ACTH

ACTH is included in my list of gout treatment for pain guide. More gout research on ACTH is needed – and here is some:

Bulletin of the NYU Hospital for Joint Diseases 2008;66(3):231-9
Update on the Management of Hyperuricemia and Gout
Michael H. Pillinger, M.D., and Robert T. Keenan, M.D.

ACTH and Melanocortin Receptors: Old Becomes New Again
ACTH (adrenocorticotropic hormone) was the first steroid pathway agent used in rheumatic disease. Although its use in gout has largely been supplanted by prednisone, and though its availability in depot form is currently limited, ACTH is an effective treatment for acute gout [Taylor CT, Brooks NC, Kelley KW. Corticotropin for acute management of gout. Ann Pharmacother. 2001;35(3):365-8], and older rheumatologists speak anecdotally of its superior efficacy.

First described by Hench and Kendall, the antiinflammatory mechanism of ACTH action has long been presumed to be due to its ability to stimulate the adrenal production of corticosterone [Hench PS, Kendall EC, Slocumb CH, Polley HF. The anti-rheumatic effects of cortisone and pituitary ACTH. Trans Stud Coll Physicians Phila. 1950;18(3):95-102.]. However, ACTH is also a precursor molecule for melanocortin and is known to have activity at melanocortin receptors (MCR) [Getting SJ. Targeting melanocortin receptors as potential novel therapeutics. Pharmacol Ther. 2006;111(1):1-15.]. Based on these observations, Getting and coworkers have examined the possibility that ACTH may act to inhibit inflammation via engagement of one or more MCR.

Using a rat model of acute gout, they confirmed the ability of ACTH, injected subcutaneously, to stimulate increases in plasma corticosterone levels, as well as to reduce signs of inflammation such as neutrophil influx. However, they also demonstrated the ability of lower concentrations of ACTH, injected directly into the joint to inhibit joint inflammation without increasing corticosterone levels [Getting SJ, Christian HC, Flower RJ, Perretti M. Activation of melanocortin type 3 receptor as a molecular mechanism for adrenocorticotropic hormone eficacy in gouty arthritis.
Arthritis Rheum. 2002;46(10):2765-75.]. Thus, ACTH must have antiinflammatory properties independent of its effect on glucocorticoid release. Further studies by Getting and associates have demonstrated the ability of MCR antagonists to reverse the antiinflammatory effect of ACTH and the ability of selective agonists of MCR—particularly MCR3—to suppress gouty inflammation [Getting SJ, Lam CW, Chen AS, et al. Melanocortin 3 receptors control crystal-induced inlammation. Faseb J. 2006;20(13):2234-41.
Getting SJ, Allcock GH, Flower R, Perretti M. Natural and synthetic agonists of the melanocortin receptor type 3 possess anti-inflammatory properties. J Leukoc Biol. 2001;69(1):98-104.]. These data suggest that MCR3 agonists may be useful antiinflammatory drugs. Whether such agents will prove useful in human gout
has yet to be tested.