Purinergic Signaling in the Regulation of Gout Flare and Resolution.

Gout flares require monosodium urate (MSU) to activate the NLRP3 inflammasome and secrete sufficient IL-1ß. However, MSU alone is not sufficient to cause a flare. This is supported by the evidence that most patients with hyperuricemia do not develop gout throughout their lives. Recent studies have shown that, besides MSU, various purine metabolites, including adenosine triphosphate, adenosine diphosphate, and adenosine bind to different purine receptors for regulating IL-1ß secretion implicated in the pathogenesis of gout flares. Purine metabolites such as adenosine triphosphate mainly activate the NLRP3 inflammasome through P2X ion channel receptors, which stimulates IL-1ß secretion and induces gout flares, while some purine metabolites such as adenosine diphosphate and adenosine mainly act on the G protein-coupled receptors exerting pro-inflammatory or anti-inflammatory effects to regulate the onset and resolution of a gout flare. Given that the purine signaling pathway exerts different regulatory effects on inflammation and that, during the inflammatory process of a gout flare, an altered expression of purine metabolites and their receptors was observed in response to the changes in the internal environment. Thus, the purine signaling pathway is involved in regulating gout flare and resolution. This study was conducted to review and elucidate the role of various purine metabolites and purinergic receptors during the process.

Pleiotropic Effects of Functional MUC1 Variants on Cardiometabolic, Renal, and Hematological Traits in the Taiwanese Population.

MUC1 is a transmembrane mucin involved in carcinogenesis and cell signaling. Functional MUC1 variants are associated with multiple metabolic and biochemical traits. This study investigated the association of functional MUC1 variants with MUC1 DNA methylation and various metabolic, biochemical, and hematological parameters. In total, 80,728 participants from the Taiwan Biobank were enrolled for association analysis using functional MUC1 variants and a nearby gene regional plot association study. A subgroup of 1686 participants was recruited for MUC1 DNA methylation analysis. After Bonferroni correction, we found that two MUC1 variants, rs4072037 and rs12411216, were significantly associated with waist circumference, systolic blood pressure, hemoglobin A1C, renal functional parameters (blood urea nitrogen, serum creatinine levels, and estimated glomerular filtration rate), albuminuria, hematocrit, hemoglobin, red blood cell count, serum uric acid level, and gout risk, with both favorable and unfavorable effects. Causal inference analysis revealed that the association between the variants and gout was partially dependent on the serum uric acid level. Both gene variants showed genome-wide significant associations with MUC1 gene-body methylation. Regional plot association analysis further revealed lead single-nucleotide polymorphisms situated at the nearby TRIM46-MUC1-THBS3-MTX1 gene region for the studied phenotypes. In conclusion, our data demonstrated the pleiotropic effects of MUC1 variants with novel associations for gout, red blood cell parameters, and MUC1 DNA methylation. These results provide further evidence in understanding the critical role of TRIM46-MUC1-THBS3-MTX1 gene region variants in the pathogenesis of cardiometabolic, renal, and hematological disorders.

Correlation of Serum Cystatin C with Renal Function in Gout Patients with Renal Injury.

The gout-induced continuous deposition of urate in the kidney tissues is the main cause of renal injury, for which cystatin C (Cys C) is an important indicator. This research analyzed the correlation between general renal injury indicators and serum Cys C level, and further investigated the potential of Cys C in renal injury diagnosis. A total of 140 gout patients with renal injury (GRI) were recruited and grouped by their glomerular filtration rate (GFR). Urea nitrogen, uric acid, creatinine, and Cys C levels in the serum were evaluated. The diagnostic efficacy of serum Cys C was evaluated by the nonparametric receiver operating characteristic analysis. Serum Cys C level was increased with decreased GFR in GRI. Urea nitrogen, uric acid, and creatinine levels in the serum showed positive correlations with Cys C level. The area under the curve for serum Cys C was 0.8589 (P < 0.001). In conclusion, this research demonstrated that the serum Cys C level was a precise diagnostic marker for GFR and renal damage evaluation, and showed a significant diagnostic value for renal injury in patients with gout.

Gout-induced endothelial impairment: The role of SREBP2 transactivation of YAP.

Gout is a multifaceted inflammatory disease involving vascular impairments induced by hyperuricemia. Experiments using human umbilical vein endothelial cells treated with uric acid (UA), monosodium urate (MSU), or serum from gout patients showed increased expression of pro-inflammatory genes (ie, VCAM1, ICAM1, CYR61, CCNA1, and E2F1) with attendant increase in monocyte adhesion. Mechanistically, UA- or MSU-induced SREBP2 expression and its transcriptional activity. RNA sequencing analysis and real-time PCR showed the induction of YAP signaling and pro-inflammatory pathways in HUVECs transfected with adenovirus-SREBP2. The SREBP2 knockdown by siRNA partially abolished UA- or MSU-induced YAP activity, pro-inflammatory gene expression, and monocytes adhesion. Vascular intima from transgenic mice overexpressing SREBP2 in endothelium or mice with hyperuricemia exhibited activated YAP signaling and increased expression of pro-inflammatory genes. Betulin, an SREBP pharmacological inhibitor, attenuated the UA-, MSU-, or gout serum-induced endothelial cell inflammation and dysfunction. In the human study, endothelial cell function, assessed by EndoPAT, was negatively correlated with serum UA level among gouty patients and healthy controls. Collectively, UA or MSU causes endothelial dysfunction via SREBP2 transactivation of YAP. Betulin inhibition of SREBP2 may restrain gout-induced endothelial dysfunction.

Presence of tophi is associated with a rapid decline in the renal function in patients with gout.

We aimed to compare clinical characteristics of patients with and without tophi at the time of the diagnosis of gout and investigate the association of tophi and renal function in gout patients. The patients who were first diagnosed with gout at the Kangwon National University Hospital were retrospectively studied. Patients were divided into 2 groups according to the presence of tophi at the diagnosis. We compared clinical characteristics and the progression of renal dysfunction between the two groups. Of 276 patients, 66 (25.5%) initially presented with tophi. Tophi group was older, had a longer symptom duration, and a higher prevalence of multiple joint involvement than those without tophi. In multivariate logistic regression analysis, prolonged symptom duration and multiple joint involvement were significantly associated with increased risk of formation of tophi. The decline in the eGFR was more prominent in patients with tophi than in those without (- 4.8 ± 14.5 vs. - 0.7 ± 11.9 ml/min/1.73 m2/year, respectively; P = 0.039). The presence of tophi was significantly associated with a rapid decline in the eGFR (ß = - 0.136; P = 0.042). In conclusion, the presence of tophi was associated with a rapid declining renal function. Therefore, an early diagnosis and closely monitoring of renal function might be important in gout patients with tophi.

Gout: Rapid Evidence Review.

Gout is caused by monosodium urate crystal deposition in joints and tissues. Risk factors include male sex; obesity; hypertension; alcohol intake; diuretic use; a diet rich in meat and seafood; chronic kidney disease; a diet heavy in fructose-rich food and beverages; being a member of certain ethnic groups, including Taiwanese, Pacific Islander, and New Zealand Maori; and living in high-income countries. Gout is characterized by swelling, pain, or tenderness in a peripheral joint or bursa, including the development of a tophus. Diagnosis of gout can be made using several validated clinical prediction rules. Arthrocentesis should be performed when suspicion for an underlying septic joint is present; synovial fluid or tophus analysis should be performed if the diagnosis is uncertain. Colchicine, nonsteroidal anti-inflammatory drugs, and corticosteroids relieve pain in adults with acute gout episodes. Indications for long-term urate-lowering therapy include chronic kidney disease, two or more flare-ups per year, urolithiasis, the presence of tophus, chronic gouty arthritis, and joint damage. Allopurinol and febuxostat are used to prevent flare-ups, although febuxostat is associated with an increase in all-cause and cardiovascular mortality and is therefore not routinely recommended.

Uric acid fluctuation had no effect on renal function among gout patients.

BACKGROUND AND AIMS: To investigate the effects of serum uric acid (SUA) level and its fluctuation on renal dysfunction in gout patients. METHODS AND RESULTS: Data on gout patients was collected from Huzhou city electronic medical record system data sharing platform, and information about relevant diagnoses, prescriptions, biochemical indexes and imaging characteristics was extracted. The gout patients with baseline normal renal function were enrolled in this analysis, and the estimated glomerular filtration rate (eGFR) < 60 mL/min/1.73 m2 was defined as renal dysfunction. The generalized estimating equation and Cox regression analysis were used. A total of 1009 patients with gout were enrolled. Compared with the reference group (normal baseline SUA with endpoint SUA to be < 6 mg/dL), endpoint SUA ≥ 10 mg/dL was associated with an increased risk of renal dysfunction (baseline normal SUA group: HR [95% CI] = 3.28 [1.21, 8.91]; baseline high SUA group: HR [95% CI] = 3.01 [1.43, 6.35]). Subgroup analysis of 771 SUA stable gout patients demonstrated that SUA levels at 8-10 (excluding 10), and ≥10 mg/dL were significantly associated with an increased risk for renal dysfunction, with HR [95%CI] to be 1.99 [1.05, 3.77], and 2.98 [1.38, 6.43], respectively. CONCLUSION: Regardless of the baseline SUA level, SUA >10 mg/dL was a significant risk factor for renal dysfunction. SUA between 6 and 10 mg/dL was a potential risk factor for renal dysfunction. No significant correlation of SUA fluctuation and renal function was found.

Synovial Biopsy in the Diagnosis of Crystal-Associated Arthropathies.

BACKGROUND/ OBJECTIVE: This study seeks to assess the utility of synovial biopsy in the diagnosis of crystal-associated arthropathies (CAAs) in a clinical setting. METHODS: In this retrospective study, we reviewed biopsy reports involving synovial tissue between 1988 and 2015. We then reviewed the records of patients where the biopsy was performed for a clinical suspicion of CAA-the clinical group-and calculated the frequency of a positive diagnosis. The t test, Mann-Whitney-Wilcoxon test, and Fisher test were used to compare clinical characteristics of patients with and without a tissue diagnosis of CAA. We also reviewed cases of unexpected detection of crystalline disease involving synovial tissue-the incidental group. RESULTS: Among 2786 biopsies involving the synovium, we identified 65 cases in the clinical group and 33 cases in the incidental group. In the clinical group, a relevant diagnosis was obtained from synovial tissue in 36.9%, and a CAA was diagnosed in 20%. Restricting analysis to clinical biopsies performed for a primary suspicion of CAA, a relevant diagnosis was obtained in 61.3%, and a CAA was diagnosed in 38.7%. The incidental group comprised 1.2% of all synovial biopsies and included 7 mass lesions. Basic calcium phosphate was not reported on any biopsy in the study period. CONCLUSIONS: Synovial biopsy is a diagnostic option when suspected CAA is resistant to conventional modes of diagnosis. Crystalline diseases should be considered in the differential diagnosis of musculoskeletal mass lesions mimicking neoplasms.

Recent approaches to gout drug discovery: an update.

INTRODUCTION: Inflammation induced by urate deposition in joints causes gout. Healthy individuals maintain serum levels of urate by balancing urate production/excretion, whereas a production/excretion imbalance increases urate levels. Hyperuricemia is diagnosed when the serum urate level is continuously above 7 mg/dl as the solubility limit, and urate accumulates in the kidneys and joints. Because hyperuricemia increases the risk of gout, therapies aim to eliminate urate deposition to prevent gouty arthritis and kidney injury. AREAS COVERED: This review discusses the mechanism underlying hyperuricemia with respect to urate production and urate transport, along with urate-lowering therapeutics, including urate synthesis inhibitors, uricolytic enzymes, and uricosuric agents. The authors asses published data on relevant commercial therapy development projects and clinical trials. EXPERT OPINION: Available treatment options for hyperuricemia are limited. Allopurinol, a urate synthesis inhibitor, is generally administered at a reduced dosage to patients with renal impairment. Some URAT1 inhibitors have an unfavorable side effect profile. A promising strategy for treatment is the use of uricosuric agents that inhibit transporters (e.g. URAT1, URATv1/GLUT9, OAT10) which reabsorb urate from the urine.

At the crossroads of gout and psoriatic arthritis: "psout".

Psoriatic arthritis and gout are frequently encountered conditions sharing a number of common risk factors, which render their independent study difficult. Epidemiological studies have demonstrated a strong link between these diseases, suggesting the presence of underlying, intertwined pathophysiological mechanisms that currently remain unknown. Indeed, sodium urate crystals could play a pathogenic role in psoriasis and psoriatic arthritis. In daily practice, the distinction between psoriatic arthritis associated with hyperuricemia and a gouty arthropathy with psoriasis is complex. Several common pathogenic features suggest a more intricate relationship than their mere coexistence in the same patient. Thus, the concurrence of these two diseases should be seen as a novel overlap syndrome, at the boundary between inflammatory and metabolic rheumatism. The present update aims to clarify the determinants of the link and to define this new nosological entity. Its recognition could have therapeutic implications that appear essential for treatment optimization in a personalized setting.Key Points• What is already known about this subject? Psoriatic arthritis (PsA) and gout have strong interconnections, including comorbidities and pathophysiology. One must note that confounding clinical symptoms and radiological signs of PsA and gout are similar and difficult to differentiate in patients whose radiological lesions become too advanced to be differentiated or with less clearly defined phenotypes.• What does this study add? The pathogenic role of chronic hyperuricemia in the development and maintenance of PsA is based on epidemiological, clinical, and fundamental arguments and hence does not appear fortuitous. These two pathological processes can influence each other.• How might this impact on clinical practice? This new line of thinking regarding the convergence of gout and PsA, involving the role of urate crystals, could prompt a potential new approach to treatment (urate-lowering therapy) among patients with active/refractory PsA.

Burden and management of gout in a multi-ethnic Asian cohort.

Gout has significant impact on the quality of life with over-utilisation of health resources. While lowering serum urate (SU) to ≤ 360 µmol/L improves clinical outcomes, this is usually not achieved. We describe the burden of gout and determine predictors of achieving SU target in gout patients in Singapore. This was a cross-sectional study of 282 gout patients from a Singapore hospital rheumatology service. Sociodemographic and lifestyle factors, co-existing medical conditions and medications, gout history and severity, SU levels and treatment were obtained. Patients with SU ≤ 360 µmol/L were compared with those > 360 µmol/L to determine factors associated with achieving SU target. Descriptive statistics and multivariate model were used. Severe disease was reported in 50%, with emergency attendances and hospitalisations in 33% and 19% respectively, and unemployment in 32%. Only 22% were at SU target and 67% on urate-lowering therapy (ULT) at recruitment. Hypertension, dyslipidaemia, chronic kidney disease and diabetes were prevalent in 56.7%, 48.2%, 32.3% and 18.8%, respectively. Malays had more comorbidities compared to Chinese participants. In multivariate analysis, ULT prescription and ≥ 2 comorbidities were associated with reaching SU target with odds ratios of 3.92 [95% confidence interval (CI) (1.75-8.71)] and 2.65 [95% CI (1.59-4.43)] respectively, independent of age, tophi, disease duration, body mass index, alcohol and diuretic use. Patients with gout have high disease burden resulting in significant healthcare utilisation. SU control is sub-optimal hence the use of ULT remains key in achieving SU target. Patients with other comorbidities are more likely to reach target than those with only gout as a single diagnosis.

Nephrolithiasis in gout: prevalence and characteristics of Brazilian patients

Abstract Background: The aims of this article were to assess the prevalence of nephrolithiasis and the factors associated with nephrolithiasis in Brazilian patients with primary gout. Methods: One hundred twenty-three patients with primary gout were recruited from a tertiary referral hospital in São Paulo, Brazil. All patients underwent ultrasonography and had their clinical and laboratory characteristics assessed. Results: One hundred fifteen (93.5%) patients were male, with a mean age of 62.9 ± 9.4 years. Twenty-three (18.7%) patients had asymptomatic nephrolithiasis (detected only by ultrasonography), 7 (6.0%) had symptomatic nephrolithiasis (detected by ultrasonography and a positive clinical history), and 13 (10.0%) had a history of kidney stones, but ultrasonography at evaluation did not show nephrolithiasis. Therefore, 35.0% of the patients had nephrolithiasis (detected either by ultrasonography and/or a positive clinical history). Nephrolithiasis was associated with male gender (43 [100%] vs 72 [90%], p = 0.049), the use of potassium citrate (13 [30.2%] vs 0, p < 0.001) and the use of medications for diabetes (10 [23.3%] vs 8 [10%], p = 0.047) and dyslipidemia (15 [34.9%] vs 10 [12.5%], p = 0.003); benzbromarone had an inverse association with nephrolithiasis (21 [48.8%] vs 55 [68.8%], p = 0.030). In patients with and without nephrolithiasis, no differences were found in the laboratory and ultrasonography characteristics, including serum uric acid levels, urinary uric acid excretion and urine pH. Conclusions: The prevalence of nephrolithiasis in primary gout was 35.0%, and 18.7% of the patients were asymptomatic. Nephrolithiasis was associated with male gender, diabetes and dyslipidemia. A positive history of nephrolithiasis probably biased the prescription of potassium citrate and benzbromarone.(AU)

Comparisons of the Incidence and Critical Risk Factors of Metabolic Syndrome in Patients With a Rheumatic Disease or Gout.

BACKGROUND: Rheumatic disease and gout are particularly known to be associated with metabolic syndrome. PURPOSE: To compare incidence, physiological indices, and risk factors of metabolic syndrome in patients with rheumatic diseases or gout. METHODS: Data were collected from medical records of 220 patients with rheumatic disease or gout. RESULTS: The incidence rate and most physiological indices of metabolic syndrome (body mass index, blood pressure, serum triglyceride, and fasting blood glucose levels) were significantly higher in the gout group than in the rheumatic disease group. In terms of risk factors of metabolic syndrome, age, gender, and steroid use were significant in the rheumatic disease group, whereas smoking and gout duration were significant in the gout group. CONCLUSIONS: Men with a rheumatic disease taking steroids warrant additional attention regarding metabolic syndrome development. Special supports are also needed for people with gout who are smokers and who have suffered from gout for a longer duration.

Hyperuricemia and acute gout after laparoscopic sleeve gastrectomy.

The aim of this study was to evaluate the prevalence of hyperuricemia and acute gout after laparoscopic sleeve gastrectomy (LSG). Risk factors for developing gout were also examined. Eighty-five patients underwent LSG were enrolled in this prospective study. Serum uric acid levels, gout attacks and total water levels % derived by bioimpedance were examined pre-operatively and 1 month post-operatively. Hyperuricemia was identified in 30.6% pre-operatively and in 18.82% of patients post-operatively. From the patients' group with pre-operative hyperuricemia, 53.9% were normalized, 46.2% had increased uric acid post-operatively while gout was observed in 11.5%. From the patients group without pre-operative hyperuricemia, hyperuricemia and gout were observed in 6.8% and 5.1% post-operatively, respectively. The relative risk for developing hyperuricemia was 6.2 (95% confidence interval [CI] 2.2-17.8) and for developing gout was 2.3 (95% CI 2.2-17.8). Statistical significant differences for gout among the groups with and without gout were indicated concerning pre-operative use of medications (P < 0.001), age (P = 0.025), post-operative uric acid levels (P < 0.001) and post-operative total water levels % (P = 0.048). The prevalence of hyperuricemia was 18.8% and gout attack of 7.1% 1 month after LSG. From the cohort of patients with pre-operative hyperuricemia, a significant proportion normalized uric acid, while 11.5% developed gout. Patients without hyperuricemia pre-operatively developed hyperuricemia and gout in 6.8% and 5.1% post-operatively, respectively. The patients who had gout were younger and had 37% water levels post-operatively.

A rare cause of back pain and radiculopathy - spinal tophi: a case report.

BACKGROUND: Gout is a monosodium urate deposition disease which is prevalent worldwide. The usual manifestations are crystal arthropathy and tophi deposition in the soft tissues. Spinal tophi may also occur and are rarely reported, resulting in various clinical manifestations such as back pain, spinal cord compression, radiculopathy, and even mimicking epidural abscess and spondylodiscitis. CASE PRESENTATION: We report a case of a 42-year-old Chinese man with underlying gout who presented with back pain and radiculopathy. The diagnosis of spinal tophi was unsuspected and he was initially treated for epidural abscess and spondylodiscitis. He underwent a laminectomy and posterolateral fusion during which tophus material was discovered. He recovered and medications for gout were started. CONCLUSION: Spinal tophi are rare. The diagnosis is difficult and spinal tophi may be mistaken for epidural abscess, spondylodiscitis, or neoplasm.

Gender-specific risk factors for gout: a systematic review of cohort studies

Abstract Background: Though gout is more prevalent in men than women, it remains unclear whether gender influences risk factors for incident gout. We aimed to systematically review all cohort studies examining risk factors for the development of gout by gender. Methods: MEDLINE, EMBASE, CINAHL and the Cochrane Library were searched from inception to March 2019. Risk factors for gout examined were: age, ethnicity, consumption of alcohol, meat, seafood, dairy products, purine-rich vegetables, coffee and fructose, vitamin C intake, the Dietary Approaches to Stop Hypertension (DASH) diet, metabolic syndrome, BMI, waist and chest circumference, waist-to-hip ratio, weight change, diabetes mellitus, dyslipidaemias, renal disease, psoriasis, hypertension, diuretic use and anti-diabetic medication. Cohort studies were included if examining (at least) one of these risk factors for gout in either gender in the general population or primary care. Sample characteristics from included articles and their reported risk estimates were described using narrative synthesis. Results: Thirty-three articles were included, 20 (60.6%)directly compared risk factors by gender, 10 (30.3%) used men-only samples, 3 (9.1%) used women-only samples. Articles comparing risk across genders found similar increases in most risk factors. However, in men, metabolic syndrome (Hazard Ratio (95% CI) 1.37(1.20-1.58)) presented a risk of incident gout compared to none in women (> 50 years 1.15(0.85-1.54); ≤50 years 1.29(0.76-2.17)). Compared to men, women showed greater associated risk with higher consumption of fish and shellfish (HR (95% CI) Men: 1.02 (0.86-1.22); Women 1.36 (1.12-1.65)). Conclusions: Risk factors for developing gout did not typically differ between genders and therefore similar preventative advice can be provided. Exceptions were metabolic syndrome in men and excessive seafood consumption in women, but these singular articles need further examination and in general more research into the risk factors for gout which includes women is required.

[Acute Gout in Emergency Admissions - Patient Characteristics and Adherence of Care Processes to Current Guidelines]. / Der akute Gichtanfall in der zentralen Notaufnahme.

BACKGROUND: Gout or hyperuricemia are both well known and common diseases. The prevalence of gout is increasing worldwide. Thus, patients with gout are becoming more common. Although there are several published guidelines for the management of gout, actual treatment of gout is inconsistent with these guidelines in many respects. Gout is usually treated by general practitioners (GP) in Germany. The aim of our study was to show which patients present to the emergency department and to record how treatment and clinical diagnostic testing of gout patients is performed in the emergency department of a university hospital in Germany. No such data have been published for Germany. METHOD: Retrospective analysis of data of patients with ICD Code M10.xx from the emergency department at a university hospital from 05/2013 until 04/2016. RESULTS: 65 patients were treated with acute gout during the study period at the emergency department (age ∅ 53.45 y, 76.9% male, 23.07% female). 42 patients (65%) came outside normal office hours of GPs. In 31 patients, hyperuricemia or gout was known in their medical history, in 22 of these acute gout was known. 48 (73%) of patients came with monoarthritis and therefrom 40 with "classic" gout, such as podagra. 57 (86%) patients were subjected to diagnostic blood analysis and 31 (48%) diagnostic X-ray of the affected joint. We defined the appropriate indications for X-ray in diagnosis of acute gout as: signs of superinfection, prior surgical intervention or uncertain trauma in case history. According to this definition, 67% of the X-rays were performed without the correct indication. Four Patients were given punction of the affected joint to demonstrate monosodium urate monohydrate (MSU) crystals. Twelve patients were admitted as inpatients for surgery and/or antibiotic treatment. 51 (78%) patients received NSAIDs, 7 in combination with steroids and 4 patients received colchicine. Of those patients who received NSAID, 17 had an unknown or impaired renal function. Seven patients received neither pharmacological treatment nor recommendations for further treatment. Ten patients (15%) received a urate-lowering therapy or an existing therapy was increased during acute gout. In 10 patients, a urate-lowering therapy was recommended as further therapy. 63% were given further treatment recommendations such as cryotherapy or diet. CONCLUSIONS: Acute gout is seldom presented in the emergency room (< 1‰). This confirms the impression that gout is mainly a disease treated in the outpatient setting. As shown in our study, the pharmacological treatment of acute gout was largely consistent with the guideline recommendations; nevertheless observance of renal function before treatment with NSAIDs should be emphasised. Furthermore, we identified overuse of diagnostic procedures. Current guidelines recommend diagnosing acute gout with clinical scores. In conclusion, our study shows that those clinical diagnostic scores should be implemented in clinical practice, in order to avoid unnecessary diagnostic procedures.

Rogue one: a story of tophaceous gout in the spine.

A 26-year-old man with history of extensive tophaceous gout presented to the referring facility with decreased bilateral lower extremity sensation and motor function that began acutely 1 week prior to admission and had progressed to urinary incontinence. The patient was admitted to the intensive care unit due to concern for sepsis secondary to epidural abscess. The patient was started on empiric vancomycin and cefepime. Neurosurgery did not recommend acute neurosurgical intervention given the lack of a compressive lesion. Aspiration of the paraspinal collection by interventional radiology subsequently showed crystals consistent with tophaceous gout. Given the high initial suspicion for gout and results of the paraspinal aspiration, the patient was started on prolonged steroid taper as well as allopurinol and colchicine. The patient eventually had partial neurological recovery with discharge to an inpatient rehabilitation facility for further physical therapy rehabilitation.

Improvement in OMERACT domains and renal function with regular treatment for gout: a 12-month follow-up cohort study.

OMERACT proposed a set of mandatory and discretionary domains to evaluate the effect of treatment in patients with gout. To determine the percentage of improvement and the effect size 6 and 12 months after starting a proper treatment in patients with gout from our cohort (GRESGO) based on the OMERACT proposal for chronic gout. GRESGO is a cohort of consecutive, new patients with gout attending either of two dedicated clinics. This report includes 141 patients evaluated at baseline and 6 months plus 101 of them completing a 12-month follow-up in 2012. Clinical data including the OMERACT domains for chronic gout were collected at baseline and every 6 months. Treatment was prescribed by their attending physician with the purpose of getting < 6 mg/dL of seric uric acid (sUA). Most patients were males (96%) with inappropriate treatment (95%); 66% had tophi, 30% metabolic syndrome, and 32% low renal function. Mean dose of allopurinol at baseline and throughout the study went from 344 ± 168 mg/day to 453 ± 198 at 12 months. Most OMERACT domains and renal function improved significantly; 73% improved > 20% from 6 to 12 months. Greater improvement was observed in the domains: flares, index tophus size, pain, general health assessment, and HAQ score, all of them associated to lower sUA values. Chronic gout patients improve significantly in most OMERACT domains when conventional and regular treatment is indicated. sUA < 6 mg/dL is associated with greater improvement.