XML Feed for RxPG News   Add RxPG News Headlines to My Yahoo!   Javascript Syndication for RxPG News

Research Health World General
 
  Home
 
   Health
 Aging
 Asian Health
 Events
 Fitness
 Food & Nutrition
 Happiness
 Men's Health
 Mental Health
 Occupational Health
 Parenting
 Public Health
 Sleep Hygiene
 Women's Health
 
   Healthcare
 Africa
 Australia
 Canada Healthcare
 China Healthcare
 India Healthcare
 New Zealand
 South Africa
 UK
 USA
 World Healthcare
 
   Latest Research
 Aging
 Alternative Medicine
 Anaethesia
 Biochemistry
 Biotechnology
 Cancer
 Cardiology
 Clinical Trials
 Cytology
 Dental
 Dermatology
 Embryology
 Endocrinology
 ENT
 Environment
 Epidemiology
 Gastroenterology
 Genetics
 Gynaecology
 Haematology
 Immunology
 Infectious Diseases
 Medicine
 Metabolism
 Microbiology
 Musculoskeletal
 Nephrology
 Neurosciences
 Obstetrics
 Ophthalmology
 Orthopedics
 Paediatrics
 Pathology
 Pharmacology
 Physiology
 Physiotherapy
 Psychiatry
 Radiology
 Rheumatology
  Arthritis
   Ankylosing Spondylitis
   Osteoarthritis
   Rheumatiod Arthritis
  Scleroderma
 Sports Medicine
 Surgery
 Toxicology
 Urology
 
   Medical News
 Awards & Prizes
 Epidemics
 Launch
 Opinion
 Professionals
 
   Special Topics
 Ethics
 Euthanasia
 Evolution
 Feature
 Odd Medical News
 Climate
Search

Last Updated: Nov 18, 2006 - 1:55:25 PM

Arthritis Channel
subscribe to Arthritis newsletter

Latest Research : Rheumatology : Arthritis

   DISCUSS   |   EMAIL   |   PRINT
Study links TNF to androgen deficiency in rheumatoid arthritis
Jun 2, 2005 - 3:59:00 PM, Reviewed by: Dr.

"In the present study, we were fortunate to demonstrate that TNF is also a strong inhibitor of the conversion of DHEAS to DHEA in synovial cells from patients with RA but absolutely not in patients with OA."

 
A protein involved in multiple cell functions, tumor necrosis factor (TNF) is perhaps best known for provoking destructive inflammation. Recently, drugs blocking the action of TNF have shown promise in the early treatment of rheumatoid arthritis (RA).

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.

On the evidence of both synovial cell and synovial fluid analysis, levels of DHEA from DHEAS were significantly lower among RA patients than OA patients. In addition, researchers found a negative correlation between converted DHEA and markers of inflammation among RA patients but not in patients with OA. They also found evidence that TNF inhibits the activity of steroid sulfatase, the key enzyme in DHEAS-to-DHEA conversion.

"This is the first study to demonstrate that the conversion of DHEAS to DHEA is decreased in patients with RA as compared with that in patients with OA," notes leading contributor Claudia Weidler. "In the present study, we were fortunate to demonstrate that TNF is also a strong inhibitor of the conversion of DHEAS to DHEA in synovial cells from patients with RA but absolutely not in patients with OA."

Providing the full picture of androgen deficiency in RA, this study affirms the need for further research into early anti-TNF antibody therapy in the treatment of this particular inflammatory disease.
 

- Article: "Tumor Necrosis Factor Inhibits Conversion of Dehydroepiandrosterone (DHEAS) TO DHEA in Rheumatoid Arthritis Synovial Cells: A Prerequisite for Local Androgen Deficiency," Claudia Weidler, Sona Struharova, Martin Schmidt, Bernhard Ugele, Jürgen Schölmerich, and Rainer H. Straub, Arthritis & Rheumatism, June 2005; 52:6; pp. 1721-1729.
 

www.interscience.wiley.com/journal/arthritis

 
Subscribe to Arthritis Newsletter
E-mail Address:

 



Related Arthritis News
DNA-covered submicroscopic bead used to deliver genes to treat rheumatoid arthritis
Rilonacept significantly reduced acute gout flares during uric acid-lowering therapy
Advances in genetics related to ankylosing spondylitis
Is Devil's Claw the key to treating arthritis?
High birth weight - risk for rheumatoid arthritis
Matrilin-3 gene discovered to prevent onset of osteoarthritis
Rituximab halts damage to joints
Tocilizumab effective in systemic juvenile idiopathic arthritis (sJIA)
Unfavourable blood fat levels predict rheumatoid arthritis up to 10 years later
Role of inflammatory leukocytes in extending tissue damage


For any corrections of factual information, to contact the editors or to send any medical news or health news press releases, use feedback form

Top of Page

 

© Copyright 2004 onwards by RxPG Medical Solutions Private Limited
Contact Us