PMID: 6984130Oct 1, 1982Paper

Etiology of rheumatoid arthritis

Medical Hypotheses
G W Rafter

Abstract

The major thesis of the proposed hypothesis is that in the absence of microbial material synovial macrophages in rheumatoid arthritis patients continue to release interleukin 1, which perpetuates the inflammation so characteristic of the disease. Its release is suggested to result from an altered synovial macrophage glutathione metabolism brought about by the action of interleukin 1 on host copper metabolism. Three anti-rheumatic drugs are suggested to act at different points in this pathogenic chain reaction. Alclofenac on interleukin 1, gold thiolates on copper-inhibited macrophage glutathione reductase, and D-penicillamine on IgC catabolism. Drawing upon the hypothesis some suggestions are made for drug design.

References

Jan 1, 1978·Scandinavian Journal of Rheumatology·P MäkisaraG L Mäkisara
Aug 1, 1979·Annals of Internal Medicine·H A BernheimE Atkins
Jun 13, 1975·Annals of the New York Academy of Sciences·C W Castor
May 19, 1972·Nature·S AokiG Aoyama
Dec 4, 1972·European Journal of Biochemistry·C GalanosD W Watson
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Jan 1, 1981·Critical Reviews in Clinical Laboratory Sciences·J M Gutteridge, J Stocks
Mar 15, 1982·Biochemical and Biophysical Research Communications·G W Rafter

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Citations

Apr 15, 1985·Experientia·T Kouri
Mar 1, 1987·Medical Hypotheses·G W Rafter
Nov 1, 1988·Medical Hypotheses·G W Rafter
Jan 1, 1990·Scandinavian Journal of Rheumatology·G W Rafter
Apr 1, 1992·Archives of Sexual Behavior·B WhippleB R Komisaruk
Jul 1, 1994·Medical Hypotheses·G W Rafter
Jan 31, 1985·Biochemical and Biophysical Research Communications·G W Rafter

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