Moving the Needle: Improving the Care of the Gout Patient

Abstract

Gout is a the most common inflammatory arthritis in the United States. It is a significant cause of morbidity, disability, lost work days, and high healthcare utilization due to intermittent attacks, chronic inflammation, and joint damage. Despite our understanding of the prelude and pathophysiology of gout, hyperuricemia, it is still poorly misunderstood by patients and poorly managed by healthcare providers. Several parallel treatment paradigms have been developed by professional societies around the world based on the understanding of how hyperuricemia occurs, gout epidemiology, expert opinion, and clinical trials data in order to lower uric acid and eventually eliminate the patient’s crystal burden. This review focuses on both the treatment of acute attacks, and more importantly, the long-term management of gout and the lowering of serum uric acid levels to a goal of < 6 mg/dl (0.360 mmol/l) or treating to target. Treating to a target serum uric acid goal is an opportunity to decrease morbidity and improve the quality of care of every gout patient.

Initiating guideline-concordant gout treatment improves arterial endothelial function and reduces intercritical inflammation: a prospective observational study

“…In this context, our data potentially argue for the importance of still-earlier initiation of gout management, prior to the establishment of comorbidities. Unfortunately, even under current, less-stringent guidelines, the quality of care remains poor in the general population of gout sufferers [ 51 ].…”

Chronic tophaceous gout causing lumbar spinal stenosis

“…Gout is the most common inflammatory arthritis worldwide, with an increasing prevalence, currently estimated between 1% and 4% in adults [1 , 2] . Gout is a type of crystalline arthropathy, triggered when monosodium urate exceeds its limit of solubility in the serum and deposits in the synovial and periarticular soft tissues, forming tophi [1] . The negatively birefringent urate crystals initiate an immune complex cascade that results in inflammation and pain.…”

“…The negatively birefringent urate crystals initiate an immune complex cascade that results in inflammation and pain. Hyperuricemia, generally defined as serum uric acid levels above 6.8 mg/dL, is the strongest risk factor for developing gout, and is most often the result of hepatic overproduction or underexcretion due to renal impairment [1] . However, about 10% of people are genetically predisposed to having increased serum urate levels, and thus are at an increased risk for developing gout [2] .…”

Identification of novel thiourea‐stilbene‐triazine conjugates as persuasive lymphoid tyrosine phosphatase inhibitors

“…[ 17 ] R263Q has been associated with a reduced risk for several diseases, including rheumatoid arthritis, [ 18 ] systemic lupus erythematosus, [ 17 ] and ulcerative colitis. [ 19 ] The SNP C1858T results in a R620W mutation, which occurs in a region responsible for binding to Csk, [ 20 ] a tyrosine kinase, which also acts as a negative regulator of TCR signaling. [ 21 ] It is currently believed that R620W results in increased TCR signaling suppression through a gain‐of‐function, but the impact this mutation has on LYP activity and the mechanism by which it functions is currently unclear.…”

“…[ 21 ] It is currently believed that R620W results in increased TCR signaling suppression through a gain‐of‐function, but the impact this mutation has on LYP activity and the mechanism by which it functions is currently unclear. [ 22 ] In contrast to the R263Q, R620W has been implicated in an increased prevalence of a number of diseases including type 1 diabetes, [ 20 ] rheumatoid arthritis, [ 23 ] systemic lupus erythematosus, [ 24 ] Graves' disease, and others. [ 25–27 ]…”