Steroid hormones and disease activity during pregnancy in systemic lupus erythematosus
Article first published online: 5 APR 2002
Copyright © 2002 by the American College of Rheumatology
Arthritis Care & Research
Volume 47, Issue 2, pages 202–209, April 2002
How to Cite
Doria, A., Cutolo, M., Ghirardello, A., Zampieri, S., Vescovi, F., Sulli, A., Giusti, M., Piccoli, A., Grella, P. and Gambari, P. F. (2002), Steroid hormones and disease activity during pregnancy in systemic lupus erythematosus. Arthritis & Rheumatism, 47: 202–209. doi: 10.1002/art.10248
- Issue published online: 5 APR 2002
- Article first published online: 5 APR 2002
- Manuscript Accepted: 28 AUG 2001
- Manuscript Received: 7 AUG 2001
- “Ministero dell'Università e della Ricerca Scientifica e Tecnologica”. Grant Number: 9906242552-003
- “Autoanticorpi e danno d'organo nelle malattie autoimmuni sistemiche.”
- Systemic lupus erythematosus;
- Steroid hormones;
- SLE activity;
To analyze the variation of steroid hormone levels during pregnancy in patients with systemic lupus erythematosus (SLE). Moreover, to investigate whether, during gestation, there is any relationship between steroid concentration and SLE activity.
Seventeen consecutive pregnant SLE patients and 8 matched healthy pregnant controls were studied prospectively. Disease activity was evaluated by European Consensus Lupus Activity Measure (ECLAM) score modified for pregnancy. The following hormones were evaluated: testosterone, 17β-estradiol (estradiol), cortisol, dehydroepiandrosterone sulfate (DHEAS), and progesterone.
Disease activity score significantly varied during pregnancy and postpartum (P< 0.05), being decreased in the third trimester and increased in the second trimester and postpartum. Serum levels of all steroids varied significantly during pregnancy and the postpartum period both in patients and in healthy subjects. In SLE patients, estradiol, progesterone, and DHEAS concentrations were found to be significantly reduced compared with controls. Serum level profiles of estradiol and progesterone were different from those observed in controls. No differences in the steroid levels were observed between patients taking prednisone ≤5 mg/day or >5 mg/day, apart from cortisol, which was, as expected, lower in the latter group.
The major hormonal alteration observed during pregnancy in SLE patients was an unexpected lack of estrogen serum level increase, and, to a lesser extent, progesterone serum level increase, during the second and—even more—the third trimester of gestation. This lack of increase probably was due to placental compromise. Therefore, these steroid hormone variations may result in a lower humoral immune response activation, probably related to a change in the estrogen/androgen balance, that in turn could account for the decrease in disease activity observed during the third trimester in pregnant SLE patients.