Gout Severity Research Articles

Gout Severity in Recipients of Kidney Transplant

PurposeThis retrospective analysis of medical chart data was performed to compare severity and treatment of gout in patients with or without a history of kidney transplantation (KT). MethodsVia an online survey, a panel of board-certified US nephrologists (N = 104) provided the following deidentified chart data for their 3 most recent patients with gout: age, sex, serum uric acid, numbers of swollen or tender joints, visible tophi, gout flare events (prior 12 months), gout drug treatment history, and KT history. The presence of “severe, uncontrolled gout” was defined as: serum uric acid ≥ 7.0 mg/dL, ≥1 tophi and ≥2 flares in the last 12 months, and history of xanthine oxidase inhibitor treatment. ResultsTwenty-five out of 312 (8.0%) gout patients had a history of KT. Univariate analysis found that patients with gout and history of kidney transplants had: greater prevalence of severe uncontrolled gout (27% vs 8%, P = .007) and tophi (36% vs 17%, P = .030), and higher rates of failure or physician perceived contraindication to allopurinol (44% vs 23%, P = .028). ConclusionThis study provides preliminary evidence that gout in patients with history of KT is more severe and poses greater challenges to pharmacologic management. Although gout has been linked to worse outcomes among kidney recipients in the literature, there are presently no publications on gout severity among patients with KT in comparison to other patients with gout. Further investigation of disease severity and appropriate, effective treatment options in recipients of kidney transplant with a diagnosis of gout, especially prior to the transplant, is warranted.

Indicators of Quality of Life and Functional Status of Patients with Arterial Hypertension and Gout

The objective: to evaluate the quality of life (QOL) and functional status of patients with arterial hypertension (AH) and gout, to determine the factors influencing the QOL in this category of patients.Materials and methods. The study included 61 patients with AH, mean age (SD) of 54,25±10,29 years, which were divided into 2 groups: group 1 (n=36, main) –patients with AH and gout, group 2 (n=25, comparison) – patients with AH. The control group included 10 patients. The QOL was evaluated using the Short Form Medical Outcomes Study (SF-36) questionnaire, the Health Assessment Questionnaire (HAQ-DI) and the 10-point Patient Global Assessment (PGA).Results. Patients with AH and gout were more likely to have lowered their physical health indicators and the role-emotional. The average value of the HAQ-DI questionnaire was significantly lower in the main group, and on the PGA scale, in the main and comparison group.Conclusion. QOL of patients with AH and gout has been reduced to a greater extent in comparison with patients without gout due to chronic pain syndrome, functional constraints, psychological problems. Factors affecting the lung in this category of patients are the clinical manifestations of AH and gout: age, number of exacerbations of AH per year, total cardiovascular risk (TCVR), total number of affected joints, severity of gout, comorbidity.

Gout Severity, Socioeconomic Status, and Work Absence: A Cross-Sectional Study in Primary Care.

To examine the association between gout severity and socioeconomic status (SES) and gout severity and work absence. Postal questionnaires were sent to adult patients who were registered with 20 general practices and who had consultations regarding gout or had been prescribed allopurinol or colchicine in the preceding 2 years. Gout severity was defined using the following proxy measures: number of attacks, history of oligoarticular/polyarticular attacks, disease duration, and allopurinol use. SES was defined using the English index of multiple deprivation (area level) and using self-reported educational attainment (individual level). Work absence was defined as taking time off from work in the past 6 months because of gout. Adjusted odds ratios (ORadj ; 95% confidence intervals [95% CIs]) were calculated using logistic regression models (adjusted for age, sex, body mass index, gout severity, and comorbidities). A total of 1,184 completed questionnaires were returned. The mean age of patients was 65.6 years, and 84% were male. Not having attended further education ("further education" is defined as attendance after the statutory minimum school-leaving age of 16 years) was associated with having had ≥2 gout attacks in the last year (ORadj 0.54 [95% CI 0.36-0.81]) and oligoarticular/polyarticular attacks (ORadj 0.72 [95% CI 0.50-1.05]). Lower area-level deprivation was associated with fewer attacks (≥2) (ORadj 0.71 [95% CI 0.51-0.98]). Work absence was associated with having had ≥2 gout attacks in the last year (ORadj 2.91 [95% CI 1.22- 6.92]), oligoarticular/polyarticular attacks (ORadj 3.10 [95% CI 1.46-6.61]), and shorter disease duration (>18 years) (ORadj 0.13 [95% CI 0.03-0.50]). Gout severity was associated with individual-level deprivation, countering the historic and negative perception of gout as a "rich man's disease." The association of gout severity with work absence reinforces the argument for earlier urate-lowering therapy to prevent attacks from becoming frequent and debilitating.

Crystal-proven Gout and Characteristic Gout Severity Factors Are Associated with Cardiovascular Disease.

Our aim was to examine the prevalence of cardiovascular disease (CVD) in patients with crystal-proven gout compared to arthritis controls. Further, we analyzed the association between characteristic gout severity factors and CVD to provide further support for a pathogenetic relationship between gout and CVD. Patients with arthritis referred for diagnosis were consecutively included in the Gout Arnhem-Liemers cohort. Joint fluid analysis was performed in all referred patients; controls were negative for crystals. Patients' characteristics and different manifestations of CVD and gout severity factors (disease duration, attack frequency, tophi, affected joints, high serum urate acid level, joint damage) were collected. Gout patients were compared with controls for the prevalence of CVD. In addition, the association between characteristic gout severity factors and presence of CVD was analyzed. Data from 700 gout patients and 276 controls were collected. CVD was present in 47% (95% CI 44%-51%) and 24% (95% CI 19%-29%) of gout patients and controls, respectively. Corrected for confounders, gout was still strongly associated with an increased prevalence of CVD compared to controls (OR 3.39, 95% CI 2.37-4.84). In patients with gout, disease duration ≥ 2 years, oligo- or polyarthritis, serum urate acid > 0.55 mmol/l at presentation, and joint damage were independently (p < 0.05) associated with prevalent CVD. Crystal-proven gout was strongly associated with an increased prevalence of CVD. In patients with gout, characteristic gout severity factors were associated with CVD.

Impaired arterial responsiveness in untreated gout patients compared with healthy non-gout controls: association with serum urate and C-reactive protein

To determine whether arterial responsiveness is impaired among patients with gout, and whether arterial responsiveness inversely correlates with serum urate and inflammatory measures. This is a cross-sectional study of untreated gout subjects (n = 34) and non-gout healthy controls (n = 64). High-resolution dynamic ultrasound-measured flow-mediated dilation (FMD) and nitroglycerin-mediated dilation (NMD) assessed endothelium-dependent and endothelium-independent arterial responsiveness respectively. Serum urate (sUA) and high-sensitivity C-reactive protein (hsCRP) were measured in the gout group, and correlated with FMD and NMD responses. Both FMD (2.20 ± 0.53 vs 3.56 ± 0.31, p = 0.021) and NMD (16.69 ± 1.54 vs 24.51 ± 0.90, p = 0.00002) were impaired in the gout versus control group. Stratification for individual comorbidities suggested that no single risk factor accounted for impaired FMD/NMD in the gout subjects. However, the degree of association between gout and FMD, but not NMD impairment, was dampened after multivariable adjustment (FMD unadjusted beta = - 1.36 (SE 0.58), p = 0.02; adjusted beta = - 1.16 (SE 0.78), p = 0.14 and NMD unadjusted beta = - 7.68 (SE 1.78), p < 0.0001; adjusted beta = - 5.33 (SE 2.46), p = 0.03). Within the gout group, there was an inverse correlation between FMD and sUA (R = - 0.5, p = 0.003), and between FMD and hsCRP (R = - 0.42, p = 0.017), but not between NMD and sUA or hsCRP. Compared with healthy controls, subjects with gout have reduced arterial function. Individual comorbidities are insufficient to account for differences between gout and control groups, but multiple comorbidities may collectively contribute to impairment in endothelium-dependent arterial responsiveness. Endothelial impairment is also related to sUA and hsCRP, markers of gout severity and inflammation respectively. Studies to determine whether gout therapy may improve arterial responsiveness are warranted.

Treatment with Allopurinol is Associated with Lower Risk of Acute Kidney Injury in Patients with Gout: A Retrospective Analysis of a Nested Cohort.

IntroductionGout is characterized by recurrent episodes of acute inflammation of joint structures, called gout flares, and flares are commonly treated with nonsteroidal anti-inflammatory drugs (NSAIDs). The objective of the study was to evaluate risk factors associated with acute kidney injury (AKI) attributed to NSAIDs in a cohort of patients who were exposed to NSAIDs to treat gout flares prior to urate-lowering therapy.MethodsRetrospective analysis of a nested cohort of 983 gout patients in whom general variables (age, gender, renal function, ethanol intake, hypertension, hyperlipidemia, diabetes, vascular events, diuretic use) and also variables related to gout and severity of gout (serum urate levels, number for flares per year, presence of tophi, joint distribution, X-ray involvement, previous urate-lowering therapy) were available for analysis. Outcomes considered were loss of renal function attributed to NSAID prescription following the RIFLE classification for (risk, injury, and failure) for acute renal events. Variables associated with increased risk in Kaplan–Meier survival analysis were tested with multivariable Cox survival analysis, using time from onset of gout to the event as time exposed to NSAIDs.ResultsOf 983 patients, 55 (5.6%) experienced AKI; the number of flares in the year previous to the renal event and polyarticular joint distribution were associated with higher risk of renal events. Other variables previously described in the literature, such as previous chronic renal disease, use of diuretics, and presence of previous vascular events, were also independently associated with increased risk of AKI. Interestingly, patients who had been previously prescribed allopurinol showed a lower risk of acute renal events.ConclusionIn addition to classic risk factors, the number of flares and extensive joint distribution were associated with higher risk for renal injury in patients with gout, while previous prescription of allopurinol was associated with lower risk.

Prophylaxis of acute flares when initiating febuxostat for chronic gouty arthritis in a real-world clinical setting

Objective: Flare prophylaxis is recommended during urate-lowering therapy (ULT) despite lack of proven benefit especially when initiating febuxostat. We investigated if colchicine or steroids administration during initiation of febuxostat for chronic gouty arthritis reduces the frequency and/or severity of acute gout flares.Methods: Patients with confirmed diagnosis of gout starting febuxostat were retrospectively studied. Frequency, severity, and length of flares were analyzed. Assessment of severity based on a visual analog scale (VAS).Results: Two hundred and seventy-three patients were studied. The mean dose of colchicine and steroids was 0.53 ± 0.15 mg PO QD and 7.55 ± 1.30 mg prednisone equivalent PO QD; while the duration was 6.13 ± 1.14 and 6.20 ± 1.36 months, respectively. Subjects treated with colchicine and steroids suffered fewer total flares (0.30, 0.96 vs 2.47, p = .000), fewer flares from 0 to 3 months (0.26, 0.71 vs 1.72, p = .000), less severe flares assessed by VAS than those without prophylactic therapy (3.65, 3.49 vs 5.54, p = .000). Both total flares (p = .003) and flares from 0 to 3 months (p = .008) of the colchicine group were fewer than the steroids group. There were no significant differences in length of flares among groups (p = .815). Both colchicine and steroids were well tolerated.Conclusion: The use of colchicine or steroids prophylaxis reduces the frequency and severity of acute gout flares during initiation of febuxostat for chronic gouty arthritis. Colchicine is superior to steroids in flares prophylaxis. Prophylactic therapy with colchicine 0.5 mg PO QD or steroids 7.5 mg prednisone equivalent PO QD for 6 months is suggested.

A variant allele of the Mediterranean-fever gene increases the severity of gout.

Gout is a clinical syndrome that occurs as an inflammatory response to increased concentration of uric acid and monosodium urate crystals. Familial Mediterranean fever (FMF) is a hereditary autoinflammatory disease with autosomal recessive inheritance. The Mediterranean fever (MEFV) gene is responsible for FMF and encodes pyrin that suppresses the inflammatory response. Most of the FMF-related mutations have been identified in exon 2 (e.g., E148Q and R202Q) and exon 10 (M680I, M694V, M694I and V726A) of the MEFV gene, and each missense mutation is known to increase production of interleukin-1, a proinflammatory cytokine. Our aim was to investigate effects of MEFV variant alleles on the manifestations of gout. Seventy-one patients diagnosed with gout (age: 61.73 ± 11.73 years, F/M: 14/57) and 50 healthy subjects (age: 61.48 ± 11.97, F/M: 10/40) as controls were included in this study. MEFV variant alleles were found in 24 (33.8%) of the gout patients and in 13 (26%) of the control subjects; the difference was not statistically significant. In the gout patients with a MEFV variant allele, the interval between the first two attacks was shorter (P = 0.014), and the platelet count was higher (P = 0.026), compared to the patients without a variant allele. In addition, the patients with a MEFV variant allele showed the higher incidence of tophus (8.5% vs. 1.4%) (P = 0.005) and the higher number of attacks per year (P = 0.001). We propose that a variant allele of the MEFV gene may be responsible for the severity of gout.

044 Gout Severity, Socio-Economic Deprivation and Work Loss: A Cross-Sectional Study in Primary Care

044 Gout Severity, Socio-Economic Deprivation and Work Loss: A Cross-Sectional Study in Primary Care

Performance of Gout Impact Scale in a longitudinal observational study of patients with gout.

The aim was to evaluate the reliability, validity and responsiveness to change of the Gout Impact Scale (GIS), a disease-specific measure of patient-reported outcomes, in a multicentre longitudinal prospective cohort of gout patients. Subjects completed the GIS, a 24-item instrument with five scales: Concern Overall, Medication Side Effects, Unmet Treatment Need, Well-Being during Attack, and Concern Over Attack. The total GIS score was calculated by averaging the GIS scale scores. HAQ-Disability Index (HAQ-DI), Short Form (SF)-36 physical and mental component summaries (PCS and MCS) and physician and patient gout severity assessments were also completed. Reliability was assessed with Cronbach's α. Baseline GIS scores were compared in subjects with and without gout attacks in the past 3 months using Wilcoxon rank sum tests. Multivariate linear regression was used to evaluate predictors of total GIS. Pearson's correlation coefficients 0.24-0.36 were considered moderate and >0.37 considered large. The effect size for responsiveness to change was interpreted as follows: 0.20-0.49 small, 0.50-0.79 medium and >0.79 large. In 147 subjects, reliability was acceptable for total GIS (0.93) and all GIS scales (0.82-0.94) except Medication Side Effects and Unmet Treatment Need. Total GIS and all scales except Medication Side Effects discriminated between subjects with and without recent gout attacks (P < 0.05). Total GIS showed moderate-to-large correlations with HAQ-DI, SF-36 PCS and MCS (0.33-0.46). Improvement in total GIS tracked with improved physician and patient severity scores. Worsening physician severity score and recent gout attack predicted worsening total GIS. Total GIS score is reliable, valid and responsive to change in patients with gout, and differentiates between subjects with and without recent gout attacks.

Management of Gouty Arthritis in Patients With Chronic Kidney Disease

Chronic kidney disease (CKD) is a comorbid condition that affects, based on recent estimates, between 47% and 54% of patients with gouty arthritis. However, data from randomized controlled trials in patients with gouty arthritis and CKD are limited, and current gouty arthritis treatment guidelines do not address the challenges associated with managing this patient population. Nonsteroidal anti-inflammatory drugs and colchicine are recommended first-line treatments for acute gouty arthritis attacks. However, in patients with CKD, nonsteroidal anti-inflammatory drugs are not recommended because their use can exacerbate or cause acute kidney injury. Also, colchicine toxicity is increased in patients with CKD, and dosage reduction is required based on level of kidney function. Allopurinol, febuxostat, and pegloticase are all effective treatments for controlling elevated uric acid levels after the treatment of an acute attack. However, in patients with CKD, required allopurinol dosage reductions may limit efficacy; pegloticase requires further investigation in this population, and febuxostat has not been studied in patients with creatinine clearance<30 mL/min. This article reviews the risks and benefits associated with currently available pharmacologic agents for the management of acute and chronic gouty arthritis including urate-lowering therapy in patients with CKD. Challenges specific to primary care providers are addressed, including guidance to help them decide when to collaborate with, or refer patients to, rheumatology and nephrology specialists based on the severity of gout and CKD.

Dietary supplements for chronic gout.

Dietary supplements are frequently used for the treatment of several medical conditions, both prescribed by physicians or self administered. However, evidence of benefit and safety of these supplements is usually limited or absent. To assess the efficacy and safety of dietary supplementation for people with chronic gout. We performed a search in the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE, EMBASE and CINAHL on 6 June 2013. We applied no date or language restrictions. In addition, we performed a handsearch of the abstracts from the 2010 to 2013 American College of Rheumatology (ACR) and European League against Rheumatism (EULAR) conferences, checked the references of all included studies and trial registries. We considered all published randomised controlled trials (RCTs) or quasi-RCTs that compared dietary supplements with no supplements, placebo, another supplement or pharmacological agents for adults with chronic gout for inclusion. Dietary supplements included, but were not limited to, amino acids, antioxidants, essential minerals, polyunsaturated fatty acids, prebiotic agents, probiotic agents and vitamins. The main outcomes were reduction in frequency of gouty attacks and trial participant withdrawal due to adverse events. We also considered pain reduction, health-related quality of life, serum uric acid (sUA) normalisation, function (i.e. activity limitation), tophus regression and the rate of serious adverse events. We used standard methodological procedures expected by The Cochrane Collaboration. We identified two RCTs (160 participants) that fulfilled our inclusion criteria. As these two trials evaluated different diet supplements (enriched skim milk powder (SMP) and vitamin C) with different outcomes (gout flare prevention for enriched SMP and sUA reduction for vitamin C), we reported the results separately.One trial including 120 participants, at moderate risk of bias, compared SMP enriched with glycomacropeptides (GMP) with unenriched SMP and with lactose over three months. Participants were predominantly men aged in their 50's who had severe gout. The frequency of acute gout attacks, measured as the number of flares per month, decreased in all three groups over the study period.The effects of enriched SMP (SMP/GMP/G600) compared with the combined control groups (SMP and lactose powder) at three months in terms of mean number of gout flares per month were uncertain (mean ± standard deviation (SD) flares per month: 0.49 ± 1.52 in SMP/GMP/G60 group versus 0.70 ± 1.28 in control groups; mean difference (MD) -0.21, 95% confidence interval (CI) -0.76 to 0.34; low-quality evidence). The number of withdrawals due to adverse effects was similar in both groups although again the results were imprecise (7/40 in SMP/GMP/G600 group versus 11/80 in control groups; risk ratio (RR) 1.27, 95% CI 0.53 to 3.03; low-quality evidence). The findings for adverse events were also uncertain (2/40 in SMP/GMP/G600 group versus 3/80 in control groups; RR 1.33, 95% CI 0.23 to 7.66; low-quality evidence). Gastrointestinal events were the most commonly reported adverse effects. Pain from self reported gout flares (measured on a 10-point Likert scale) improved slightly more in the SMP/GMP/G600 group compared with controls (mean ± SD reduction -1.97 ± 2.28 points in SMP/GMP/G600 group versus -0.94 ± 2.25 in control groups; MD -1.03, 95% CI -1.96 to -0.10; low-quality evidence). This was an absolute reduction of 10% (95% CI 20% to 1% reduction), which may not be of clinical relevance. Results were imprecise for the outcome improvement in physical function (mean ± SD Health Assessment Questionnaire (HAQ)-II (scale 0 to 3, 0 = no disability): 0.08 ± 0.23 in SMP/GMP/G60 group versus 0.11 ± 0.31 in control groups; MD -0.03, 95% CI -0.14 to 0.08; low-quality evidence). Similarly, results for sUA reduction were imprecise (mean ± SD reduction: -0.025 ± 0.067 mmol/L in SMP/GMP/G60 group versus -0.010 ± 0.069 in control groups; MD -0.01, 95% CI -0.04 to 0.01; low-quality evidence). The study did not report tophus regression and health-related quality of life impact.One trial including 40 participants, at moderate to high risk of bias, compared vitamin C alone with allopurinol and with allopurinol plus vitamin C in a three-arm trial. We only compared vitamin C with allopurinol in this review. Participants were predominantly middle-aged men, and their severity of gout was representative of gout in general. The effect of vitamin C on the rate of gout attacks was not assessed. Vitamin C did not lower sUA as much as allopurinol (-0.014 mmol/L in vitamin C group versus -0.118 mmol/L in allopurinol group; MD 0.10, 95% CI 0.06 to 0.15; low-quality evidence). The study did not assess tophus regression, pain reduction or disability or health-related quality of life impact. The study reported no adverse events and no participant withdrawal due to adverse events. While dietary supplements may be widely used for gout, this review has shown a paucity of high-quality evidence assessing dietary supplementation.

Impact of gout on left atrial function: a prospective speckle-tracking echocardiographic study.

The purpose of our study was to evaluate the left ventricular (LV) and left atrial (LA) function in patients with gout. A total of 173 patients underwent a comprehensive Doppler-echocardiography examination. Participants were divided into four groups–Stage 0: control (n = 35), Stage I: asymptomatic hyperuricemia (n = 30), Stage II: gouty arthritis without tophi (n = 58), and Stage III: tophaceous gout (n = 50). Serum uric acid levels were not significantly different between stage I, II and III. Stage III patients demonstrated a higher ratio of the transmitral and myocardial peak early diastolic velocities (E/Em) (10.50±3.18 vs. 8.58±2.07; P = 0.008), and larger maximal LA volume index (LAVi) (29.60±9.89 vs. 20.07±4.76 ml/m2; P<0.001) compared with controls. Stage III patients had decreased LV global longitudinal systolic strain (LVε) compared with controls (−20.2±3.06 vs. −21.79±2.27; P = 0.002). Stage III patients also had decreased peak atrial longitudinal strain rate during ventricular systole (ALSRsyst), peak atrial longitudinal strain rate during ventricular early diastole (ALSRearly), and peak atrial longitudinal strain rate during ventricular late diastole (ALSRlate) compared with controls (1.73±0.48 vs. 2.05±0.55 1/s, −1.44±0.53 vs. −2.07±0.84 1/s, −2.07±0.7 vs. −2.66±0.91 1/s, respectively; all P<0.005). Multiple regression analysis revealed severity of gout had an independent negative impact on LA pump function (ALSRlate). In conclusion, gout caused LV diastolic dysfunction, LV subclinical systolic dysfunction and LA reservoir, conduit, and booster pump dysfunction.

FRI0174 A Comparative Evaluation of the Health Economic Outcomes of Febuxostat and Allopurinol in Gout Patients with Chronic Kidney Disease

BackgroundAllopurinol (ALP) and febuxostat (FBX) are indicated for the treatment of hyperuricemia due to gout. Scant real-world research has compared the economic outcomes of these agents in renally compromised patients.ObjectivesTo...

SAT0530 Development of A Patient Reported Outcome Measure of Tophus Burden: the Tophus Impact Questionnaire (TIQ-20)

BackgroundThe tophus represents a chronic foreign body granulomatous response to monosodium urate crystals. Tophi have been associated with activity limitation, joint damage and mortality in people with gout. Currently, tophus...

65. Anxiety and Depression Comorbidity in Primary Care Gout: A Matched Retrospective Cohort Study

Background: Chronic conditions such as diabetes mellitus and cardiovascular disease are common in people with gout and are associated with poorer quality of life and higher mortality. However, our understanding of the role of psychological comorbidity in gout remains unclear. Frequent experience of severe pain, social isolation and strained family relationships may impact negatively on psychological health and influence health-seeking behaviour. This matched retrospective cohort study aimed to examine the association between gout and subsequent consultation for anxiety & depression in a UK primary care population. Methods: The study was undertaken using data from a general practice consultation database (CiPCA), gathered from nine general practices in North Staffordshire. Patients aged 18 years who consulted with gout between 2000 and 2008 were identified by Read code and each matched to 4 controls by age, gender, year of consultation and general practice. A consultation for either anxiety or depression, subsequent to the gout diagnosis, was defined from a relevant Read code gained between 2000 and 2011. Several other gout-related comorbidities (e.g. hypertension) were also recorded by Read code. Cox regression model was used to examine the association between gout and subsequent anxiety & depression consultation (new episodes), adjusting for age, gender, deprivation, year of consultation, general practice and comorbidities. Hazard ratio (HR) and 95% CI were reported for gout cases vs matched controls. Results: 1689 patients with gout were compared with 6,756 control patients. Mean age was 63 years (Standard deviation 16) and 24% were female. Of gout patients, 15.3% & 9.7% had consulted for anxiety & depression respectively, this was in comparison with 14.2% & 9.5% of the controls. Adjusted cox regression analysis found no association between gout and time to consultation for anxiety (HR 1.04, 95% CI 0.9, 1.2) or depression [0.88 (0.7, 1.1)] compared with controls. Across gout patients and matched controls, being younger and female was associated with a propensity to consult for anxiety & depression. With each year from first diagnosis (gout and controls), there was a trend of increasing consultation for anxiety. The presence of hypertension and alcoholism comorbidity was associated with an increased probability of consultation for anxiety & depression. Conclusion: Despite the psychological burden which gout may be expected to impart on patients, time to consultation for anxiety & depression in UK primary care was equivalent to matched controls. This may relate to the prolonged asymptomatic inter-critical period between gout attacks during which psychological burden may ease. However, as under-reporting of both anxiety & depression in primary care is common and the severity & disease characteristics of gout, anxiety & depression could not be established from medical records, further research considering these factors would be of benefit. Disclosure statement: The authors have declared no conflicts of interest.

The effects of gout on left atrial volume remodelling: a prospective echocardiographic study

The aim of the present study was to investigate the effect of gout on left ventricular (LV) diastolic function and left atrial volume (LAV). A total of 173 patients were divided into four groups: control (n = 35), asymptomatic hyperuricaemia (n = 30), gouty arthritis without tophi (n = 58) and gouty tophi (n = 50). Patients underwent a comprehensive Doppler echocardiography examination to evaluate LV volume, systolic and diastolic function and LAV and function. Serum uric acid levels were not significantly different in the asymptomatic hyperuricaemia, gouty arthritis without tophi and gouty tophi groups. However, the ratio of the transmitral and myocardial peak early diastolic velocities (E/e') and LAV index (LAVi) progressively increased from the control group to the gouty tophi group. The tophi group had significantly higher E/e' [10.5 (s.d. 3.2) vs 8.6 (s.d. 2.1), P = 0.008] and larger maximal, pre-contraction and minimal LAVi [29.6 ml/m(2) (s.d. 9.9) vs 20.1 ml/m(2) (s.d. 4.8); 19.1 ml/m(2) (s.d. 8.5) vs 11.5 ml/m(2) (s.d. 3.4); 9.6 ml/m(2) (s.d. 4.2) vs 6.1 ml/m(2) (s.d. 2.2); all P < 0.001] than the control group. By binary logistic analysis, maximal LAVi was an independent predictor for the development of tophi in gout patients, with an odds ratio of 1.068 (95% CI 1.02, 1.118; P = 0.005). The severity of gout had a significant effect on LV diastolic dysfunction and LA enlargement in gout patients. Additionally, a high maximal LAVi predicted the development of tophi and may be a predictor of adverse cardiovascular events related to LA and LV remodelling in this clinical setting.

CaseBook Challenges: Managing Gout, Hyperuricemia and Comorbidities—Dialogue with the Experts

The prevalence of gout and hyperuricemia are on the rise in the United States corresponding with an increase in risk factors for these conditions, such as obesity, metabolic syndrome, and the use of diuretics. A progressive disorder, untreated gout can be debilitating and result in tophi, chronic arthropathy, and recurrent kidney stones. Although joint aspiration is needed for a definitive diagnosis, the majority of patients are diagnosed presumptively based on medical history and presentation with characteristic signs and symptoms. Patients with gout also often have multiple comorbidities, and there is an increasing body of evidence that shows hyperuricemia is associated with incidence hypertension, diabetes, chronic kidney disease, and heart failure. Clinical strategies for the management of gout and hyperuricemia must include considerations for these and other common cardiometabolic and renal conditions. In addition to acute flare therapy and prophylaxis, the treatment of gout involves lowering serum uric acid (SUA) levels with the urate-lowering therapies (ULTs) allopurinol or febuxostat. Once begun, treatment with ULT is lifelong. However, inadequate dosing and patient nonadherence or intolerance to therapy often lead to treatment failure. Recent guidelines from the American College of Rheumatology stress tailoring therapy and target SUA level (traditionally <6 mg/dL, but lower levels may be needed for certain patients) based on gout severity and the presence of comorbid conditions. Because painful acute gout flares may result in trips to the emergency department and because the majority of gout cases are managed in primary care, it is important for clinicians practicing in these settings to be able to diagnose and treat this condition and communicate with patients to improve their understanding of the disease process and adherence to treatment.

FRI0385 Factors associated with refractoriness to NSAIDS in GOUTY arthritis

BackgroundIn gouty arthritis, we most often start with a non-steroid anti-inflammatory drug (NSAID). Many patients with gout have comorbidities that make NSAIDs use problematic. In clinical practice, we observe more...

OP0102 Presence of tophi and high level hyperuricemia are associated with increased risk of mortalty in patients with gout

BackgroundSeveral studies have linked gout with increased risk of cardiovascular events and mortality. There is no study linking severity of gout with mortality, as specific clinical evaluation of gout is...