Gout is a type of inflammatory arthritis condition that affects the joints and other tissues, most commonly the feet. Inflammation arises in the areas where monosodium urate (MSU) crystals deposit. These crystal deposits are the result of hyperuricemia (abnormally high levels of uric acid in the blood). Recently, a multinational team of 78 rheumatologists from 14 countries acting under the 3e scientific initiative reviewed the collection of clinical literature on gout and compiled a list of recommendations for its diagnosis and treatment, which we summarize in this article.
Diagnosis for gout is usually performed with standard laboratory and X-ray techniques, but ultrasound and dual-energy CT have recently been proven superior. The essential requirement for diagnosis is the identification of MSU crystals. Hyperuricemia is associated with gout and increases the risk for diabetes, hypertension, and renal disease. Gout also increases the risk for kidney disease, metabolic syndrome, Coronary Heart Disease (CHD), and other cardiovascular disorders. Therefore, screening for and diagnosis of the potential development of these complications is necessary.
The committee reviewed several different treatment options:
- For inflammation: low doses of colchicines (1.8mg daily) are as effective and safer than high doses (4.8mg), and glucocorticoids and NSAIDs show comparable efficacy and safety outcomes.
- Oral colchicines, NSAIDs administered into the joint, and intramuscular glucocorticoids all show success in treating acute gout flare-ups.
- Urate Lowering Therapy (ULT) is specified as the method for reducing levels of serum uric acid (SUA). Allopurinol and febuxostat are both effective in this outcome. Emphasis is placed on the importance of starting ULT at low doses and gradually increasing to more potent levels. Uricase is indicated as the drug of choice for severe cases after all other treatment options have been exhausted.
- Finally, pegloticase is another drug of considerable effectiveness, but more adverse events are associated with it, and precautions are made against combining it with ULT.
In general, each individual patient should be assessed for the precise type of treatment according to their flare-up frequency, duration of disease, and presence and size of tophi (bulky protrusions in the skin, joints, and bones). Monitoring for SUA is crucial in gout because lowered levels correlate to decreased flare-ups, disappearance of crystal deposits, and regression of tophi. Target SUA levels for experiencing these positive healing effects is 0.36 mmol/L. Surgery to remove tophi should be considered only in rare cases where nerve compression, mechanical impingement, or infection, render it necessary.
The limitations of the presented review were that only rheumatologists participated in the decision making process, while specialists from other disciplines, like nephrologists and primary care physicians, were excluded. It is then unclear how the specified recommendations will hold up in cases of gout in conjunction with other diseases. Nevertheless, the guidelines listed here should provide a useful multinational standard for the treatment of gout.
Sivera, F. et al. “Multinational evidence-based recommendations for the diagnosis and management of gout: integrating systematic literature review and expert opinion of a broad panel of rheumatologists in the 3e initiative.” Annals of the Rheumatic Diseases: the EULAR Journal. Available from: http://www.ncbi.nlm.nih.gov/pubmed/23868909. July 18, 2013.
Written by Julia Yusupova