To expand the understanding of TNF's function in chronic inflammatory diseases, researchers at University Hospital Regensburg in Germany and the National Institute of Rheumatic Diseases in the Slovak Republic decided to take a closer look at this cytokine's impact on androgen production. Androgens are thought to play a critical anti-inflammatory role in rheumatic diseases, including various forms of arthritis and lupus, based on extensive clinical trials and animal models. For their study, the team investigated the role of TNF in the conversion of biologically inactive DHEAS--short for dehydroepiandrosterone sulfate--to biologically active DHEA, the steroid hormone parent of androgen, estrogen, and testosterone. Their findings, featured in the June 2005 issue of Arthritis & Rheumatism (http://www.interscience.wiley.com/journal/arthritis), shed new light on suppression of androgen by TNF in RA patients, as well as on the different nature of inflammation in RA from the most common inflammatory disease: osteoarthritis (OA).

To get a clear picture of how TNF affects hormone production and regulation, the research team analyzed samples of inflamed synovial tissue--obtained immediately after opening the knee joint capsules of 37 patients who underwent elective joint replacement surgery. 15 of the patients had a longstanding history of RA, with disease duration averaging 15 years. 22 of the patients were OA sufferers. Using tools for biochemical analysis, the team assessed the process of converting DHEAS to DHEA. The results revealed marked differences in the cellular activity of RA and OA patients.

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Contact: Amy Molnar
amolnar@wiley.com
John Wiley & Sons, Inc.
2-Jun-2005