http://jama.ama-assn.org/issues/v286n19/ffull/jha10011-3.html

Brian Vastag

Women with autoimmune disorders often have fewer symptoms during late pregnancy. Conversely, in the year following pregnancy, symptoms often worsen and women without autoimmune disorders are at higher risk for developing them. Scientists now think that roller-coaster levels of two immune hormones, interleukin 12 (IL-12) and tumor necrosis factor ga (TNF-a), drive both phenomena.

Earlier work had suggested that the two hormones may be responsible for the tissue swelling and destruction characteristic of rheumatoid arthritis and multiple sclerosis. To follow up, George P. Chrousos, MD, and colleagues at the National Institute of Child Health and Human Development and the National Institute of Arthritis and Musculoskeletal and Skin Diseases recruited 18 women with healthy pregnancies. The researchers measured IL-12 and TNF-a levels during and after pregnancy. After birth, the women experienced threefold higher levels of IL-12 than they had during their third trimester. Similarly, TNF-a levels rose by 40% after birth.

Additional data led Chrousos to conclude that the master stress hormone, corticotropin-releasing hormone (CRH), powers the IL-12 and TNF-a changes via intermediary stress hormones such as norepinephrine. During pregnancy, the placenta secretes extra CRH into the mother's bloodstream, driving down levels of IL-12 and TNF-a. After birth, CRH levels plummet, reversing the trend.

"This appears to be a rebound effect that could exacerbate autoimmune disorders," said Chrousos. The work appears in the October issue of The Journal of Clinical Endocrinology and Metabolism.

 
© 2001 American Medical Association