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Journal of Peking University (Health Sciences) ›› 2023, Vol. 55 ›› Issue (6): 1053-1057. doi: 10.19723/j.issn.1671-167X.2023.06.015

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Clinical characteristics of fetal cardiac disease in patients with anti-SSA antibody positive

Yu-fei LI1,Ya-ni YAN2,Jia-yang JIN1,Chun LI1,*(),Qiu-yan PEI2,*()   

  1. 1. Department of Rheumatology and Immunology, Peking University People' s Hospital, Beijing 100044, China
    2. Department of Obstetrics & Gynecology, Peking University People' s Hospital, Beijing 100044, China
  • Received:2023-08-22 Online:2023-12-18 Published:2023-12-11
  • Contact: Chun LI,Qiu-yan PEI E-mail:fiona_leechun@163.com;pqypei@126.com
  • Supported by:
    China lnternational Medical Foundation(Z-2018-40-2101);Peking University People' s Hospital Scientific Research Development Funds(RD 2022-66)

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Abstract:

Objective: To investigate the clinical manifestations and laboratory indicators of anti-Sjögren's-syndrome-related antigen A (SSA) antibody associated fetal cardiac disease. Methods: Pregnant women hospitalized at Peking University People's Hospital from January 2013 to July 2023 were included. Eleven patients with anti-SSA antibody positive were eventually diagnosed with fetal cardiac di-sease. And patients with anti-SSA antibody positive without fetal cardiac disease were selected as controls. Clinical manifestations, laboratory indications and drug usage were compared between the two groups. Results: Among these 11 patients, congenital heart block was confirmed in seven, which was the most common manifestations of fetal cardiac malformation. The proportion of the patients diagnosed with autoimmune disease before pregnancy in fetal cardiac malformation group was significantly lower than that in the control group (P=0.032), while most of the patients in the fetal cardiac malformation group received immune-related examinations for the first time because of this time's fetal cardiac diagnosis. While most of the patients in the control group received routine examinations because of autoimmune diseases diagnosed before pregnancy. During pregnancy, the white blood cell level [(9.29±2.58)×109/L vs. (7.10±1.90×109/L, t=3.052, P=0.004], erythrocyte sedimentation rate [(49.50 (48.00, 51.00) mm/h vs. 23.00 (15.00, 30.25) mm/h, Z=-2.251, P=0.024], IgA level [3.46 (2.30, 5.06) g/L vs. 2.13 (1.77, 2.77) g/L, Z=-2.181, P=0.029], and antinuclear antibody (ANA) titers [1∶320 (1∶160, 1∶320) vs. 1∶80 (1∶40, 1∶160), Z=-3.022, P=0.003] were significantly higher in fetal cardiac malformation group than in the control group. The proportion of positive anti-SSB antibody during pregnancy did not show a statistically significant difference between the two groups (37.5% vs. 7.7%, P=0.053). There was no significant difference in hydroxychloroquine dosage and initiation time between the two groups. The dosage of prednisone in the second and third trimesters was significantly higher in the cardiac malformation group than that in the control group, but there was no significant difference in the first trimester. Conclusion: Fetal cardiac disease is rare in pregnant women with anti-SSA antibody. White blood cell, erythrocyte sedimentation rate, IgA, the titer of ANA positivity were higher in the fetal heart disease group during pregnancy. Since congenital heart block is difficult to reverse, its prevention and monitoring are more important than remedial treatment.

Key words: Anti-Sjögren's-syndrome-related antigen A antibody, Congenital heart defects, Heart block, Pregnancy, Risk factors

CLC Number: 

  • R593.2

Table 1

The comparison of clinical symptoms and complications during pregnancy between the cardial malformation and the control group"

Parameters Cardiac malformation (n=11) Control (n=44) P
Clinical feature, n(%)
  History of miscarriage 5 (45.5) 22 (50.0) > 0.999
  Leukopenia during pregnancy 0 7 (15.9) 0.323
  Thrombocytopenia during pregnancy 2 (18.2) 10 (22.7) > 0.999
  Diagnosis of autoimmune disease before pregnancy 6 (54.5) 38 (86.4) 0.032
Complicating disease, n(%)
  Hashimoto thyroiditis 2 (18.2) 2 (4.5) 0.175
  Hyperthyroidism 0 0 > 0.999
  Hypothyroidism 1 (9.1) 8 (18.2) 0.669
  Gestational diabetes mellitus 1 (9.1) 3 (6.8) > 0.999
  Ovarian tumor 0 2 (4.5) > 0.999

Table 2

The comparison of laboratory parameters between the cardiac malformation and the control group"

Parameters Cardiac malformation (n=11) Control (n=44) Z/t/χ2 P
WBC during pregnancy/(×109/L) 9.29±2.58 7.10±1.90 3.052 0.004
PLT during pregnancy/(×109/L) 202.20±79.05 171.51±56.68 1.428 0.159
ESR during pregnancy/(mm/h) 49.50 (48.00, 51.00) 23.00 (15.00, 30.25) -2.251 0.024
IgA during pregnancy/(g/L) 3.46 (2.30, 5.06) 2.13 (1.77, 2.77) -2.181 0.029
ANA positive during pregnancy 10/10 (100.0) 38/40 (95.0) > 0.999
ANA titer during pregnancy 1∶320 (1∶160, 1∶320) 1∶80 (1∶40, 1∶160) -3.022 0.003
Anti-SSB positive during pregnancy 3/8 (37.5) 3/39 (7.7) 0.053

Table 3

The comparison of medication between the cardiac malformation and the control group"

Parameters Cardiac malformation (n=11) Control (n=44) Z/t/χ2 P
HCQ
  Use of HCQ during pregnancy, n(%) 10 (90.9) 35 (79.5) 0.667
  Use of HCQ during the first trimester, n(%) 6 (54.5) 33 (75.0) 0.266
  HCQ dose in the first trimester/mg, M (P25, P75) 200 (0, 200) 200 (25, 200) -1.117 0.264
  HCQ dose in the second trimester/mg, M (P25, P75) 200 (200, 200) 200 (100, 200) -0.555 0.579
  HCQ dose in the third trimester/mg, M (P25, P75) 200 (200, 200) 200 (125, 200) -1.098 0.272
Prednisone
  Use of prednisone during pregnancy, n(%) 9 (81.8) 16 (36.4) 0.015
  Prednisone dose in the first trimester/mg, M (P25, P75) 0 (0, 10.00) 0 (0, 5.00) -0.593 0.553
  Prednisone dose in the second trimester/mg, M (P25, P75) 10.00 (0, 20.00) 0 (0, 5.00) -2.924 0.003
  Prednisone dose in the third trimester/mg, M (P25, P75) 10.00 (5.00, 26.70) 0 (0, 5.00) -3.347 0.001
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