1952
DOI: 10.1038/jid.1952.100
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Comparative Effects of Aminopterin, Cortisone and Acth in Experimental Formaldehyde Arthritis and Psoriatic Arthritis*

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Cited by 10 publications
(6 citation statements)
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“…Madonia (1952) suggested that methyl thiouracil acted via the pituitary/adrenal axis in suppressing the development of formalin arthritis. Gubner, Cote, Hughes, Oleson, Ruegsegger, and Williams (1952) confirmed the benefits of cortisone and of ACTH. Bacchus (1952) found that ascorbic acid did not influence the formalin changes in adrenalectomized rats, suggesting that ascorbic acid acted on the intact adult animal by influencing the adrenal cortical hormones.…”
Section: Experimental Production Of Arthritismentioning
confidence: 56%
“…Madonia (1952) suggested that methyl thiouracil acted via the pituitary/adrenal axis in suppressing the development of formalin arthritis. Gubner, Cote, Hughes, Oleson, Ruegsegger, and Williams (1952) confirmed the benefits of cortisone and of ACTH. Bacchus (1952) found that ascorbic acid did not influence the formalin changes in adrenalectomized rats, suggesting that ascorbic acid acted on the intact adult animal by influencing the adrenal cortical hormones.…”
Section: Experimental Production Of Arthritismentioning
confidence: 56%
“…The rationale for the introduction of MTX for the treatment of RA was assumed on its capacity to inhibit inflammatory and proliferative response of connective tissue. The closely related antifolate aminopterin, a synthetic derivative of pterin, was shown to suppress exudative and proliferative changes in experimental formaldehyde arthritis [21]. Aminopterin was gradually replaced by MTX due to its less toxic nature and the first documented clinical use of MTX for the treatment of RA was in 1951 [22].…”
Section: Historymentioning
confidence: 99%
“…While part of Acthar Gel’s efficacy is mediated through the production of steroids from the adrenal cortex, the non-steroidogenic anti-inflammatory effects via MCR activation are the most interesting. Studies in animal models of inflammation suggest responses to ACTH in the absence of adrenal steroid production 12 . Additionally, Bomback et al 18 have demonstrated previously that cortisol levels after administration of Acthar Gel were within normal limits, supporting a limited contribution for cortisol in responses to Acthar Gel, at least in this population of patients on long-term prednisone therapy.…”
Section: Discussionmentioning
confidence: 99%
“…The MC1R-selective agonists inhibited tumor necrosis factor α (TNF-α)-induced activation of NF-κB and down-regulated expression and secretion of endothelial cell selectin, vascular cell adhesion molecule, and intercellular adhesion molecule in human dermal vascular endothelial cells treated with TNF-α 4 , 11 . In a study with adrenalectomized rats, Acthar Gel decreased experimental arthritis, indicating a steroid-independent action 12 .…”
Section: Introductionmentioning
confidence: 96%