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Rheumatic Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Neonatal lupus is rare. Clinically, there may be a transient rash or permanent congenital heart block, which is related to SS-A (Ro), SS-B (La) antibody in maternal serum. The neonate may have a transient positive ANA test and thrombocytopenia resulting from maternal antiplatelet antibodies, haemolytic anaemia and leucopaenia.
Autoimmune disorders
Published in Judy Bothamley, Maureen Boyle, Medical Conditions Affecting Pregnancy and Childbirth, 2020
Neonatal lupus is a rare condition and can involve dermatological, haematological or cardiac anomalies. It occurs in around 5% of children born to mothers with anti-Ro antibodies and anti-La antibodies6. The most common presentation of neonatal lupus is cutaneous neonatal lupus, when, the newborn develops a characteristic rash, commonly on the face and scalp, typically after sunlight exposure at around two weeks old. The rash usually disappears within six months6.
Connective tissue disease
Published in Catherine Nelson-Piercy, Handbook of Obstetric Medicine, 2020
The risk of neonatal lupus is increased if a previous child has been affected, rising to 16%–18% with one affected child and 50% if two children are affected; subsequent infants tend to be affected in the same way as their siblings.
Gut dysbiosis and the clinical spectrum in anti-Ro positive mothers of children with neonatal lupus
Published in Gut Microbes, 2022
Robert M. Clancy, Miranda C. Marion, Hannah C. Ainsworth, Miao Chang, Timothy D. Howard, Peter M. Izmirly, Mala Masson, Jill P. Buyon, Carl D. Langefeld
Autoantibodies can antecede overt clinical disease by years, as demonstrated by the fact that serological positivity for anti-SSA/Ro autoantibodies can be detected long before clinical symptoms of Systemic Lupus Erythematosus (SLE);1 however, autoantibody profiles alone cannot predict which patients will develop clinically significant disease versus those who will remain in a benign autoimmune state. In this respect, mothers whose children have neonatal lupus represent a unique population at risk for overt clinical autoimmunity. Despite the presence of high titer anti-SSA/Ro antibodies clearly pathogenic to the developing fetus, many women are asymptomatic and subsequently unaware of their autoantibody status, learning of their autoimmunity only because of disease in their offspring. Follow-up of these at-risk mothers in one U.S. registry revealed that women who were asymptomatic at the time of their child’s birth had 10-year probabilities of developing SLE and Sjögren’s Syndrome (SS) of 18.6% and 27.9%, respectively.2
Clinical outcomes and predictors of maternal and fetal complications in pregnancies of patients with systemic lupus erythematosus
Published in Expert Review of Clinical Immunology, 2019
Maddalena Larosa, Teresa Del Ross, Antonia Calligaro, Maria Favaro, Elisabetta Zanatta, Luca Iaccarino, Andrea Doria
Neonatal lupus (NL) is a syndrome characterized by different clinical features, including cutaneous, hematological and/or hepatic manifestations, which are usually transient, and a severe condition named congenital atrioventricular block (CHB) which can be permanent. NL is due to a passive immunization of the fetus by maternal anti-SSA/Ro and anti-SSB/La Abs [1,23]. These are actively transported across placenta starting from 16th WG [1]. These Abs are specific for three different proteins (Ro52, Ro60, and La) and one or more non-coding RNAs, showed Y RNAs particles [87]. The majority of NL features tend to resolve within 6–9 months after birth, when maternal Abs are cleared from neonatal circulation [23].
The role of sialic acid-binding immunoglobulin-like-lectin-1 (siglec-1) in immunology and infectious disease
Published in International Reviews of Immunology, 2023
Shane Prenzler, Santosh Rudrawar, Mario Waespy, Sørge Kelm, Shailendra Anoopkumar-Dukie, Thomas Haselhorst
Neonatal lupus (congenital heart block (CHB), neonatal transient skin rash, hematological and hepatic abnormalities) is caused by a passive autoimmunity whereby circulating maternal auto-antibodies are able to be transferred to the developing offspring via trophoblastic neonatal Fc receptors [20]. The antibodies are targeted toward SSA/Ro and SSB/La and are common amongst autoimmune diseases including Sjögren’s syndrome and SLE [20]. Circulating maternal auto-antibodies are transferred to the developing infant from the mother resulting into cardiac abnormalities, such as advanced atrioventricular node (AV) conduction abnormalities and to a lesser extent cardiomyopathy [20]. Macrophages aggregate in congenital heart tissue along with large multinucleated cells [20]. The mechanism underlying the connection between macrophages and CHB has been proposed as anti-SSA/Ro associated ssRNA binds to Toll-like receptors (TLRs) of macrophages which results in the release of pro-inflammatory and pro-fibrosing cytokines [20]. This then causes the trans-differentiation of fibroblasts to myofibroblasts resulting in cardiac scarring and fibrosis [20]. Mothers which are positive to SSA/Ro and SSB/La antibodies have a greater chance of having a child with CHB [20]. Some evidence suggests that women who simultaneously have elevated IFN-α levels are more consistently at risk of having their child develop CHB; as it was observed that there are cases of women with SSA/Ro and SSB/La antibodies and lower IFN-α infants did not develop CHB [20]. It is possible that the maternal IFN-α is also capable of passively being given to the fetus from the mother that consequently contributes to the upregulation of Siglec-1, which has been associated with fibrosis in other autoimmune conditions including SLE [20].