Rheumatoid arthritis (RA) affects 1 to 2 percent of the adult population in the United States. There is a female predominance in RA, and many female patients are of childbearing age . Thus, the management of RA during pregnancy is a common challenge. In many patients with RA, disease activity improves substantially in the gravid state. However, modification of treatment so as to minimize the potential for fetal toxicity while maintaining adequate disease control can be difficult in patients whose RA flares or remains active.
HORMONES AND RHEUMATOID ARTHRITIS
The increased incidence of RA in women suggests that sex hormones may have an influence on RA. As an example, women have noted improved symptoms during the luteal phase of the menstrual cycle, the time when the production of gonadal steroids, particularly progesterone, is maximal . In addition, oophorectomized female mice demonstrate a heightened susceptibility to collagen-induced arthritis .
Pregnancy-related changes in circulating hormones may contribute to alterations in the immune system that may affect disease activity. Both premenopausal and postmenopausal women with RA appear to have lower serum levels of adrenal androgens (eg, dehydroepiandrosterone [DHEA]) [4,5]. DHEA, cortisol, estrogen, progesterone, and norepinephrine, all of which are elevated in pregnancy, contribute to the Th2 dominant cytokine profile that emerges in pregnancy . (See 'Immunology of pregnancy' below.)
In contrast, no significant differences in the serum estrogen concentration have been found between patients with RA and controls . Furthermore, hormone replacement therapy has no effect on the course of RA .
Oral contraceptives — The data on the effect of oral contraceptives on RA are conflicting: