Treating to target: A strategy to cure gout

Rheumatology Division, Hospital de Cruces, 48600 Baracaldo, Vizcaya, Spain.
Rheumatology (Oxford, England) (Impact Factor: 4.48). 05/2009; 48 Suppl 2(2):ii9-ii14. DOI: 10.1093/rheumatology/kep087
Source: PubMed


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.

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    • "The prevalence of gout has increased over the past few decades to 3.9% of US adults (8.3 million individuals) [1], which is further complicated by a high level of cardiovascular, metabolic, and renal comorbidities [2]. The pathogenesis of gout is well understood; high levels of circulating serum uric acid (SUA) lead to the acute and chronic manifestations of gout via the deposition of monosodium urate crystals in the joints and the soft tissues [3]. Reducing SUA levels effectively " cures " the disease [4], and guidelines including the American College of Rheumatology [5] and the European League Against Rheumatism [6] recommend lowering SUA levels to target levels (o 6 mg/dL or o 5 mg/dL), as well as reducing recurrent attacks, destructive arthropathy, renal disease, and comorbidity. "
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    ABSTRACT: Gout is a painful and disabling joint disease that constitutes the most common inflammatory arthritis in the US. To clarify the economic impact of gout, we systematically reviewed the literature on the direct and indirect costs associated with this disease. We conducted a literature search of MEDLINE, EMBASE, International Pharmaceutical Abstracts, NHS Economic Evaluation, and CINAHL databases to identify studies of gout and economics. We systematically reviewed published studies that met our inclusion criteria and extracted and summarized all relevant economic parameters. Reported costs were inflation-adjusted to 2013 US dollars (USD). A total of 15 studies met all eligibility criteria. Three controlled studies reported all-cause total direct costs based on specific populations (i.e., $4733, $16,925, and $18,362 per capita among employed, elderly, and treatment-refractory gout populations, respectively, and $2562, $10,590, and $7188 among corresponding non-gout patients). Two additional studies, although uncontrolled, allowed for estimation of total all-cause direct costs in unselected gout populations ($11,080 and $13,170). Gout-related costs ranged from $172 to $6179, depending on population characteristics. Six studies reported positive associations of direct costs with SUA level, gout attack frequency, or presence of tophi. Four studies reported on indirect costs, which were estimated to be as high as $4341 USD. The available data suggest that gout patients incur substantially greater direct and indirect costs as compared with gout-free individuals among elderly and treatment-refractory gouty patients, whereas the costs are considerably less among younger, employed gouty patients. Further, direct costs increased with worsening disease characteristics. Copyright © 2015 Elsevier Inc. All rights reserved.
    Seminars in Arthritis and Rheumatism 02/2015; 45(1). DOI:10.1016/j.semarthrit.2015.02.004 · 3.93 Impact Factor
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    • "In the case of gout, medical intervention is indicated in order to prevent progression and to eliminate any tophi [4]. A sustained reduction of serum uric acid levels is "
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    ABSTRACT: Introduction. Febuxostat, a novel xanthine oxidase inhibitor for the treatment of symptomatic hyperuricemia, showed superiority over allopurinol in the reduction of serum uric acid levels in pivotal studies. Whether this holds true the FORTE (febuxostat in the oral urate lowering treatment: effectiveness and safety) study was conducted to evaluate treatment with febuxostat under daily practice conditions. Materials/Methods. The multicentre, open-label, and prospective observational study was conducted in 1,690 German medical practices from 9/2010 to 5/2011. Safety and efficacy data were assessed at baseline and week 4. Results. Data from 5,592 gout patients (72.6% male, mean age 63.7 years) were collected. Under urate lowering treatment with febuxostat mean serum uric acid levels decreased significantly from 8.9 ± 1.9 mg/dL (534.0 ± 114.6 μmol/L) at baseline to 6.2 ± 2.5 mg/dL (372.0 ± 150.0 μmol/L) at week 4. 67% which reached the mean uric acid target (6.1 ± 1.0 mg/dL [366.0 ± 59.4 μmol/L]). Only 43.1% of patients received concomitant flare prophylaxis. A total of 178 adverse events (mostly gout flares) were reported in 152 patients (2.6%). Conclusion. Febuxostat lowers serum uric acid levels effectively in routine clinical practice. Overall, treatment with febuxostat in both available dosages (80 mg/120 mg) was safe and well tolerated.
    International Journal of Rheumatology 09/2014; 2014:123105. DOI:10.1155/2014/123105
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    • "Disease-related variables were used as predictors and were coded as follows: symptom duration (>5 years), cumulative joint involvement (1 joint, monoarticular; 2 to 4 joints, oligoarticular; >4 joints, polyarticular), number of attacks in the last year, attacks in the last month, presence of tophi, number of swollen joints, number of tender joints, sUA (<5 mg/dl; ≥5 to 6 mg/dl; ≥6 to 7 mg/dl; >7 mg/dl) [31], current ULT, current nonsteroidal anti-inflammatory drugs or colchicine use, and systemic corticosteroid use at any time (previous or current). "
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    ABSTRACT: Gout is the most prevalent arthritis and significantly impacts on function and quality of life. Given that gout associates with disabling comorbid conditions, it is not clear whether such a complex of diseases accounts for the increased disability or if gout may play a role by itself. This study aims to evaluate the specific influence of gout and disease-related features on functional disability and health-related quality of life (HRQoL) in patients with gout followed in rheumatology clinics. A random sample of patients was drawn from clinical registries of 30 rheumatology clinics across Italy. Sociodemographic, general health and gout-specific variables were collected. Functional disability and HRQoL were assessed by the health assessment questionnaire (HAQ) and the Physical and Mental Component Summary scores (PCS and MCS) of the Short Form-36 (SF-36). Crude and adjusted ordinal logistic and linear regression models were applied to investigate the specific contribution of different variables on HAQ and SF-36 scores. Results are presented as odds ratio (OR) or mean difference (MD) and 95% confidence intervals. Out of 446 patients with gout, 90% were males with a mean age of 63.9 years and median disease duration of 3.8 years; the majority of patients were overweight or obese, and with several comorbidities; 21.1% showed at least moderate disability; the PCS score was significantly lower than expected age- and gender-matched samples in the general population, while MCS score was not. After adjusting for potential sociodemographic and general-health confounders, gout-specific variables significantly impacted on HAQ, including polyarticular involvement OR 3.82 (1.63, 8.95), presence of tophi OR 1.92 (1.07, 3.43) and recent attacks OR 2.20 (1.27, 3.81). Consistent results were found for PCS. The impairment of PCS compared to the general population was limited to patients with features of chronic gout. MCS was only affected by recent attacks (MD -2.72 [-4.58, -0.86]) and corticosteroid treatment (-3.39 [-5.30,-1.48]). The data from the KING study confirm that gout impacts on disability and provide evidence for an independent association of gout and gout-related features with functional outcome and HRQoL. This result supports the need to improve specific treatment in gout.
    Arthritis research & therapy 09/2013; 15(5):R101. DOI:10.1186/ar4281 · 3.75 Impact Factor
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