Aetiology and pathogenesis of rheumatoid arthritis

Dresner, Ellis

doi:10.1016/0002-9343(55)90207-2

Cited by 20 publications

(2 citation statements)

References 270 publications

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“…These hormones are still in use for the management of RA. Structural changes in the adenohypophysis have been observed in RA patients, along with altered adrenal corticosteroid metabolism (10)(11)(12)(13). Oral contraceptives and testosterone may alter the course of RA (14,15).…”

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confidence: 99%

The influence of pituitary hormones on adjuvant arthritis

Berczi

Nagy

Sylvia

et al. 1984

Arthritis & Rheumatism

112

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Adjuvant arthritis was induced in female Fisher rats by injecting their right hind paw with 0.1 ml Freund's complete adjuvant. The development of adjuvant arthritis was inhibited by hypophysectomy and by daily treatment of intact animals with the dopaminergic agent bromocriptine. Adjuvant arthritis developed normally if hypophysectomized or bromocriptine-suppressed animals were treated with either prolactin or growth hormone. Additional treatment with adrenocorticottopic hormone inhibited this restoration. Treatment of hypophysectomized rats with follicle-stimulating hormone, luteinizing hormone, aud thyroidstimulating hormone had no effect. These results indicate that prolactin and/or growth hormone are necessary for the development of adjuvant arthritis, whereas adrenocorticotropic hormone has an inhibitory effect.Women are more prone to autoimmune disease than men. Approximately 90% of patients with systemic lupus erythematosus (SLE) are female (1). Rheumatoid arthritis (RA) is 2-3 times more frequent

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confidence: 99%

The influence of pituitary hormones on adjuvant arthritis

Berczi

Nagy

Sylvia

et al. 1984

Arthritis & Rheumatism

112

View full text Add to dashboard Cite

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“…In addition to the decreased bioactivity of PRL in rheumatoid arthritis, a number of other findings support the existence of abnormal endocrine function in this disease: (1) structural changes in the adenohypophysis, 228 (2) abnormal diurnal rhythm of Cortisol secretion, 229,230 (3) a blunted glucocorticoid response after ACTH administration, 231 (4) reduced serum androgen levels and impaired testosterone response after stimulation with HCG, 232 (5) a blunted TSH and exaggerated PRL response after stimulation with TRH, 214 (6) paradoxical elevation of GH during glucose infusion, 233 and (7) a blunted erythropoietin response to anemia. 227 These abnormalities suggest that a neurohormonal imbalance exists in RA, which could play an etiological role in the immune abnormalities observed.…”

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confidence: 91%