Treating to target: a strategy to cure gout.
ABSTRACT Acute gout attacks and the long-term complications of gout are associated with the deposition of monosodium urate (MSU) monohydrate crystals in the joints and soft tissues, causing acute and chronic inflammation. The aim of long-term treatment is to reduce the serum urate (sUA) level to 6 mg/dl (< or =360 micromol/l), below the saturation point of MSU, so that new crystals cannot form and existing crystals are dissolved. Serial joint aspiration studies confirmed the disappearance of crystals with effective urate-lowering therapy. There is good evidence that achieving sUA <6 mg/dl (360 micromol/l) results in freedom from acute gout attacks, and shrinkage and eventual disappearance of tophi. Gout patients must be informed about their diagnosis and educated about gout management including the importance of compliance with long-term treatment. Patients starting urate-lowering therapy need to understand the importance of prophylactic therapy with colchicine or NSAIDs to reduce the risk of 'mobilization flares' in the first few months. In the long term, reduction in the sUA below the target level will result in gout being effectively cured.
SourceAvailable from: Timothy Shao Ern Tan[Show abstract] [Hide abstract]
ABSTRACT: Introduction: The soaring incidence of gout in the United Kingdom suggests that medical practitioners should be increasingly aware of optimizing management of gout, which is aimed at pain relief, preservation of joint function and preventing recurrent attacks. Recent guidelines published by the British Society of Rheumatology (BSR), have provided clinicians with a framework for achieving these aims. Aims: To evaluate the management of gout in a primary care centre in North West England against recognized standards. Methods: An electronic search on EMIS Web using the Read codes “gout” and “gouty arthritis”, with a specified period of 2010–2013, generated a cohort of patients who were categorized into 2 groups: those prescribed urate-lowering therapy (allopurinol) and those not. Patients on febuxostat were excluded. Clinical data from the patients were extracted and retrospectively audited. Results: A total of 112 patients were identified, of which only 46% (n = 52) of patients were reviewed after an acute attack. Among those who were prescribed allopurinol, only 19% (n = 12) achieved target serum urate levels while only 67% (n = 42) had their serum urate levels checked regularly and 31% (n = 20) had dosage adjustments. Comparatively, in patients not prescribed allopurinol, a few indications for initiating allopurinol were detected: 29% (n = 12) had more than one attack of gout in a year, 27% (n = 11) suffered from renal insufficiency, 2% (n = 1) presented with tophi, and 17% (n = 7) were on diuretics. Conclusion: Gout management in this primary care centre is not fully concordant to the BSR guidelines. Clearly, there is a need to improve adherence, particularly in the tight monitoring of serum uric acid levels, medications review, appropriate use of allopurinol, where indicated, and patient follow-up.
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ABSTRACT: To investigate whether monosodium urate (MSU) crystals induce interleukin (IL)-1β in human fibroblast-like synoviocytes (FLS), and whether the NLRP3 inflammasome is involved in the inflammatory mechanism. Human FLS isolated from explants of synovial tissue were stimulated with MSU crystals (0.001 to 0.5 mg/ml) for different time course (6 hours to 48 hours). The expressions of IL-1β, IL-6, TNF-α and NLRP3 were evaluated with ELISA, Western blot and quantitative real-time PCR. Exposure of FLS to MSU crystals transiently induced a significant increase in IL-1β expression in culture medium with a peak at 6 h. The mRNA level of IL-1β in the FLS cells had a similar pattern at this time point. Changes in IL-6 and TNF-α expression were not observed. Simultaneously, intercellular pro-IL-1β was detected at 6 h. Furthermore, MSU crystals also induced NLRP3 mRNA and protein expression at 6 h to 48 h after MSU treatment. MSU crystals directly increased IL-1β and intercellular NLRP3 expression in FLS cells. It is suggested that the NLRP3 inflammasome may be associated with IL-1β in FLS treated with MSU. Altogether, MSU could induce production and release of IL-1β through the NLRP3 inflammasome in human synoviocytes.Journal of Inflammation 12/2015; 12(1). DOI:10.1186/s12950-015-0070-7 · 2.22 Impact Factor
09/2011; 18(3):163-174. DOI:10.1016/S0121-8123(11)70051-2