautiously earlier in pregnancy, avoid systemic use from 20 weeks unless clinically necessary and stop by 30 weeks; low-dose aspirin for obstetric prevention is a separate indication.
Continue hydroxychloroquine in lupus unless a specific contraindication exists because withdrawal increases flare risk; monitor maternal disease and placental function rather than stopping treatment reflexively.
Certolizumab has minimal placental transfer and does not alter the infant live-vaccine schedule. Fc-containing TNF inhibitors continued late can require deferral of live vaccines to six months.
Prednisolone is the preferred systemic glucocorticoid when needed, ideally below 20 mg daily with steroid-sparing therapy, while monitoring diabetes, pressure, infection and adrenal risk.
Breastfeeding compatibility is not identical to pregnancy compatibility: hydroxychloroquine, sulfasalazine, azathioprine, tacrolimus, prednisolone and TNF inhibitors are generally compatible, while methotrexate, mycophenolate, leflunomide and JAK inhibitors are not.
Document a postpartum plan before delivery: flare surveillance, thromboprophylaxis when indicated, medicine restart, wound and infection review, breastfeeding and the infant live-vaccine schedule.

02Indications, selection and cautionsWho may benefit, who needs urgent treatment and important alternatives.

Preconception high-risk disease

Recent nephritis, pulmonary hypertension, severe lung or heart disease, active vasculitis or thrombosis warrants disease stabilisation and tertiary counselling before conception.

Lupus flare pattern

New inflammatory symptoms, active urine sediment, increasing proteinuria, falling complement and rising anti-dsDNA support disease activity, while infection remains an important mimic.

Pre-eclampsia patternRed flag

New hypertension after 20 weeks with proteinuria or maternal organ or placental dysfunction requires urgent maternity assessment and can coexist with lupus nephritis.

Antiphospholipid complicationRed flag

Thrombosis, recurrent early loss, fetal death, severe placental insufficiency or early pre-eclampsia with persistent antibodies defines different APS treatment intensities.

Anti-Ro fetal signalRed flag

Fetal bradycardia or conduction delay between 16 and 26 weeks in an anti-Ro or anti-La pregnancy needs urgent fetal cardiology confirmation.

Postpartum flare or thrombosisRed flag

Increasing arthritis, rash, renal change, chest symptoms or unilateral swelling in the first weeks after birth should not be dismissed as normal recovery.

Red flags requiring action

Severe headache, visual disturbance, epigastric pain, hypertension, thrombocytopenia or increasing proteinuria requires urgent pre-eclampsia assessment even when lupus nephritis is also plausible.
Chest pain, unilateral leg swelling, sudden dyspnoea, hypoxaemia or haemoptysis requires emergency venous-thromboembolism assessment, particularly with antiphospholipid antibodies.
Fever, rigors, urinary or respiratory symptoms, painful rash or reduced fetal movement during immunosuppression needs same-day maternity and infection review.
Rising creatinine, active urine sediment, falling complement, increasing anti-dsDNA or systemic lupus features may indicate nephritis flare and needs joint renal-rheumatology care.
Fetal bradycardia or conduction abnormality in an anti-Ro or anti-La pregnancy requires urgent fetal-medicine assessment, not maternal steroid escalation without confirmation.
Pregnancy exposure to methotrexate, mycophenolate, leflunomide, cyclophosphamide, a JAK inhibitor or another incompatible medicine requires immediate specialist advice.
Severe postpartum headache, neurological deficit, chest symptoms, haemorrhage or hypertensive features remain emergencies because thrombosis and flare risk persists after birth.

03Assessment before treatmentTests and checks that guide safe selection.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
First-line preconception disease assessmentFirst stepFirst line
Why
Define whether activity and organ reserve are safe enough for pregnancy.
Interpretation and limitations
Measure disease-specific activity, FBC, renal and liver profiles, pressure, urine sediment and protein, and arrange cardiac or pulmonary testing when previous organ disease makes pregnancy high risk.
02
Anti-Ro, anti-La and antiphospholipid antibodies
Why
Predict neonatal lupus, congenital heart block, thrombosis and placental complications that require specialised surveillance.
Interpretation and limitations
Confirm the complete aPL pattern on two occasions at least twelve weeks apart outside acute confounders when establishing APS; antibody presence alone does not define anticoagulant dose.
03
Medicine and last-dose reconciliation
Why
Apply exact washout, elimination and infant-vaccine intervals.
Interpretation and limitations
Record methotrexate, mycophenolate and leflunomide stop dates, biologic brand and gestational last dose, JAK contraception interval and every over-the-counter NSAID.
04
Serial blood pressure, urine and renal profile
Why
Detect pre-eclampsia, nephritis and medication toxicity throughout pregnancy.
Interpretation and limitations
Interpret pressure, sediment, protein trend, creatinine, platelets, liver tests, complement and anti-dsDNA together; pregnancy lowers baseline creatinine, so a value within the non-pregnant range may still be abnormal.
05
Fetal growth and placental surveillance
Why
Identify growth restriction and placental insufficiency in lupus, APS, renal disease or hypertension.
Interpretation and limitations
Use fetal-medicine ultrasound and Doppler intervals based on maternal phenotype and prior outcome; reduced movement requires immediate maternity assessment between planned scans.
06
Fetal rhythm surveillance
Why
Detect conduction disease in an anti-Ro or anti-La pregnancy during the period of greatest risk.
Interpretation and limitations
Use local fetal-medicine echocardiographic or heart-rate protocol; an abnormal screen requires specialist confirmation before transplacental treatment decisions.
07
Breastfeeding and infant-vaccine assessment
Why
Match postpartum medicines and neonatal immune exposure to feeding and immunisation plans.
Interpretation and limitations
Record gestational biologic exposure, infant prematurity, jaundice and health, and place any live-vaccine deferral in discharge, GP and immunisation records.

04Treatment approachPreparation, options, escalation and aftercare.

01Preconception first-lineStabilise disease on compatible treatmentFirst stepFirst lineA person with rheumatic disease plans pregnancy but is not yet pregnant.

1Assess activity and organ, thrombotic and obstetric history and aim for approximately six months of stable low disease activity before conception.
2Continue or introduce compatible hydroxychloroquine, sulfasalazine, azathioprine, calcineurin inhibitor or TNF treatment appropriate to the disease.
3Stop or wash out incompatible medicines at their exact interval and verify leflunomide elimination before attempts at conception.

02Antenatal controlTreat mother and monitor placentaPregnancy is established on a compatible regimen or inflammatory disease becomes active.

1Continue effective compatible DMARDs, use prednisolone at the lowest effective dose and do not delay organ-saving induction for a severe flare.
2Monitor blood pressure, urine, renal and disease markers and arrange fetal growth, anti-Ro or APS surveillance according to phenotype.
3Coordinate obstetric aspirin, LMWH and delivery planning through maternal medicine, keeping APS intensity separate from antibody positivity alone.

03Incompatible exposureStop, remove and counsel without assumptionsPregnancy occurs during methotrexate, mycophenolate, leflunomide, cyclophosphamide, JAK or another incompatible treatment.

1Stop the relevant medicine immediately unless abrupt cessation itself requires specialist control, document dose and timing and contact rheumatology and fetal medicine.
2Give folic acid 5 mg daily after methotrexate exposure and perform accelerated elimination with level verification after leflunomide.
3Provide individual teratology counselling and targeted fetal assessment; do not promise safety or presume that exposure mandates one pregnancy outcome.

04Late biologic exposureProtect maternal control and plan infant vaccinesAn Fc-containing biologic is needed beyond the gestation at which stopping would permit routine live vaccination.

1Continue treatment when maternal flare risk outweighs theoretical infant exposure and record the exact agent and final antenatal dose.
2Tell neonatology, primary care and the vaccination team to defer live vaccines until six months or the product-specific safe point.
3Use certolizumab when clinically appropriate if continuous TNF inhibition and an unaltered live-vaccine schedule are priorities.

05Postnatal and breastfeedingPrevent flare, infection and conflicting adviceDelivery is approaching or the patient is restarting treatment while feeding an infant.

1EscalationAgree thromboprophylaxis, flare review and compatible medicine continuation before birth and check wound, infection and blood loss before postpartum escalation.
2Use lactation-compatible hydroxychloroquine, sulfasalazine, azathioprine, calcineurin inhibitor, prednisolone or TNF therapy when clinically indicated.
3Avoid incompatible breast-milk exposure and preserve the written infant live-vaccine plan through every transition of care.

05Regimens, contraindications and interactionsTreatment details and the circumstances that modify them.

Core compatible treatment for lupus and selected inflammatory rheumatic disease that reduces maternal flare risk.

Hydroxychloroquine

Continue 200–400 mg orally daily, keeping long-term dose at no more than 5 mg/kg actual body weight each day, throughout pregnancy and breastfeeding when clinically indicated.

Continue retinal and renal risk review; assess QT or cardiac symptoms and do not stop reflexively at conception because loss of disease control can harm pregnancy.

Pregnancy-compatible conventional DMARD for rheumatoid and peripheral spondyloarthritis.

Sulfasalazine with folic acid

Titrate sulfasalazine to the effective rheumatology dose, commonly 2 g orally daily in divided doses, and give folic acid 5 mg orally daily during periconception and the first trimester.

Monitor FBC, liver and renal function; review allergy, G6PD and male reversible oligospermia. Breastfeeding needs paediatric caution for a premature, jaundiced or G6PD-deficient infant.

Compatible steroid-sparing treatment for lupus, vasculitis and selected organ disease.

Azathioprine

Use up to 2 mg/kg orally daily during pregnancy and breastfeeding when required for maternal disease, with dose and monitoring directed by rheumatology, renal or other specialty care.

Check FBC and liver profile and review TPMT or NUDT15 status, infection and allopurinol interaction; neonatal blood monitoring may be considered after high maternal exposure or prematurity.

Preferred systemic glucocorticoid because placental inactivation limits fetal exposure compared with fluorinated steroids.

Prednisolone

Use the lowest effective oral dose, preferably below 20 mg once daily when sustained treatment is required; higher disease-specific doses or IV methylprednisolone are acceptable for organ-threatening maternal disease.

Monitor diabetes, pressure, infection, bone, mood and adrenal suppression. After a single dose above 20 mg, waiting about four hours before breastfeeding can minimise infant exposure when practical.

TNF inhibition with minimal placental transfer, supporting continuous disease control without routine deferral of infant live vaccines.

Certolizumab pegol

Give 400 mg subcutaneously at weeks 0, 2 and 4, then 200 mg every two weeks or 400 mg every four weeks for licensed rheumatic indications throughout pregnancy when needed.

Screen TB, hepatitis B and active infection and review heart failure or demyelination; postpartum treatment still requires maternal wound and infection assessment.

Rapid removal before maternal conception or after pregnancy exposure to a long-persisting teratogenic DMARD.

Leflunomide accelerated elimination

Stop leflunomide and give cholestyramine 8 g orally three times daily for 11 days or activated charcoal 50 g four times daily for 11 days, then verify teriflunomide below 0.02 mg/L twice at least 14 days apart.

Ordinary tablet withdrawal can leave metabolite for up to two years; repeat washout if levels remain above target and coordinate fetal-medicine counselling after exposure.

Prevents placental and maternal thrombosis in selected persistent-aPL and APS pregnancies; intensity belongs to the APS and obstetric pathway.

Low-dose aspirin and LMWH for APS

Use aspirin 75–150 mg orally once daily and prophylactic or treatment-dose low-molecular-weight heparin according to the obstetric or thrombotic APS phenotype, body weight, renal function and maternity-haematology protocol.

Check bleeding, platelet count, renal function, neuraxial and delivery timing. Antibody positivity alone does not justify treatment-dose anticoagulation, and obstetric aspirin is distinct from analgesic NSAID advice.

06Complications, monitoring and follow-upAdverse effects, response and longer-term review.

Before conception and at each trimester or disease-defined interval, record clinical activity, pressure, urine sediment and protein, renal and liver function, blood counts and steroid dose.
For lupus, trend complement and anti-dsDNA with symptoms and urine; investigate infection and pre-eclampsia in parallel rather than assuming every laboratory change is flare.
For calcineurin inhibitors, follow trough concentrations, creatinine, potassium, magnesium, blood pressure and glucose because pregnancy changes volume and drug handling.
Use fetal growth, placental Doppler and fetal-rhythm surveillance according to renal, hypertensive, APS and anti-Ro risk, and respond immediately to reduced fetal movement.
Review every medicine and intended feeding plan near delivery and record which stopped treatment restarts, when blood monitoring resumes and whether wound or infection delays it.
At postnatal review, check flare, mood, thrombosis, pressure, renal disease, contraception and infant live-vaccine communication rather than ending rheumatology care at delivery.

07Special situationsVariants, exceptions and circumstances that change the usual approach.

Untreated disease is an exposure

Maternal inflammation, nephritis, hypertension and thrombosis can harm placental and fetal outcomes, so compatible DMARD continuation is active risk reduction.

Creatinine should fall in pregnancy

A value labelled normal for a non-pregnant adult can signal renal impairment because glomerular filtration usually increases during healthy pregnancy.

Aspirin is not one class decision

Low-dose obstetric antiplatelet treatment can continue when analgesic-dose NSAIDs are avoided after 20 weeks.

Placental transfer accelerates later

Fc-containing antibodies cross increasingly in the second and third trimesters, whereas certolizumab's lack of Fc produces minimal active transfer.

Neonatal records carry maternal pharmacology

The exact last biologic dose determines live-vaccine safety months later and must survive discharge and GP handover.

Postpartum is immunologically active

Delivery can be followed by inflammatory flare while surgery, infection, feeding and thrombosis risks constrain immediate medicine restart.

08Common pitfallsFrequent interpretation and management errors.

01
Stopping every DMARD at a positive pregnancy test and provoking a severe flare instead of distinguishing compatible from incompatible treatment.
02
Using the same washout for methotrexate, mycophenolate and leflunomide despite different persistence and elimination requirements.
03
Calling new proteinuria lupus nephritis without assessing hypertension and placental disease, or calling it pre-eclampsia without urine sediment and lupus trends.
04
Stopping low-dose aspirin because of the systemic NSAID warning even though it was prescribed for an obstetric or APS indication.
05
Continuing an Fc-containing biologic late but omitting infant rotavirus and BCG deferral from the newborn record.
06
Treating pregnancy compatibility as proof of breastfeeding compatibility without considering infant prematurity, jaundice and drug-specific milk evidence.