Hormonal control of rheumatoid inflammation.
As other contributors to this volume have discussed, the genetic basis of rheumatoid arthritis (RA) is multifactorial. One aim of this chapter is to propose that perhaps an additional, non-MHC genetic factor contributing to the pathogenesis of RA may reside in a defective response of the neuroendocrine system to inflammatory stimuli. This proposal is based on work carried out in patients with RA and on lessons learned from animal models of chronic inflammatory disease. This chapter will not consider the effect of sex hormones on the pathogenesis of RA because the data are often contradictory and have yet to crystallize into a coherent hypothesis with testable predictions.
Panayi
G S
GS
Rheumatology Unit, UMDS, Guy's Hospital, London, UK.
D000208:Acute Disease; D000818:Animals; D001172:Arthritis, Rheumatoid / Q000209:etiology*; D002908:Chronic Disease; D002940:Circadian Rhythm; D006801:Humans; D007030:Hypothalamo-Hypophyseal System / Q000503:physiopathology*; D010913:Pituitary-Adrenal System / Q000503:physiopathology*; D011388:Prolactin / Q000378:metabolism; D051381:Rats; D011917:Rats, Inbred Lew; D013312:Stress, Physiological / Q000378:metabolism; D013601:T-Lymphocytes / Q000276:immunology
D011388:Prolactin