More MS news articles for Nov 2001

Postpartum Cytokine Rebound May Explain Autoimmune Disease Activity

WESTPORT, CT (Reuters Health) Oct 31 - Monocytic production of the cytokines interleukin-12 (IL-12) and tumor necrosis factor-alpha (TNF-alpha) fall sharply during the third trimester of pregnancy, researchers at the National Institutes of Health report.

They believe that postpartum rebound of these cytokines, along with hormonal changes, may account for the frequently observed exacerbation or onset of rheumatoid arthritis, multiple sclerosis, and some other autoimmune illnesses following pregnancy.

Dr. Ilia J. Elenkov, of the National Institute of Arthritis and Musculoskeletal and Skin Diseases in Bethesda, Maryland, and associates obtained blood and urine samples from 18 healthy pregnant women during week 33 to 36 of gestation and 3 to 6 weeks after delivery.

Urinary cortisol and norepinephrine excretion, as well as serum levels of 1,25-dihydroxyvitamin D-3, were 50% to 400% higher in the third trimester than postpartum, the investigators report in the Journal of Clinical Endocrinology and Metabolism for October. They note that they and others have shown that these hormones directly suppress IL-12 and TNF-alpha production in vitro.

Indeed, monocytic production of IL-12 was about three times lower during pregnancy than postpartum, the investigators found, and production of TNF-alpha was approximately 40% lower.

Dr. Elenkov's group speculates that "postpartum, when [stress] hormones return to normal or low normal levels, the removal of their inhibitory effects may induce a rebound of IL-12 and TNF-alpha production and a Th1 shift."

The authors suggest that "further studies of the role of neuroendocrine factors in the regulation of IL-12, TNF-alpha/IL-10, and Th1/Th2 balance may suggest novel diagnostic and therapeutic approaches for [certain autoimmune] diseases."

J Clin Endocrinol Metab 2001;86:4933-4938.

Copyright © 2001 Reuters Ltd