Medical expert of the article
New publications
Autoimmune disorders in pregnancy
Last reviewed: 07.07.2025

All iLive content is medically reviewed or fact checked to ensure as much factual accuracy as possible.
We have strict sourcing guidelines and only link to reputable media sites, academic research institutions and, whenever possible, medically peer reviewed studies. Note that the numbers in parentheses ([1], [2], etc.) are clickable links to these studies.
If you feel that any of our content is inaccurate, out-of-date, or otherwise questionable, please select it and press Ctrl + Enter.
Systemic lupus erythematosus in pregnancy
Systemic lupus erythematosus may first appear during pregnancy; women who have a history of unexplained second-trimester stillbirth, fetal growth restriction, preterm labor, or spontaneous abortion are often later diagnosed with systemic lupus erythematosus. The course of preexisting systemic lupus erythematosus during pregnancy cannot be predicted, but systemic lupus erythematosus may worsen, especially immediately after delivery.[ 3 ]
Complications include fetal growth restriction, preterm labor due to preeclampsia, and congenital heart block secondary to maternal antibodies crossing the placenta.[ 4 ] Preexisting significant renal or cardiac complications increase the risk of maternal morbidity and mortality. Diffuse nephritis, hypertension, or the presence of circulating antiphospholipid antibodies increase the risk of perinatal mortality. Women with anticardiolipin antibodies ( lupus anticoagulant ) account for approximately 5-15% of patients with systemic lupus erythematosus and have an increased risk of abortion, stillbirth, and thromboembolic disorders.[ 5 ]
Treatment consists of prednisone at the lowest dose. It is necessary to take 10-60 mg orally once a day. Some patients are treated with aspirin (81 mg orally once a day) and prophylaxis with sodium heparin (5000-10,000 IU subcutaneously) or low-molecular-weight heparins. If a woman has severe, refractory systemic lupus erythematosus, the need for continuing immunosuppressants during pregnancy is considered individually.
Rheumatoid arthritis in pregnancy
Rheumatoid arthritis may begin during pregnancy or, more commonly, in the postpartum period. Pre-existing symptoms of rheumatoid arthritis generally improve during pregnancy. There are no specific fetal injuries, but delivery may be difficult if the woman has hip or lumbar spine injuries. [6 ], [ 7 ]
Myasthenia gravis of pregnancy
The course changes during pregnancy. Frequent acute myasthenic episodes may require increasing doses of anticholinesterase drugs (eg, neostigmine), which cause symptoms of cholinergic action (eg, abdominal pain, diarrhea, vomiting, weakness); atropine may be prescribed. [ 8 ]
In general, myasthenia gravis does not have a serious adverse effect on pregnancy.[ 9 ] Reports do not indicate an increased risk of spontaneous abortion or preterm birth in women with myasthenia gravis.[ 10 ] In contrast, infants may develop transient neonatal myasthenia. This occurs in 10–20% of cases due to placental transfer of immunoglobulin G antibodies during the second and third trimesters.[ 11 ] In the newborn, symptoms usually appear 2–4 days after birth, including breathing problems, muscle weakness, weak cry, poor sucking, and ptosis, requiring close monitoring.[ 12 ],[ 13 ] This condition usually resolves within 3 weeks without complications due to degradation of maternally derived antibodies.
Myasthenia gravis is sometimes resistant to standard therapy and requires the use of corticosteroids or immunosuppressants. During labor, women often require assisted ventilation and are extremely sensitive to drugs that depress respiration (eg, sedatives, opioids, magnesium). Because the IgG responsible for myasthenia crosses the placenta, transient myasthenia occurs in 20% of newborns, and is more common in mothers who have not had a thymectomy. [ 14 ]
Immune thrombocytopenic purpura in pregnancy
Immune thrombocytopenic purpura due to maternal antiplatelet IgG tends to worsen during pregnancy and the risk of maternal complications increases. Corticosteroids reduce IgG levels and induce remission in most women, but long-term improvement occurs in 50% of cases. Subsequent immunosuppressive therapy and plasma exchange reduce IgG, increasing platelet counts. Rarely, splenectomy is required for refractory cases; this is best performed in the 2nd trimester, with long-term remission achieved in 80% of cases. Intravenous immunoglobulin significantly increases platelet counts, but only briefly, and may induce labor in women with low platelet counts. Platelet transfusions are used only if cesarean section is necessary and the maternal platelet count is less than 50,000/μL.[ 15 ]
Although IgG can cross the placenta causing fetal and neonatal thrombocytopenia, this is rare. Maternal antiplatelet antibody levels (measured directly or indirectly) do not predict fetal pathology, but the fetus may be involved even in mothers treated with corticosteroids or with previous splenectomy and who do not have thrombocytopenia. A subcutaneous cord blood sample may be diagnostic. If the fetal platelet count is less than 50,000/μL, intracerebral hemorrhage may occur during labor and cesarean delivery is necessary.[ 16 ]