Ro52, Ro60 and La IgG autoantibody levels and Ro52 IgG subclass profiles longitudinally throughout pregnancy in congenital heart block risk pregnancies.
Congenital heart block occurs in fetuses of Ro/SSA and La/SSB positive women. To investigate the stability of maternal autoantibody levels during pregnancy, we followed Ro52, Ro60 and La autoantibody IgG level variation and Ro52 subclass profiles longitudinally in selected congenital heart block risk pregnancies. Serum samples were obtained from 12 Ro/La positive women diagnosed with a systemic rheumatic disease and followed on average 60 months (range two to 84) which included 13 pregnancies. Seven children were affected by neonatal lupus, whereof four developed complete congenital heart block. Serum was also collected from the babies at birth. Ro52, Ro60 and La IgG as well as subclass antibodies were analysed by ELISA using recombinant antigens. Six Ro/La negative rheumatic patients were included as controls for antibody levels during pregnancy. Ro52, Ro60 and La IgG levels decreased progressively from early to late pregnancy, significantly for Ro52 and Ro60 (P < 0.01). No peaks or persistent elevation of antibody levels were noted in any of the CHB risk pregnancies. Ro52 IgG1 antibody levels were significantly higher than IgG2 (P < 0.01), IgG3 (P < 0.01) and IgG4 (P < 0.05) levels in the mothers during pregnancy. Ro52 IgG1 and IgG4 levels decreased significantly from early to late pregnancy (P = 0.02), while levels of IgG2 and IgG3 were low and the decrease was not significant. All IgG subclasses were transferred to the children. We conclude that maternal levels of Ro52, Ro60 and La autoantibodies tended rather to decrease than to increase during pregnancy.
Strandberg
L
L
Rheumatology Unit, Department of Medicine, Karolinska Institutet, Stockholm, Sweden.
Salomonsson
S
S
Bremme
K
K
Sonesson
S- E
S
Wahren-Herlenius
M
M
D000328:Adult; D000974:Antibodies, Antinuclear / Q000097:blood / Q000276:immunology*; D016736:Antiphospholipid Syndrome / Q000097:blood / Q000276:immunology; D001324:Autoantigens / Q000276:immunology*; D015331:Cohort Studies; D005260:Female; D005500:Follow-Up Studies; D006327:Heart Block / Q000151:congenital* / Q000453:epidemiology / Q000276:immunology; D006801:Humans; D007112:Immunity, Maternally-Acquired; D007074:Immunoglobulin G / Q000097:blood / Q000276:immunology*; D007231:Infant, Newborn; D008180:Lupus Erythematosus, Systemic / Q000097:blood / Q000276:immunology*; D008431:Maternal-Fetal Exchange; D008947:Mixed Connective Tissue Disease / Q000097:blood / Q000276:immunology; D011247:Pregnancy; D011248:Pregnancy Complications / Q000097:blood / Q000276:immunology*; D020733:RNA, Small Cytoplasmic / Q000276:immunology*; D012261:Ribonucleoproteins / Q000276:immunology*; D012306:Risk; D012859:Sjogren's Syndrome / Q000097:blood / Q000276:immunology*; D000097585:SS-B Antigen; D000099207:SS-A Antigen
D000974:Antibodies, Antinuclear; D001324:Autoantigens; D007074:Immunoglobulin G; D020733:RNA, Small Cytoplasmic; D012261:Ribonucleoproteins; D000097585:SS-B Antigen; D000099207:SS-A Antigen; C116006:RO60 protein, human