Article Text

Download PDFPDF
Glucocorticoid receptor polymorphisms in Korean patients with rheumatoid arthritis
  1. E B Lee,
  2. J Y Kim,
  3. Y J Lee,
  4. Y W Song
  1. Department of Internal Medicine, Clinical Research Institute, Medical Research Centre, Seoul National University College of Medicine, Seoul, Korea
  1. Correspondence to:
    Professor Y W Song
    Department of Internal Medicine, Seoul National University College of Medicine, 28 Yungon-dong, Chongno-gu, Seoul 110–744, Korea;

Statistics from

Request Permissions

If you wish to reuse any or all of this article please use the link below which will take you to the Copyright Clearance Center’s RightsLink service. You will be able to get a quick price and instant permission to reuse the content in many different ways.

It has been suggested that dysregulation of the neuroendocrine system is an important pathogenetic mechanism of rheumatoid arthritis (RA). The dramatic response of patients with RA to glucocorticoids, the aggravation of RA after resection of bilateral adrenal glands, the inappropriately normal plasma cortisol levels in patients with RA, the blunted plasma cortisol responses after surgical stress, and the essential role of glucocorticoids in the development of streptococcal cell wall induced arthritis in Lewis rats provide evidence that dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis or relative glucocorticoid deficiency might play a part in the development of RA.1,2 The involvement of glucocorticoids in the development of thymocytes further supports the role of glucocorticoid in autoimmune diseases like RA.3

The human glucocorticoid receptor (hGR) is a transcriptional factor …

View Full Text