Elevated uric acid levels and the incidence of clinical gout are exceedingly rare in women before menopause but rise after cessation of menses, potentially explained by an effect of estrogen on the renal handling of uric acid. Despite this well established association, little is known about the effect of post-menopausal estrogen replacement on uric acid levels in women.
Chronic tophaceous gout remains difficult to treat with available medications. Replacement of uricase, an enzyme essential for uric acid metabolism yet functionally deficient in humans, represents a promising therapy for uric acid lowering and resolution of tophi. Rasburicase, an available recombinant form of uricase, is limited in its use for gout due to immunogenicity.
Antibodies against citrullinated proteins have emerged as powerful diagnostic and prognostic tools in RA that may contribute to the initiation phases of the disease. The enzymes that catalyze the citrullination process, known as peptidyl argenine deiminases (or PADs), may also be involved in the initiation and propagation steps of the RA disease process. Additionally, autoimmunity to these catalysts may identify a subset of RA patients with unique disease phenotypes.
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