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Gout: HELP
Articles by Naomi Schlesinger
Based on 35 articles published since 2010
(Why 35 articles?)
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Between 2010 and 2020, Naomi Schlesinger wrote the following 35 articles about Gout.
 
+ Citations + Abstracts
Pages: 1 · 2
1 Editorial Can ultrasonography make identification of asymptomatic hyperuricemic individuals at risk for developing gouty arthritis more crystal clear? 2011

Schlesinger, Naomi. · ·Arthritis Res Ther · Pubmed #21542883.

ABSTRACT: Hyperuricemia is the most important risk factor for gouty arthritis. The quandary is how to predict which patient with asymptomatic hyperuricemia will develop gouty arthritis. Can ultrasonography help identify hyperuricemic individuals at risk for developing gouty arthritis? In the previous issue of Arthritis Research & Therapy, Pineda and colleagues found ultrasonography changes suggestive of gouty arthritis in 25% of hyperuricemic individuals. These were found exclusively in hyperuricemic individuals but not in normouricemic patients. Ultrasonography may serve as a noninvasive means to diagnose gouty arthritis in hyperuricemic individuals who have yet to develop symptomatic gouty arthritis.

2 Review Chronic tophaceous gout as the first manifestation of gout in two cases and a review of the literature. 2018

Bieber, Amir / Schlesinger, Naomi / Fawaz, Abdallah / Mader, Reuven. ·Rheumatic Diseases Unit, Ha'Emek Medical Center, Afula 18101, Israel. Electronic address: amir.bieber@gmail.com. · Division of Rheumatology, Department of Medicine, Rutgers, Robert Wood Johnson Medical School, New Brunswick, NJ. · Rheumatic Diseases Unit, Ha'Emek Medical Center, Afula 18101, Israel. · Rheumatic Diseases Unit, Ha'Emek Medical Center, Afula 18101, Israel; The Technicon Institute of Technology, Haifa, Israel. ·Semin Arthritis Rheum · Pubmed #29275830.

ABSTRACT: OBJECTIVES: Acute gout is a common arthritis that may eventually develop into chronic tophaceous gout (CTG). CTG usually is manifested by recurrent gout attacks. The diagnosis and treatment of CTG is challenging. Although the emergence of CTG without previous gout attacks is uncommon, it is important to recognize this unusual gout presentation. METHODS: Herein, we present two cases of CTG, occurring in elderly patients with chronic kidney disease (CKD) on diuretics, who presented without a prior history of acute gout attacks. We also searched PUBMED, Ovid MEDLINE, and Google scholar (1970-2017), for "tophi as the initial manifestation of gout" and "chronic gout without previous attacks", and extracted relevant data. RESULTS: The search disclosed one retrospective study and several case reports and case series describing 96 patients. Clinical and laboratory data was extracted from 34 patients. We found that a specific group of patients, e.g., elderly patients, most often female patients, suffering from CKD, and treated with diuretics, are specifically reported in the English medical literature to present with CTG as their first manifestation of gout. CONCLUSION: The two cases and our literature review try to emphasize the many faces of chronic gout, in particular, its presentation without previous gout attacks.

3 Review The safety of treatment options available for gout. 2017

Schlesinger, Naomi. ·a Department of Medicine Rutgers , Robert Wood Johnson Medical School , New Brunswick , NJ , USA. ·Expert Opin Drug Saf · Pubmed #28095258.

ABSTRACT: INTRODUCTION: Gout is the most common inflammatory arthritis in humans. Gout treatment includes rapid initiation of anti-inflammatory medications for acute attacks and chronically treating with urate lowering drugs as well as chronic anti-inflammatory prophylaxis. Areas covered: This review aims to provide an overview and discussion of the safety concerns of current treatment options available for gout. Expert opinion: Gout is a curable disease with appropriate treatment. The advent of new therapies provides encouraging opportunities to improve gout management. However, clinicians should be aware of some of the safety concerns of medications used to treat acute and chronic gout. When prescribing medications for gout one has to be mindful of the presence of comorbidities commonly affecting gout patients that may affect drug safety and efficacy, especially in the elderly and in patients treated with multiple drugs. The benefits of gout drugs, usually, outweigh their safety concerns. Studies are needed in gout patients with chronic kidney disease and/or cardiovascular disease, so that escalation of dosing /combination of anti-inflammatory drugs needed to suppress gouty inflammation as well as escalation of dosing/combination of urate lowering drugs needed to achieve target serum urate level will lead to better understanding of gout treatment safety issues.

4 Review Beyond Joints: a Review of Ocular Abnormalities in Gout and Hyperuricemia. 2016

Sharon, Yael / Schlesinger, Naomi. ·Department of Ophthalmology, Rabin Medical Center-Beilinson Hospital, 39 Jabotinsky St., Petach Tikva, 494149, Israel. yaelpauker@gmail.com. · Division of Rheumatology, Rutgers-Robert Wood Johnson Medical School, New Brunswick, 08903-0019, NJ, USA. ·Curr Rheumatol Rep · Pubmed #27138165.

ABSTRACT: Gout is a common inflammatory arthritis among middle-aged men and postmenopausal women and can be a debilitating disease. Gout results from an elevated body uric acid pool, which leads to deposition of monosodium urate (MSU) crystals, mainly in and around the joints. The MSU crystals trigger release of proinflammatory cytokines, such as interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α. Ocular manifestations have been uncommonly reported in patients with gout. These include descriptions of tophaceous deposits in different locations of the eye including the eyelids, conjunctiva, cornea, iris, sclera, and orbit. Some depositions were coincidentally diagnosed in asymptomatic patients, while the majority were symptomatic. Other ocular abnormalities include dry eye syndrome, red eye, uveitis, intraocular hypertension, glaucoma, and cataracts. Herein, we review the medical literature pertaining to ocular manifestations in gout and hyperuricemia and propose a possible association between ocular abnormalities, hyperuricemia, and gout, including their common risk factors and comorbidities.

5 Review New and Pipeline Drugs for Gout. 2016

Keenan, Robert T / Schlesinger, Naomi. ·Department of Medicine, Duke University School of Medicine, Durham, NC, USA. robert.keenan@duke.edu. · Division of Rheumatology, Duke University Medical Center, 200 Trent Drive DUMC 3544, Durham, NC, USA. robert.keenan@duke.edu. · Department of Medicine, Rutgers-Robert Wood Johnson Medical School, New Brunswick, NJ, USA. ·Curr Rheumatol Rep · Pubmed #27097819.

ABSTRACT: Gout is the most common inflammatory arthropathy in the western world. Affecting millions and accounting for lost wages, increased health care costs, and significant disability, it remains a burden for those afflicted, their families, and the health care system. Despite the availability of a number of effective therapies, gout is often inadequately treated, and its impact on the patients overall health and well-being is underestimated by physicians and patients alike. For many decades, controlling acute flares was the priority in the management of gout. More recently, however, a deeper understanding of gout pathophysiology has resulted in a new appreciation that gout impacts the patient with consequences well beyond the episodes of acute inflammatory arthritis. Reflecting the chronic nature of the disease, gout treatment needs to be chronic as well, and aimed at reducing the underlying cause of gout-hyperuricemia-as well as the symptom of acute attacks. Therapy therefore requires both urate lowering and anti-inflammatory strategies. Unfortunately, the most commonly used urate lowering and anti-inflammatory treatments may be problematic in some gout patients, who often have multiple comorbidities that establish relative contraindications. Novel urate lowering therapies, and new medications to treat and prevent acute gouty flares, can not only improve care of the individual; they can also lead to a better discourse for the edification of those who manage and are managed for this underestimated disease. In this paper, we discuss new and pipeline drugs for acute gout, prophylactic anti-inflammatory therapies as well as urate lowering therapies.

6 Review Non-steroidal anti-inflammatory drugs for acute gout. 2014

van Durme, Caroline M P G / Wechalekar, Mihir D / Buchbinder, Rachelle / Schlesinger, Naomi / van der Heijde, Désirée / Landewé, Robert B M. ·Department of Rheumatology, Centre Hospitalier Universitaire de Liège, Avenue de l'Hopital 1, Liège, Belgium, 4000. ·Cochrane Database Syst Rev · Pubmed #25225849.

ABSTRACT: BACKGROUND: Gout is an inflammatory arthritis that is characterised by the deposition of monosodium urate crystals in synovial fluid and other tissues. The natural history of articular gout is generally characterised by three periods: asymptomatic hyperuricaemia, episodes of acute gout and chronic gouty arthritis. Non-steroidal anti-inflammatory drugs (NSAIDs) including selective cyclo-oxygenase-2 (COX-2) inhibitors (COXIBs) are commonly used to treat acute gout. Published guidelines recommend their use to treat acute attacks, using maximum recommended doses for a short time. OBJECTIVES: To assess the benefit and safety of NSAIDs (including COXIBs) for acute gout. SEARCH METHODS: We searched the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE and EMBASE for studies to 7 October 2013, the 2010 and 2011 ACR and EULAR abstracts and performed a handsearch of reference lists of articles. We searched the World Health Organization (WHO) trial register and ClinicalTrials.gov. We applied no date or language restrictions. SELECTION CRITERIA: We considered all published randomised controlled trials (RCTs) and quasi-randomised controlled clinical trials that compared NSAIDs with placebo or another therapy (including non-pharmacological therapies) for acute gout. Major outcomes were pain (proportion with 50% or more reduction in pain or mean pain when the dichotomous outcome was unavailable), inflammation (e.g. measured by joint swelling/erythema/tenderness), function of target joint, participant's global assessment of treatment success, health-related quality of life, withdrawals due to adverse events and total adverse events. DATA COLLECTION AND ANALYSIS: Two review authors independently selected the studies for inclusion, extracted the data, performed a risk of bias assessment and assessed the quality of the evidence using the GRADE approach. MAIN RESULTS: We included 23 trials (2200 participants).One trial (30 participants) of low-quality evidence compared an NSAID (tenoxicam) with placebo. It found that significantly more participants had more than 50% reduction in pain after 24 hours (11/15 participants) compared with those taking placebo (4/15 participants) (risk ratio (RR) 2.75, 95% confidence interval (CI) 1.13 to 6.72). A similar outcome was seen for more than 50% improvement in joint swelling after 24 hours (5/15 participants taking NSAIDs versus 2/15 participants taking placebo; RR 2.50, 95% CI 0.57 to 10.93). The trial did not measure function, participant global assessment of treatment success and health-related quality of life. There were no adverse events reported with the use of tenoxicam; two adverse events (nausea and polypuria) were reported in the placebo group. No between-group differences in outcome were observed after four days.Moderate-quality evidence based upon four trials (974 participants) indicated that NSAIDs and COXIBs produced similar benefits in terms of pain, swelling and global improvement, but COXIBs were associated with fewer adverse events. Pain reduction was 1.9 points on a 0- to 10-point scale with COXIBs (0 was no pain) while pain reduction with NSAIDs was 0.03 points lower or better (mean difference (MD) -0.03, 95% CI -0.19 to 0.13). Joint swelling in the COXIB group was 1.64 points on a 0- to 3-point scale (0 is no swelling) and 0.13 points higher with NSAIDs (MD 0.13, 95% CI -0.08 to 0.34). Function was not reported. Participant-reported global assessment was 1.56 points on a 0- to 4-point scale with COXIBs (0 was the best score) and was 0.04 points higher with NSAIDs (MD 0.04, 95% CI -0.12 to 0.20). Health-related quality of life assessed using the 36-item Short Form showed no evidence of a statistically significant between-group difference (MD 0.49, 95% CI -1.61 to 2.60 for the physical component). There were significantly fewer withdrawals due to adverse events in participants treated with COXIBs (3%) compared with NSAIDs (8%) (RR 2.39, 95% CI 1.34 to 4.28). There was a significantly lower number of total adverse events in participants treated with COXIBs (38%) compared with NSAIDs (60%) (RR 1.56, 95% CI 1.30 to 1.86).There was moderate-quality evidence based on two trials (210 participants) that oral glucocorticoids did not differ in pain reduction, function or adverse events when compared with NSAIDs. Pain reduction was 9.5 on a 0- to 100-point scale with glucocorticoids, pain reduction with NSAIDs was 1.74 higher or worse (MD 1.74, 95% CI -1.44 to 4.92). The trials did not assess inflammation. Function measured as walking disability was 17.4 points on a 0- to 100-point scale with glucocorticoids, function with NSAIDs was 0.1 lower or better (MD -0.10, 95% CI -4.72 to 4.52). The trials did not measure participant-reported global assessment and health-related quality of life. There were no withdrawals due to adverse events. There was no evidence of a difference in total number of adverse events with glucocorticoids (31%) versus NSAIDs (49%) (RR 1.58, 95% CI 0.76 to 3.28). AUTHORS' CONCLUSIONS: Limited evidence supported the use of NSAIDs in the treatment of acute gout. One placebo-controlled trial provided evidence of benefit at 24 hours and little or no harm. We downgraded the evidence due to potential selection and reporting biases, and imprecision. While these data were insufficient to draw firm conclusions, they did not conflict with clinical guideline recommendations based upon evidence from observational studies, other inflammatory arthritis and expert consensus, which support the use of NSAIDs in acute gout.Moderate-quality evidence suggested that selective COX-2 inhibitors and non-selective NSAIDs are probably equally beneficial although COX-2 inhibitors are likely to be associated with significantly fewer total and gastrointestinal adverse events. We downgraded the evidence due to an unclear risk of selection and reporting biases. Moderate-quality evidence indicated that systemic glucocorticoids and NSAIDs were also equally beneficial in terms of pain relief. There were no withdrawals due to adverse events and total adverse events were similar between groups. We downgraded the evidence due to unclear risk of selection and reporting bias. There was low-quality evidence that there was no difference in function. We downgraded the quality due to unclear risk of selection bias and imprecision.

7 Review Colchicine for acute gout. 2014

van Echteld, Irene / Wechalekar, Mihir D / Schlesinger, Naomi / Buchbinder, Rachelle / Aletaha, Daniel. ·Department of Rheumatology, St Elisabeth Hospital, Hilvarenbeekseweg 60, Tilburg, Netherlands, 5022GC. ·Cochrane Database Syst Rev · Pubmed #25123076.

ABSTRACT: BACKGROUND: This is an update of a Cochrane review first published in 2006. Gout is one of the most common rheumatic diseases worldwide. Despite the use of colchicine as one of the first-line therapies for the treatment of acute gout, evidence for its benefits and harms is relatively limited. OBJECTIVES: To evaluate the benefits and harms of colchicine for the treatment of acute gout. SEARCH METHODS: We searched the following electronic databases from inception to April 2014: Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE and EMBASE. We did not impose any date or language restrictions in the search. We also handsearched conference proceedings of the American College of Rheumatology and the European League against Rheumatism (2010 until 2013) and reference lists of identified studies. We searched the clinical trials register clinicaltrials.gov and the WHO trials register. SELECTION CRITERIA: We considered published randomised controlled trials (RCTs) and controlled clinical trials (CCTs) evaluating colchicine therapy compared with another therapy (active or placebo) in acute gout. The primary benefit outcome of interest was pain, defined as a proportion with 50% or greater decrease in pain, and the primary harm outcome was study participants withdrawal due to adverse events. DATA COLLECTION AND ANALYSIS: Two authors independently screened search results for relevant studies, extracted data into a standardised form and assessed the risk of bias of included studies. We pooled data if deemed to be sufficiently clinically homogeneous. We assessed the quality of the body of evidence for each outcome using the GRADE approach. MAIN RESULTS: Two RCTs (124 participants) were included in this updated review, including one new RCT. We considered one trial to be at low risk of bias, while we considered the newly included trial to be at unclear risk of bias. Both trials included a placebo and a high-dose colchicine arm, although the colchicine regimens varied. In one trial 0.5 mg colchicine was given every two hours until there was either complete relief of symptoms or toxicity and the total doses were not specified. In the other trial a total of 4.8 mg colchicine was given over six hours. The newly identified trial also included a low-dose colchicine arm (total 1.8 mg over one hour).Based upon pooled data from two trials (124 participants), there is low-quality evidence that a greater proportion of people receiving high-dose colchicine experience a 50% or greater decrease in pain from baseline up to 32 to 36 hours compared with placebo (35/74 in the high-dose colchicine group versus 12/50 in the placebo group (risk ratio (RR) 2.16, 95% confidence interval (CI) 1.28 to 3.65), with a number needed to treat to benefit (NNTB) of 4 (95% CI 3 to 12). However, the total number of adverse events (diarrhoea, vomiting or nausea) is greater in those who receive high-dose colchicine versus placebo (62/74 in the high-dose colchicine group versus 11/50 in the placebo group (RR 3.81, 95% CI 2.28 to 6.38), with a number needed to treat to harm (NNTH) of 2 (95% CI 2 to 5). Only one trial included reduction of inflammation as part of a composite measure comprising pain, tenderness, swelling and erythema, each graded on a four-point scale (none 0 to severe 3) to derive a maximum score for any one joint of 12. They reported the proportion of people who achieved a 50% reduction in this composite score. Based upon one trial (43 participants), there was low-quality evidence that more people in the high-dose colchicine group had a 50% or greater decrease in composite score from baseline up to 32 to 36 hours than people in the placebo group (11/22 in the high-dose colchicine group versus 1/21 in the placebo group (RR 10.50, 95% CI 1.48 to 74.38) and 45% absolute difference).Based upon data from one trial (103 participants), there was low-quality evidence that low-dose colchicine is more efficacious than placebo with respect to the proportion of people who achieve a 50% or greater decrease in pain from baseline to 32 to 36 hours (low-dose colchicine 31/74 versus placebo 5/29 (RR 2.43, 95% CI 1.05 to 5.64)), with a NNTB of 5 (95% CI 2 to 20). There are no additional harms in terms of adverse events (diarrhoea, nausea or vomiting) with low-dose colchicine compared to placebo (19/74 and 6/29 respectively (RR 1.24, 95% CI 0.55 to 2.79)).Based upon data from one trial (126 participants), there is low-quality evidence that there are no additional benefits in terms of the proportion of people achieving 50% or greater decrease in pain from baseline up to 32 to 36 hours with high-dose colchicine compared to low-dose (19/52 and 31/74 respectively (RR 0.87, 95% CI 0.56 to 1.36). However, there were statistically significantly more adverse events in those who received high-dose colchicine (40/52 versus 19/74 in the low-dose group (RR 3.00, 95% CI 1.98 to 4.54)), with a NNTH of 2 (95% CI 2 to 3).No trials reported function of the target joint, patient-reported global assessment of treatment success, health-related quality of life or withdrawals due to adverse events. We identified no studies comparing colchicine to non-steroidal anti-inflammatory drugs (NSAIDs) or other active treatments such as glucocorticoids (by any route). AUTHORS' CONCLUSIONS: Based upon only two published trials, there is low-quality evidence that low-dose colchicine is likely to be an effective treatment for acute gout. We downgraded the evidence because of a possible risk of selection and reporting biases and imprecision. Both high and low-dose colchicine improve pain when compared to placebo. While there is some uncertainty around the effect estimates, compared with placebo, high-dose but not low-dose colchicine appears to result in a statistically significantly greater number of adverse events. Therefore low-dose colchicine may be the preferred treatment option. There are no trials about the effect of colchicine in populations with comorbidities or in comparison with other commonly used treatments, such as NSAIDs and glucocorticoids.

8 Review Treatment of acute gout. 2014

Schlesinger, Naomi. ·Division of Rheumatology, Department of Medicine, Rutgers - Robert Wood Johnson Medical School, One Robert Wood Johnson Place, PO Box 19, New Brunswick, NJ 08903-0019, USA. Electronic address: schlesna@rwjms.rutgers.edu. ·Rheum Dis Clin North Am · Pubmed #24703350.

ABSTRACT: This article presents an overview of the treatment of acute gout. Nonpharmacologic and pharmacologic treatments, monotherapy versus combination therapy, suggested recommendations, guidelines for treatment, and drugs under development are discussed.

9 Review Anti-interleukin-1 therapy in the management of gout. 2014

Schlesinger, Naomi. ·Division of Rheumatology, Department of Medicine, Rutgers- Robert Wood Johnson Medical School, New Brunswick, NJ, USA, schlesna@rwjms.rutgers.edu. ·Curr Rheumatol Rep · Pubmed #24407823.

ABSTRACT: Gout is the most common inflammatory arthritis in humans. Current treatment options to control the pain and inflammation of acute and chronic gout include nonsteroidal anti-inflammatory drugs, colchicine, and corticosteroids. However, patients are commonly unresponsive to, intolerant of, or have contraindications to current treatments. Interleukin-1 (IL-1), a proinflammatory cytokine, plays a major role in mediating gouty inflammation. This role of IL-1 has led investigators to explore a new class of anti-inflammatory drugs that inhibit IL-1 signal transduction. IL-1 inhibitors currently in trials for gout include anakinra, rilonacept, and canakinumab. Anakinra is an IL‑1 receptor antagonist that inhibits the activity of both IL‑1α and IL‑1β, rilonacept is a soluble decoy receptor and canakinumab is an anti‑IL‑1β monoclonal antibody. In case cohorts, anakinra was found to be efficacious in combating acute gout pain and inflammation, whereas rilonacept has been found to be efficacious for reducing the risk of recurrent attacks. Canakinumab has been shown to be efficacious in both reducing pain and inflammation in acute attacks, and for reducing the risk of recurrent attacks. All three IL-1 inhibitors are generally well tolerated. This article reviews the current IL-1 inhibitors and the results of trials in which they have been tested for the management of acute and chronic gouty inflammation.

10 Review Intra-articular glucocorticoids for acute gout. 2013

Wechalekar, Mihir D / Vinik, Ophir / Schlesinger, Naomi / Buchbinder, Rachelle. ·Rheumatology Unit, Repatriation GeneralHospital, Daw Park, Australia. mihir.w@gmail.com. ·Cochrane Database Syst Rev · Pubmed #23633379.

ABSTRACT: BACKGROUND: Although intra-articular glucocorticoids are a commonly used intervention in the treatment of acute gout, there is little evidence to support their safety and efficacy in this setting. OBJECTIVES: To evaluate the safety and efficacy of intra-articular glucocorticoids in the treatment of acute gout. SEARCH METHODS: We searched the Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library), Ovid MEDLINE and Ovid EMBASE for studies to 16th October 2012. We also searched the 2010 to 2011 American College of Rheumatology (ACR) and European League against Rheumatism (EULAR) abstracts and performed a handsearch of the reference lists of articles considered for inclusion. SELECTION CRITERIA: Studies were eligible for inclusion if they were randomised controlled trials (RCTs) or controlled clinical trials (CCTs) that used quasi-randomisation methods to allocate participants to treatment and compared intra-articular glucocorticoids to another therapy (active or placebo) in adults with acute gout. Outcomes selected for inclusion were pain, the proportion of participant withdrawals due to adverse events, inflammation, function, patient global assessment of treatment success, quality of life and proportion of particpants with serious adverse events. DATA COLLECTION AND ANALYSIS: Two review authors independently selected the studies for inclusion and planned to extract the data and perform a risk of bias assessment. MAIN RESULTS: No trials were identified that evaluated the efficacy and safety of intra-articular glucocorticoids for acute gout. AUTHORS' CONCLUSIONS: There is presently no evidence from randomised trials to support the use of intra-articular glucocorticoid treatment in acute gout. Evidence suggests intra-articular glucocorticoids may be a safe and effective treatment in osteoarthritis and rheumatoid arthritis. These results may be generalisable to people with acute gout, and the treatment may be especially useful in people when non-steroidal anti-inflammatory drugs or colchicine are contraindicated.

11 Review Canakinumab in gout. 2012

Schlesinger, Naomi. ·Division of Rheumatology, Department of Medicine, UMDNJ/RWJMS , MEB 468, PO Box 19, New Brunswick, NJ 08903-0019, USA. schlesna@umdnj.edu ·Expert Opin Biol Ther · Pubmed #22784099.

ABSTRACT: INTRODUCTION: Gout is a painful inflammatory arthritis with a prevalence of approximately 4% in the United States, affecting an estimated 8.3 million adults. The past 20 years have shown significant increases in the number of patients with gout and its incidence may still be increasing. Current treatment options to control the pain and inflammation of acute gout include nonsteroidal anti-inflammatory drugs, colchicine and corticosteroids, although patients are often unresponsive to, intolerant of, or have contraindications for, these therapies. Additional treatment options are therefore needed for this population with difficult-to-treat gout. AREAS COVERED: Currently available and investigational anti-inflammatory agents for acute and chronic gout will briefly be reviewed. Canakinumab , a fully human monoclonal anti-interleukin (IL)-1β antibody that selectively blocks IL-1β and that is being investigated for the treatment of gout, will be discussed in greater detail. EXPERT OPINION: Canakinumab has been found to be superior to triamcinolone acetonide in acute gout and to colchicine in gout attack prophylaxis in reducing pain and risk of new gout attacks. Canakinumab's long half-life contributes to its prolonged anti-inflammatory effects.

12 Review Treatment of chronic gouty arthritis: it is not just about urate-lowering therapy. 2012

Schlesinger, Naomi. ·Division of Rheumatology, Department of Medicine, UMDNJ/RWJMS, New Brunswick, NJ, USA. schlesna@umdnj.edu ·Semin Arthritis Rheum · Pubmed #22542277.

ABSTRACT: OBJECTIVES: The management of gouty arthritis is focused on treating pain and inflammation associated with acute flares and preventing further acute flares and urate crystal deposition. A challenge associated with the successful management of gouty arthritis is an increased risk of acute flares during the first months after initiation of urate-lowering therapy (ULT). This increase in flare frequency can occur regardless of the choice of ULT and is linked to suboptimal patient adherence to ULT. Current treatment recommendations for the use of prophylaxis are limited. There are no definitive recommendations as to which agents should be used or for how long therapy is beneficial after starting ULT. This article aims to improve awareness of the importance of gouty arthritis flare prophylaxis when initiating ULT and to summarize current recommendations and clinical findings related to the efficacy and safety of currently available and investigational new therapies. METHODS: This review discusses the pathophysiology of acute gouty arthritis flares during initiation of ULT and examines the literature on the use of anti-inflammatory prophylaxis for reduction of these flares. RESULTS: It has recently become clear that, even when the patient is asymptomatic, chronic inflammation is often present in patients with chronic gouty arthritis. Chronic anti-inflammatory therapy should therefore be added to chronic ULT. Prophylaxis with colchicine as well as with nonsteroidal anti-inflammatory drugs (NSAIDs) during ULT initiation can reduce the incidence and severity of gouty arthritis flares substantially; however, safety concerns associated with colchicine and NSAIDs may limit their use. CONCLUSION: When colchicine and NSAIDs are contraindicated or poorly tolerated, rilonacept and canakinumab, interleukin-1 inhibitors in trials, may prove to be useful alternatives for flare prevention. (Of note, although both inhibit the IL-1β pathway, rilonacept also binds to IL-1α and IL-1RA, in contrast to canakinumab, which binds selectively to IL-1β.).

13 Review Difficult-to-treat gouty arthritis: a disease warranting better management. 2011

Schlesinger, Naomi. ·Division of Rheumatology, Department of Medicine, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, New Brunswick, NJ, USA. schlesna@umdnj.edu ·Drugs · Pubmed #21812506.

ABSTRACT: Gouty arthritis is the most common inflammatory arthritis in adults and is characterized by very painful flares. Gouty arthritis results from an elevated body uric acid pool, which leads to deposition of monosodium urate crystals, mainly in the joints. These crystals trigger the release of proinflammatory cytokines, in particular interleukin (IL)-1β, which stimulates inflammation. Gouty arthritis can progress to a chronic, deforming and physically disabling disease through the development of disfiguring tophi, joint destruction and persistent pain. Standard treatments are effective in most patients. Acutely, anti-inflammatory therapies provide rapid pain relief and resolution of flares. Chronically, urate-lowering therapies reduce serum urate levels and, in combination with anti-inflammatory prophylaxis, reduce the risk of flares. However, for a growing number of patients, current standard treatments are ineffective or are contraindicated, largely due to the presence of co-morbidities. Indeed, metabolic syndrome, hypertension, dyslipidaemia, cardiovascular disease, diabetes mellitus and renal impairment are all highly prevalent in individuals with gouty arthritis, and may lead to standard treatments being ineffective or inappropriate. Such patients with difficult-to-treat disease require alternative therapies. Gouty arthritis can have a major impact on health-related quality of life (HR-QOL), especially in patients with difficult-to-treat disease, as revealed by recent studies comparing HR-QOL for patients with gouty arthritis with that of the general population. All studies revealed clinically significant reductions in physical functioning for individuals with gouty arthritis compared with the general population. The difference was particularly marked for patients with difficult-to-treat disease. Gouty arthritis also constitutes an important economic burden through absence from work and medical costs. Again, the burden is greater in patients with difficult-to-treat disease. The development of difficult-to-treat disease reflects the short-comings of current standard treatments in a growing number of gouty arthritis patients. This has been recognized by the pharmaceutical industry and has promoted the development of innovative therapies. An appreciation of the key role of IL-1β in inflammation in gouty arthritis has led to the development of a new class of anti-inflammatory agents that block IL-1β signal transduction. The current IL-1β blockers in trials are rilonacept and canakinumab. Canakinumab, a fully human anti-IL-1β monoclonal antibody, has been shown to produce rapid and sustained pain relief from acute flares in patients with difficult-to-treat disease, and both rilonacept and canakinumab have been shown to reduce the risk of recurrent flares. Promising new therapies for reducing serum urate levels are also being developed. These include the recently approved therapies pegloticase (a pegylated form of the enzyme uricase that converts urate to allantoin), inhibitors of renal urate transporter proteins, and inhibitors of purine nucleotide phosphorylase, an enzyme involved in purine metabolism. Further studies are warranted to establish the value and role of these new therapies in the management of gouty arthritis. These new options should help reduce the growing human burden associated with gouty arthritis, lowering the tophaceous burden, minimizing the risk of flares, and enabling patients to achieve rapid and effective pain relief when flares do occur.

14 Review New agents for the treatment of gout and hyperuricemia: febuxostat, puricase, and beyond. 2010

Schlesinger, Naomi. ·Division of Rheumatology, Department of Medicine, University of Medicine and Dentistry of New Jersey/Robert Wood Johnson Medical School, One Robert Wood Johnson Place, New Brunswick, NJ 08903, USA. schlesna@umdnj.edu ·Curr Rheumatol Rep · Pubmed #20425022.

ABSTRACT: The rising prevalence of gout has led the pharmaceutical industry to rediscover what it had considered a forgotten disease. In April 2009, the Food and Drug Administration (FDA) approved febuxostat (Takeda Pharmaceuticals; Deerfield, IL), the first new urate-lowering gout drug in more than 40 years. In August 2009, the FDA approved colchicine for the treatment of acute gout. Several other pharmaceutical companies are also conducting clinical trials to test new drugs for acute and chronic gout. This article reviews new drugs and drugs in development in the management of acute and chronic gout.

15 Review Diagnosing and treating gout: a review to aid primary care physicians. 2010

Schlesinger, Naomi. ·Department of Medicine, UMDNJ-Robert Wood Johnson Medical School, New Brunswick, NJ 08903, USA. schlesna@umdnj.edu ·Postgrad Med · Pubmed #20203467.

ABSTRACT: Generalist physicians, specifically general internists and primary care physicians, are often the first to see patients with gout and therefore play a critical role in the diagnosis and management of these patients. The aim of this review is to aid generalist physicians in diagnosing and treating gout. A case report example is presented to highlight some of the problems in diagnosing and treating gout. Practical practice points are also highlighted.

16 Clinical Trial Canakinumab for the treatment of acute flares in difficult-to-treat gouty arthritis: Results of a multicenter, phase II, dose-ranging study. 2010

So, Alexander / De Meulemeester, Marc / Pikhlak, Andrey / Yücel, A Eftal / Richard, Dominik / Murphy, Valda / Arulmani, Udayasankar / Sallstig, Peter / Schlesinger, Naomi. ·University Hospital of Lausanne, Lausanne, Switzerland. AlexanderKai-Lik.So@chuv.ch ·Arthritis Rheum · Pubmed #20533546.

ABSTRACT: OBJECTIVE: To assess the efficacy and tolerability of canakinumab, a fully human anti-interleukin-1β monoclonal antibody, for the treatment of acute gouty arthritis. METHODS: In this 8-week, single-blind, double-dummy, dose-ranging study, patients with acute gouty arthritis whose disease was refractory to or who had contraindications to nonsteroidal antiinflammatory drugs and/or colchicine were randomized to receive a single subcutaneous dose of canakinumab (10, 25, 50, 90, or 150 mg; n = 143) or an intramuscular dose of triamcinolone acetonide (40 mg; n = 57). Patients assessed pain using a 100-mm visual analog scale. RESULTS: Seventy-two hours after treatment, a statistically significant dose response was observed for canakinumab. All canakinumab doses were associated with numerically less pain than triamcinolone acetonide; thus, a dose with equivalent efficacy to triamcinolone acetonide 72 hours after treatment could not be determined. The reduction from baseline in pain intensity with canakinumab 150 mg was greater than with triamcinolone acetonide 24, 48, and 72 hours after treatment (differences of -11.5 mm [P = 0.04], -18.2 mm [P = 0.002], and -19.2 mm [P < 0.001], respectively), and 4, 5, and 7 days after treatment (all P < 0.05). Canakinumab significantly reduced the risk of recurrent flares versus triamcinolone acetonide (P ≤ 0.01 for all doses) (relative risk reduction 94% for canakinumab 150 mg versus triamcinolone acetonide). The overall incidence of adverse events was similar for canakinumab (41%) and triamcinolone acetonide (42%); most were mild or moderate in severity. CONCLUSION: Our findings indicate that canakinumab 150 mg provides rapid and sustained pain relief in patients with acute gouty arthritis, and significantly reduces the risk of recurrent flares compared with triamcinolone acetonide.

17 Article Gout, Hyperuricaemia and Crystal-Associated Disease Network (G-CAN) consensus statement regarding labels and definitions of disease states of gout. 2019

Bursill, David / Taylor, William J / Terkeltaub, Robert / Abhishek, Abhishek / So, Alexander K / Vargas-Santos, Ana Beatriz / Gaffo, Angelo Lino / Rosenthal, Ann / Tausche, Anne-Kathrin / Reginato, Anthony / Manger, Bernhard / Sciré, Carlo / Pineda, Carlos / van Durme, Caroline / Lin, Ching-Tsai / Yin, Congcong / Albert, Daniel Arthur / Biernat-Kaluza, Edyta / Roddy, Edward / Pascual, Eliseo / Becce, Fabio / Perez-Ruiz, Fernando / Sivera, Francisca / Lioté, Frédéric / Schett, Georg / Nuki, George / Filippou, Georgios / McCarthy, Geraldine / da Rocha Castelar Pinheiro, Geraldo / Ea, Hang-Korng / Tupinambá, Helena De Almeida / Yamanaka, Hisashi / Choi, Hyon K / Mackay, James / ODell, James R / Vázquez Mellado, Janitzia / Singh, Jasvinder A / Fitzgerald, John D / Jacobsson, Lennart T H / Joosten, Leo / Harrold, Leslie R / Stamp, Lisa / Andrés, Mariano / Gutierrez, Marwin / Kuwabara, Masanari / Dehlin, Mats / Janssen, Matthijs / Doherty, Michael / Hershfield, Michael S / Pillinger, Michael / Edwards, N Lawrence / Schlesinger, Naomi / Kumar, Nitin / Slot, Ole / Ottaviani, Sebastien / Richette, Pascal / MacMullan, Paul A / Chapman, Peter T / Lipsky, Peter E / Robinson, Philip / Khanna, Puja P / Gancheva, Rada N / Grainger, Rebecca / Johnson, Richard J / Te Kampe, Ritch / Keenan, Robert T / Tedeschi, Sara K / Kim, Seoyoung / Choi, Sung Jae / Fields, Theodore R / Bardin, Thomas / Uhlig, Till / Jansen, Tim / Merriman, Tony / Pascart, Tristan / Neogi, Tuhina / Klück, Viola / Louthrenoo, Worawit / Dalbeth, Nicola. ·Department of Health and Medical Sciences, The University of Adelaide, Adelaide, South Australia, Australia davebursill@bigpond.com. · Department of Medicine, University of Otago, Wellington, New Zealand. · Wellington Regional Rheumatology Unit, Hutt Valley District Health Board, Lower Hutt, New Zealand. · Department of Rheumatology, UCSD/ VA Medical Center, San Diego, California, USA. · Department of Academic Rheumatology, University of Nottingham, Nottingham, UK. · Department of Musculoskeletal Medicine, Service de RMR, Lausanne, Switzerland. · Department of Internal Medicine, Rheumatology Unit, State University of Rio de Janeiro, Rio de Janeiro, Brazil. · Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA. · Division of Rheumatology, Medical College of Wisconsin, Milwaukee, Wisconsin, USA. · Translational Research Unit, Clement J Zablocki VA Medical Center, Milwaukee, Wisconsin, USA. · Department of Rheumatology, University Hospital 'Carl Gustav Carus' of the Technical University Dresden, Dresden, Germany. · Division of Rheumatology, The Warren Alpert School of Medicine at Brown University, Providence, Rhode Island, USA. · Rheumatology and Immunology, Universität Erlangen-Nürnberg, Erlangen, Germany. · Section of Rheumatology, Department of Medical Sciences, University of Ferrara, Ferrara, Italy. · Epidemiology Unit, Italian Society for Rheumatology, Milan, Italy. · Department of Rheumatology, Instituto Nacional de Rehabilitación Luis Guillermo Ibarra Ibarra, Mexico City, Mexico. · Department of Internal Medicine, Division of Rheumatology, Maastricht University Medical Centre, Maastricht, The Netherlands. · Division of Allergy, Immunology and Rheumatology, Taichung Veterans General Hospital, Taichung, Taiwan. · Department of Immunology and Dermatology, Henry Ford Health System, Detroit, Michigan, USA. · Department of Rheumatology, Dartmouth-Hitchcock Medical Center, Hanover, New Hampshire, USA. · Outpatient Rheumatology Clinic, Nutritional and Lifestyle Medicine Centre, ORLIK, Warsaw, Poland. · Research Institute for Primary Care and Health Sciences, Keele University, Keele, UK. · Department of Rheumatology, Hospital General Universitario de Alicante, Alicante, Spain. · Departamento de Medicina Clínica, Universidad Miguel Hernández, Alicante, Spain. · Department of Diagnostic and Interventional Radiology, University of Lausanne, Lausanne, Switzerland. · Rheumatology Division, Cruces University Hospital, Baracaldo, Spain. · Department of Medicine, University of the Basque Country, Biscay, Spain. · Investigation Group for Arthritis, Biocruces Health Research Institute, Baracaldo, Spain. · Department of Rheumatology, Hospital General Universitario Elda, Elda, Spain. · Department of Rhumatologie, Hôpital Lariboisière, Assistance Publique-Hopitaux de Paris, Paris, France. · Department of Rhumatologie, INSERM UMR-1132 and Université Paris Diderot, Paris, France. · Department of Internal Medicine III, Friedrich-Alexander University Erlangen-Nürnberg and Universitatsklinikum Erlangen, Erlangen, Germany. · Insititute of Genetics and Molecular Medicine, University of Edinburgh, Edinburgh, UK. · Department of Rheumatology, Mater Misericordiae University Hospital, Dublin, Ireland. · School of Medicine and Medical Science, University College Dublin, Dublin, Ireland. · Department of Rheumatology, Hôpital Lariboisière, Paris, France. · Rheumatology, State University of Rio de Janeiro, Rio de Janeiro, Brazil. · Institute of Rheumatology, Tokyo Women's Medical University Hospital, Tokyo, Japan. · School of Medicine, Tokyo Women's Medical University, Tokyo, Japan. · Section of Rheumatology and Clinical Epidemiology, Harvard Medical School and Massachusetts General Hospital, Boston, Massachusetts, USA. · President and CEO, Aristea Therapeutics, San Diego, California, USA. · Division of Rheumatology, University of Nebraska Medical Center, Omaha, Nebraska, USA. · Department of Rheumatology, Hospital General de Mexico and Universidad Nacional Autónoma de México, Mexico City, Mexico. · Department of Medicine at School of Medicine, University of Alabama at Birmingham, Birmingham, Alabama, USA. · Medicine Service, Birmingham Veterans Affairs Medical Center, Birmingham, Alabama, USA. · Division of Epidemiology at School of Public Health, University of Alabama at Birmingham, Birmingham, Alabama, USA. · Department of Medicine/Rheumatology, David Geffen School of Medicine at the University of California, Los Angeles, Los Angeles, California, USA. · Department of Rheumatology and Inflammation Research, Institute of Medicine, The Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. · Department of Internal Medicine, Radboud University Medical Center Nijmegen, Nijmegen, The Netherlands. · Department of Medicine, University of Massachusetts Medical School, Worcester, Massachusetts, USA. · Chief Scientific Officer, Corrona, LLC, Southborough, Massachusetts, USA. · Department of Medicine, Otago University, Christchurch, New Zealand. · Department of Rheumatology, Hospital Universitario de Alicante, Alicante, Spain. · Division of Musculoskeletal and Rheumatic Diseases, Instituto Nacional Rehabilitación, México City, México. · Division of Renal Diseases and Hypertension, University of Colorado Denver School of Medicine, Aurora, Colorado, USA. · Department of Cardiology, Toranomon Hospital, Minato-ku, Japan. · Department of Rheumatology and Inflammation Research, Sahlgrenska Academy, University of Göteborg, Göteborg, Sweden. · Department of Rheumatology, VieCuri Medical Centre, Venlo, The Netherlands. · Division of Rheumatology, Duke University Medical Center, Durham, North Carolina, USA. · Department of Rheumatology/Medicine, New York University School of Medicine, New York City, New York, USA. · College of Medicine, University of Florida, Gainesville, Florida, USA. · Department of Medicine, Rutgers-Robert Wood Johnson Medical School, New Brunswick, New Jersey, USA. · Department of Internal Medicine, Division of Cardiovascular Medicine, University of Michigan, Ann Arbor, Detroit, Michigan, USA. · Department of Rheumatology, Copenhagen Center for Arthritis Research, Center for Rheumatology and Spinal Disorders, Rigshospitalet Glostrup, Glostrup, Denmark. · Department of Rheumatology, Bichat-Claude Bernard Hospital, University of Sorbonne Paris Cité, Paris, France. · Service de Rhumatologie, Hôpital Lariboisière, Assistance Publique-Hopitaux de Paris, and INSERM UMR-1132 and Université de Paris, Paris, France. · Division of Rheumatology, University of Calgary, Calgary, Alberta, Canada. · Department of Rheumatology, Immunology and Allergy, Canterbury District Health Board, Christchurch, New Zealand. · CEO and CMO, AMPEL BioSolutions, LLC, Charlottesville, Virginia, USA. · School of Clinical Medicine, Faculty of Medicine, The University of Queensland, Brisbane, Queensland, Australia. · Department of Rheumatology, University of Michigan, Ann Arbor, Michigan, USA. · Clinic of Rheumatology, University Hospital 'St. Ivan Rilski', Sofia, Bulgaria. · Department of Medicine, University of Otago, Wellington, Wellington, New Zealand. · Division of Renal Diseases and Hypertension, University of Colorado Denver, Denver, Colorado, USA. · Division of Rheumatology, Duke University School of Medicine, Durham, North Carolina, USA. · Division of Rheumatology, Immunology and Allergy, Brigham and Women's Hospital, Boston, Massachusetts, USA. · Arthritis Center, Harvard Medical School, Boston, Massachusetts, USA. · Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts, USA. · Division of Rheumatology, Department of Internal Medicine, Korea University Medical College, Ansan, South Korea. · Weill Cornell Medical College, Hospital for Special Surgery, New York City, New York, USA. · Department of Rheumatology, Hôpital Lariboisière, Assistance Publique-Hopitaux de Paris, and INSERM UMR-1132 and Université de Paris, Paris, France. · Department of Rheumatology, Diakonhjemmet Hospital, Oslo, Norway. · Department of Biochemistry, University of Otago, Dunedin, New Zealand. · Department of Rheumatology, Lille Catholic University, Saint-Philibert Hospital, Lomme, France. · Section of Rheumatology, Department of Medicine, Boston University School of Medicine, Boston, Massachusetts, USA. · Department of Internal Medicine, Radboud Institute for Molecular Life Sciences, Radboud University Medical Center, Nijmegen, The Netherlands. · Division of Rheumatology, Department of Internal Medicine, Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand. · Department of Medicine, Faculty of Medical and Health Sciences, University of Auckland, Auckland, New Zealand. ·Ann Rheum Dis · Pubmed #31501138.

ABSTRACT: OBJECTIVE: There is a lack of standardisation in the terminology used to describe gout. The aim of this project was to develop a consensus statement describing the recommended nomenclature for disease states of gout. METHODS: A content analysis of gout-related articles from rheumatology and general internal medicine journals published over a 5-year period identified potential disease states and the labels commonly assigned to them. Based on these findings, experts in gout were invited to participate in a Delphi exercise and face-to-face consensus meeting to reach agreement on disease state labels and definitions. RESULTS: The content analysis identified 13 unique disease states and a total of 63 unique labels. The Delphi exercise (n=76 respondents) and face-to-face meeting (n=35 attendees) established consensus agreement for eight disease state labels and definitions. The agreed labels were as follows: 'asymptomatic hyperuricaemia', 'asymptomatic monosodium urate crystal deposition', 'asymptomatic hyperuricaemia with monosodium urate crystal deposition', 'gout', 'tophaceous gout', 'erosive gout', 'first gout flare' and 'recurrent gout flares'. There was consensus agreement that the label 'gout' should be restricted to current or prior clinically evident disease caused by monosodium urate crystal deposition (gout flare, chronic gouty arthritis or subcutaneous tophus). CONCLUSION: Consensus agreement has been established for the labels and definitions of eight gout disease states, including 'gout' itself. The Gout, Hyperuricaemia and Crystal-Associated Disease Network recommends the use of these labels when describing disease states of gout in research and clinical practice.

18 Article Gout, Hyperuricemia, and Crystal-Associated Disease Network Consensus Statement Regarding Labels and Definitions for Disease Elements in Gout. 2019

Bursill, David / Taylor, William J / Terkeltaub, Robert / Kuwabara, Masanari / Merriman, Tony R / Grainger, Rebecca / Pineda, Carlos / Louthrenoo, Worawit / Edwards, N Lawrence / Andrés, Mariano / Vargas-Santos, Ana Beatriz / Roddy, Edward / Pascart, Tristan / Lin, Ching-Tsai / Perez-Ruiz, Fernando / Tedeschi, Sara K / Kim, Seoyoung C / Harrold, Leslie R / McCarthy, Geraldine / Kumar, Nitin / Chapman, Peter T / Tausche, Anne-Kathrin / Vazquez-Mellado, Janitzia / Gutierrez, Marwin / da Rocha Castelar-Pinheiro, Geraldo / Richette, Pascal / Pascual, Eliseo / Fisher, Mark C / Burgos-Vargas, Ruben / Robinson, Philip C / Singh, Jasvinder A / Jansen, Tim L / Saag, Kenneth G / Slot, Ole / Uhlig, Tillmann / Solomon, Daniel H / Keenan, Robert T / Scire, Carlo Alberto / Biernat-Kaluza, Edyta / Dehlin, Mats / Nuki, George / Schlesinger, Naomi / Janssen, Matthijs / Stamp, Lisa K / Sivera, Francisca / Reginato, Anthony M / Jacobsson, Lennart / Lioté, Frédéric / Ea, Hang-Korng / Rosenthal, Ann / Bardin, Thomas / Choi, Hyon K / Hershfield, Michael S / Czegley, Christine / Choi, Sung Jae / Dalbeth, Nicola. ·University of Auckland, Auckland, New Zealand, and Adelaide Medical School, University of Adelaide, South Australia, Australia. · University of Otago, Wellington, and Hutt Valley District Health Board, Lower Hutt, New Zealand. · Veterans Affairs Medical Center and University of California, San Diego. · Toranomon Hospital, Tokyo, Japan, and University of Colorado Denver, Aurora. · University of Otago, Dunedin, New Zealand. · Instituto Nacional Rehabilitación Luis Guillermo Ibarra Ibarra, Mexico City, Mexico. · Chiang Mai University, Chiang Mai, Thailand. · University of Florida College of Medicine, Gainesville. · Hospital Universitario de Alicante and Universidad Miguel Hernández, Alicante, Spain. · State University of Rio de Janeiro, Rio de Janeiro, Brazil. · Keele University, Keele, UK. · Lille Catholic University and Saint-Philibert Hospital, Lomme, France. · Taichung Veterans General Hospital, Taichung, Taiwan. · University of the Basque Country, Biscay, and Cruces University Hospital and Biocruces Health Research Institute, Baracaldo, Spain. · Harvard Medical School, and Brigham and Women's Hospital, Boston, Massachusetts. · Corrona, LLC, Waltham, and University of Massachusetts Medical School, Worcester. · Mater Misericordiae University Hospital and University College, Dublin, Ireland. · Henry Ford Hospital, Detroit, Michigan. · Christchurch Hospital, Christchurch, New Zealand. · University Hospital Carl Gustav Carus, Technical University Dresden, Dresden, Germany. · Hospital General de México and Universidad Nacional Autónoma de México, Mexico City, Mexico. · Instituto Nacional Rehabilitación, Mexico City, Mexico. · Hôpital Lariboisière, Assistance Publique-Hopitaux de Paris, and INSERM UMR-1132 and Université Paris Diderot, Paris, France. · Harvard Medical School and Massachusetts General Hospital Boston. · University of Queensland School of Medicine and Royal Brisbane and Women's Hospital, Herston, Queensland, Australia. · Veterans Affairs Medical Center, Birmingham, and University of Alabama at Birmingham. · Viecuri Medical Centre, Venlo, The Netherlands. · University of Alabama at Birmingham. · Rigshospitalet Glostrup, Glostrup, Denmark. · Diakonhjemmet Hospital, Oslo, Norway. · Duke University School of Medicine, Durham, North Carolina. · University of Ferrara, Ferrara, and Italian Society for Rheumatology, Milan, Italy. · ORLIK, Warsaw, Poland. · Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden. · University of Edinburgh, Edinburgh, UK. · Rutgers-Robert Wood Johnson Medical School, Piscataway, New Jersey. · University of Otago, Christchurch, New Zealand. · Hospital General Universitario de Elda, Alicante, Spain. · Warren Alpert School of Medicine at Brown University, Providence, Rhode Island. · Medical College of Wisconsin and the Clement J. Zablocki Veterans Affairs Medical Center, Milwaukee. · Duke University Medical Center, Durham, North Carolina. · Friedrich-Alexander University Erlangen-Nuremberg, Erlangen, Germany. · University of California, San Diego, and Korea University Ansan Hospital, Ansan, South Korea. · University of Auckland, Auckland, New Zealand. ·Arthritis Care Res (Hoboken) · Pubmed #29799677.

ABSTRACT: OBJECTIVE: The language currently used to describe gout lacks standardization. The aim of this project was to develop a consensus statement on the labels and definitions used to describe the basic disease elements of gout. METHODS: Experts in gout (n = 130) were invited to participate in a Delphi exercise and face-to-face consensus meeting to reach consensus on the labeling and definitions for the basic disease elements of gout. Disease elements and labels in current use were derived from a content analysis of the contemporary medical literature, and the results of this analysis were used for item selection in the Delphi exercise and face-to-face consensus meeting. RESULTS: There were 51 respondents to the Delphi exercise and 30 attendees at the face-to-face meeting. Consensus agreement (≥80%) was achieved for the labels of 8 disease elements through the Delphi exercise; the remaining 3 labels reached consensus agreement through the face-to-face consensus meeting. The agreed labels were monosodium urate crystals, urate, hyperuric(a)emia, tophus, subcutaneous tophus, gout flare, intercritical gout, chronic gouty arthritis, imaging evidence of monosodium urate crystal deposition, gouty bone erosion, and podagra. Participants at the face-to-face meeting achieved consensus agreement for the definitions of all 11 elements and a recommendation that the label "chronic gout" should not be used. CONCLUSION: Consensus agreement was achieved for the labels and definitions of 11 elements representing the fundamental components of gout etiology, pathophysiology, and clinical presentation. The Gout, Hyperuricemia, and Crystal-Associated Disease Network recommends the use of these labels when describing the basic disease elements of gout.

19 Article Gout and the Risk of Incident Erectile Dysfunction: A Body Mass Index-matched Population-based Study. 2018

Schlesinger, Naomi / Lu, Na / Choi, Hyon K. ·From the Division of Rheumatology, Department of Medicine, Rutgers Robert Wood Johnson Gout Center, Rutgers University, Robert Wood Johnson Medical School, New Brunswick, New Jersey; Harvard Medical School; Gout and Crystal Arthropathy Center, Clinical Epidemiology, Division of Rheumatology, Allergy, and Immunology, Massachusetts General Hospital, Boston, Massachusetts, USA. schlesna@rutgers.edu. · N. Schlesinger, MD, Professor, Chief, Division of Rheumatology, Department of Medicine, and Rutgers Robert Wood Johnson Gout Center, Rutgers Robert Wood Johnson Medical School; N. Lu, MPH, Harvard Medical School, and Clinical Epidemiology, Division of Rheumatology, Allergy, and Immunology, Massachusetts General Hospital; H.K. Choi, MD, PhD, Professor, Harvard Medical School, and Gout and Crystal Arthropathy Center, Clinical Epidemiology, Division of Rheumatology, Allergy, and Immunology, Massachusetts General Hospital. schlesna@rutgers.edu. · From the Division of Rheumatology, Department of Medicine, Rutgers Robert Wood Johnson Gout Center, Rutgers University, Robert Wood Johnson Medical School, New Brunswick, New Jersey; Harvard Medical School; Gout and Crystal Arthropathy Center, Clinical Epidemiology, Division of Rheumatology, Allergy, and Immunology, Massachusetts General Hospital, Boston, Massachusetts, USA. · N. Schlesinger, MD, Professor, Chief, Division of Rheumatology, Department of Medicine, and Rutgers Robert Wood Johnson Gout Center, Rutgers Robert Wood Johnson Medical School; N. Lu, MPH, Harvard Medical School, and Clinical Epidemiology, Division of Rheumatology, Allergy, and Immunology, Massachusetts General Hospital; H.K. Choi, MD, PhD, Professor, Harvard Medical School, and Gout and Crystal Arthropathy Center, Clinical Epidemiology, Division of Rheumatology, Allergy, and Immunology, Massachusetts General Hospital. ·J Rheumatol · Pubmed #30008453.

ABSTRACT: OBJECTIVE: Gout is the most common inflammatory arthritis. Erectile dysfunction (ED) is common in the general population; however, evidence regarding ED among patients with gout is limited. Our purpose was to study the association between incident gout and the risk of incident ED in the general population. METHODS: We conducted a cohort study using The Health Improvement Network, an electronic medical record database in the United Kingdom. Up to 5 individuals without gout were matched to each case of incident gout by age, enrollment time, and body mass index (BMI). Multivariate HR for ED were calculated after adjusting for smoking, alcohol consumption, comorbidities, and medication use. RESULTS: We identified 2290 new cases of ED among 38,438 patients with gout (mean age 63.6 yrs) and 8447 cases among 154,332 individuals in the comparison cohort over a 5-year median followup (11.9 vs 10.5 per 1000 person-years, respectively). Univariate (matched for age, entry time, and BMI) and multivariate HR for ED among patients with gout were 1.13 (95% CI 1.08-1.19) and 1.15 (95% CI 1.09-1.21), respectively. In our sensitivity analysis, by restricting gout cases to those receiving anti-gout treatment (n = 27,718), the magnitude of relative risk was stronger than the primary analysis (multivariate HR 1.31, 95% CI 1.23-1.39). CONCLUSION: This population-based study suggests that gout is associated with an increased risk of developing ED, supporting a possible role for hyperuricemia and inflammation as independent risk factors for ED.

20 Article Sex differences in gout characteristics: tailoring care for women and men. 2017

Harrold, Leslie R / Etzel, Carol J / Gibofsky, Allan / Kremer, Joel M / Pillinger, Michael H / Saag, Kenneth G / Schlesinger, Naomi / Terkeltaub, Robert / Cox, Vanessa / Greenberg, Jeffrey D. ·Department of Medicine and Orthopedics, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA, 01655, USA. leslie.harrold@umassmed.edu. · Corrona, LLC, Southborough, MA, USA. · Department of Epidemiology, UT MD Anderson Cancer Center, Houston, TX, USA. · Hospital for Special Surgery-Weill Medical College of Cornell University, New York, NY, USA. · Albany Medical College and The Center for Rheumatology, Albany, NY, USA. · NYU School of Medicine, New York, NY, USA. · University of Alabama at Birmingham, Birmingham, AL, USA. · Rutgers-Robert Wood Johnson Medical School, New Brunswick, NJ, USA. · VA Medical Center, UCSD, San Diego, CA, USA. ·BMC Musculoskelet Disord · Pubmed #28292303.

ABSTRACT: BACKGROUND: To characterize the differences between women and men with gout. METHODS: We analyzed a US national cohort of gout patients cared for by rheumatologists. RESULTS: Compared with the 1012 men with gout, women with gout (n = 262) were older (71 vs. 61 years, p < 0.001) and had a greater burden of comorbid conditions (p < 0.001 for hypertension, diabetes, renal disease and obesity). Risk factors for gout differed with women more often taking diuretics (p < 0.001), while men more frequently had dietary triggers (p < 0.05). CONCLUSIONS: The profiles of women and men with gout are markedly different, suggesting a need to tailor treatment recommendations.

21 Article Gout Prophylaxis Evaluated According to the 2012 American College of Rheumatology Guidelines: Analysis from the CORRONA Gout Registry. 2016

Schlesinger, Naomi / Etzel, Carol J / Greenberg, Jeff / Kremer, Joel / Harrold, Leslie R. ·From the Division of Rheumatology, Department of Medicine, Rutgers-Robert Wood Johnson Medical School, New Brunswick, New Jersey; Corrona LLC, Southborough, Massachusetts; Department of Epidemiology, University of Texas MD Anderson Cancer Center, Houston, Texas; Division of Rheumatology, Department of Medicine, New York University School of Medicine, New York, New York; the Center for Rheumatology, Albany Medical College, Albany, New York; Department of Orthopedics, University of Massachusetts Medical School, Worcester, Massachusetts, USA.N. Schlesinger, MD, Professor of Medicine and Chief, Division of Rheumatology, Department of Medicine, Rutgers-Robert Wood Johnson Medical School; C.J. Etzel, PhD, Corrona LLC, and the Department of Epidemiology, University of Texas MD Anderson Cancer Center; J. Greenberg, MD, MPH, Associate Professor, Division of Rheumatology, Department of Medicine, New York University School of Medicine, and Corrona LLC; J. Kremer, MD, Director, the Center for Rheumatology, Albany Medical College; L.R. Harrold, MD, MPH, Associate Professor, Department of Orthopedics, University of Massachusetts Medical School. ·J Rheumatol · Pubmed #26980578.

ABSTRACT: OBJECTIVE: To analyze prophylaxis using the CORRONA (COnsortium of Rheumatology Researchers Of North America) Gout Registry according to the American College of Rheumatology (ACR) guidelines, and to evaluate whether differences in disease characteristics influenced prophylaxis. METHODS: All patients with gout in the CORRONA Gout Registry between November 1, 2012, and November 26, 2013, were included. They were divided into 2 groups: "receiving prophylaxis" versus "not receiving prophylaxis" at the time of enrollment. Patients having a flare at time of visit were excluded. Descriptive statistics and multivariable logistic regression models were performed to evaluate the factors associated with prophylaxis. RESULTS: There were 1049 patients with gout available for analysis. There were 441 patients (42%) receiving prophylaxis and 608 (58%) not receiving prophylaxis. The most common drugs used for prophylaxis were colchicine (78%) and nonsteroidal antiinflammatory drugs (32%). Prophylaxis drug combination was used by 45 patients (10.2%). Patients in the "receiving prophylaxis" group were more likely to have a gout duration of ≤ 1 year (n = 68, p < 0.001), ≥ 1 flare in the year previous to enrollment (p < 0.001), ≥ 1 healthcare uses in the last year [Emergency Department (p = 0.029); outpatient visit to primary care, rheumatologist, or urgent care clinic (p < 0.001)], have tophi (p < 0.001), report pain > 3 (p = 0.001), and have disease activity > 10 (p < 0.001) compared with patients in the "not receiving prophylaxis" group. CONCLUSION: Forty-two percent of patients with gout in the CORRONA Gout Registry were receiving prophylaxis. Prophylaxis was significantly more common in patients with a higher disease burden and activity, which is in agreement with the ACR guidelines. Our study highlights disease characteristics influencing prophylaxis and furthers our knowledge on current use of flare prophylaxis.

22 Article Development of Preliminary Remission Criteria for Gout Using Delphi and 1000Minds Consensus Exercises. 2016

de Lautour, Hugh / Taylor, William J / Adebajo, Ade / Alten, Rieke / Burgos-Vargas, Ruben / Chapman, Peter / Cimmino, Marco A / da Rocha Castelar Pinheiro, Geraldo / Day, Ric / Harrold, Leslie R / Helliwell, Philip / Janssen, Matthijs / Kerr, Gail / Kavanaugh, Arthur / Khanna, Dinesh / Khanna, Puja P / Lin, Chingtsai / Louthrenoo, Worawit / McCarthy, Geraldine / Vazquez-Mellado, Janitzia / Mikuls, Ted R / Neogi, Tuhina / Ogdie, Alexis / Perez-Ruiz, Fernando / Schlesinger, Naomi / Ralph Schumacher, H / Scirè, Carlo A / Singh, Jasvinder A / Sivera, Francisca / Slot, Ole / Stamp, Lisa K / Tausche, Anne-Kathrin / Terkeltaub, Robert / Uhlig, Till / van de Laar, Mart / White, Douglas / Yamanaka, Hisashi / Zeng, Xuejun / Dalbeth, Nicola. ·Auckland District Health Board, Auckland, New Zealand. · University of Otago, Wellington, New Zealand. · University of Sheffield, Sheffield, UK. · Schlosspark-Klinik, Charité, University Medicine Berlin, Berlin, Germany. · Hospital General de México, Mexico City, Mexico. · Christchurch Hospital, Christchurch, New Zealand. · Università di Genova, Genova, Italy. · Pedro Ernesto University Hospital, Rio de Janeiro, Brazil. · University of New South Wales and St Vincent's Hospital, Sydney, Australia. · University of Massachusetts Medical School, Worcester, and Corrona, LLC, Southborough. · Leeds Institute of Rheumatic and Musculoskeletal Medicine, Leeds, UK. · Rijnstate Hospital, Arnhem, The Netherlands. · Veterans Affairs Medical Center, Georgetown and Howard University Hospitals, Washington, DC. · University of California School of Medicine, San Diego. · University of Michigan, Ann Arbor. · University of Michigan and Ann Arbor VA Medical Center, Ann Arbor. · Taichung Veteran's General Hospital, Taichung, Taiwan. · Faculty of Medicine, Chiang Mai University, Chiang Mai, Thailand. · Mater Misericordiae University Hospital and University College, Dublin, Ireland. · Nebraska-Western Iowa Health Care System and University of Nebraska Medical Center, Omaha. · Boston University School of Medicine, Boston, Massachusetts. · University of Pennsylvania, Philadelphia. · Hospital Universitario Cruces, OSI-EEC, and Biocruces Health Research Institute, Biscay, Spain. · Rutgers University Robert Wood Johnson Medical School, New Brunswick, New Jersey. · IRCCS Policlinico San Matteo Foundation, University of Pavia, Pavia, Italy. · University of Alabama at Birmingham and the Birmingham VA Medical Center, Birmingham. · Hospital General Universitario Elda, Elda, Spain. · Copenhagen University Hospital Glostrup, Glostrup, Denmark. · University of Otago, Christchurch, New Zealand. · University Hospital Carl Gustav Carus, Dresden, Germany. · University of California San Diego VA Medical Center, La Jolla. · National Advisory Unit on Rehabilitation in Rheumatology, Diakonhjemmet Hospital, Oslo, Norway. · Universiteit Twente, Erschede, The Netherlands. · Waikato DHB and Waikato Clinical School, University of Auckland, Hamilton, New Zealand. · Tokyo Women's Medical University, Tokyo, Japan. · Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, and Peking Union Medical College, Beijing, China. · University of Auckland and Auckland District Health Board, Auckland, New Zealand. ·Arthritis Care Res (Hoboken) · Pubmed #26414176.

ABSTRACT: OBJECTIVE: To establish consensus for potential remission criteria to use in clinical trials of gout. METHODS: Experts (n = 88) in gout from multiple countries were invited to participate in a web-based questionnaire study. Three rounds of Delphi consensus exercises were conducted using SurveyMonkey, followed by a discrete-choice experiment using 1000Minds software. The exercises focused on identifying domains, definitions for each domain, and the timeframe over which remission should be defined. RESULTS: There were 49 respondents (56% response) to the initial survey, with subsequent response rates ranging from 57% to 90%. Consensus was reached for the inclusion of serum urate (98% agreement), flares (96%), tophi (92%), pain (83%), and patient global assessment of disease activity (93%) as measurement domains in remission criteria. Consensus was also reached for domain definitions, including serum urate (<0.36 mm), pain (<2 on a 10-point scale), and patient global assessment (<2 on a 10-point scale), all of which should be measured at least twice over a set time interval. Consensus was not achieved in the Delphi exercise for the timeframe for remission, with equal responses for 6 months (51%) and 1 year (49%). In the discrete-choice experiment, there was a preference towards 12 months as a timeframe for remission. CONCLUSION: These consensus exercises have identified domains and provisional definitions for gout remission criteria. Based on the results of these exercises, preliminary remission criteria are proposed with domains of serum urate, acute flares, tophus, pain, and patient global assessment. These preliminary criteria now require testing in clinical data sets.

23 Article Did Michelangelo Have Gout? 2015

Pinals, Robert S / Schlesinger, Naomi. ·From the Division of Rheumatology, Department of Medicine, Rutgers Robert Wood Johnson Medical School, New Brunswick, NJ. ·J Clin Rheumatol · Pubmed #26398464.

ABSTRACT: Michelangelo, the great Renaissance artist, is often included on lists of celebrated gout patients. His letters describe a single acute attack of foot pain at the age of 80, but a case for early onset has been presented, based on a fresco by a contemporary artist, Raphael. A figure resembling Michelangelo at the age of 36 appears to have nodules resembling tophi over his knees.In this report, we review Michelangelo's medical history, discuss the proposal that he had tophaceous gout, and address the significance of "knobby" knees in his works and those of other artists.

24 Article Adherence to the 2012 American College of Rheumatology (ACR) Guidelines for Management of Gout: A Survey of Brazilian Rheumatologists. 2015

Vargas-Santos, Ana Beatriz / Castelar-Pinheiro, Geraldo da Rocha / Coutinho, Evandro Silva Freire / Schumacher, H Ralph / Singh, Jasvinder A / Schlesinger, Naomi. ·Division of Rheumatology, Internal Medicine Department, Universidade do Estado do Rio de Janeiro, Rio de Janeiro, Rio de Janeiro, Brazil. · Epidemiology Department, Escola Nacional de Saúde Pública Sergio Arouca, Fundação Oswaldo Cruz, Rio de Janeiro, Rio de Janeiro, Brazil. · Division of Rheumatology, University of Pennsylvania School of Medicine and Veterans Affairs Medical Center, Philadelphia, Pennsylvania, United States of America. · Medicine Service, Birmingham Veterans Affairs Medical Center, Birmingham, Alabama, United States of America; Department of Medicine at the School of Medicine, and the Division of Epidemiology at School of Public Health, University of Alabama, Birmingham, Alabama, United States of America; Department of Orthopedic Surgery, Mayo Clinic College of Medicine, Rochester, Minnesota, United States of America. · Division of Rheumatology, Department of Medicine, Rutgers-Robert Wood Johnson Medical School, New Brunswick, New Jersey, United States of America. ·PLoS One · Pubmed #26274585.

ABSTRACT: OBJECTIVE: To describe the current pharmacological approach to gout treatment reported by rheumatologists in Brazil. METHODS: We performed a cross-sectional survey study using an online questionnaire e-mailed to 395 rheumatologists, randomly selected, from among the members of the Brazilian Society of Rheumatology. RESULTS: Three hundred and nine rheumatologists (78.2%) responded to the survey. For acute gout attacks, combination therapy (NSAIDs or steroid + colchicine) was often used, even in monoarticular involvement, and colchicine was commonly started as monotherapy after 36 hours or more from onset of attack. During an acute attack, urate-lowering therapy (ULT) was withdrawn by approximately a third of rheumatologists. Anti-inflammatory prophylaxis (98% colchicine) was initiated when ULT was started in most cases (92.4%), but its duration was varied. Most (70%) respondents considered the target serum uric acid level to be less than 6 mg/dl. Approximately 50% of rheumatologists reported starting allopurinol at doses of 100 mg daily or less and 42% reported the initial dose to be 300 mg daily in patients with normal renal function. ULT was maintained indefinitely in 76% of gout patients with tophi whereas in gout patients without tophi its use was kept indefinitely in 39.6%. CONCLUSION: This is the first study evaluating gout treatment in a representative, random sample of Brazilian rheumatologists describing common treatment practices among these specialists. We identified several gaps in reported gout management, mainly concerning the use of colchicine and ULT and the duration of anti-inflammatory prophylaxis and ULT. Since rheumatologists are considered as opinion leaders in this disease, a program for improving quality of care for gout patients should focus on increasing their knowledge in this common disease.

25 Article Diagnosis and Treatment of Acute Gout at a University Hospital Emergency Department. 2015

Schlesinger, Naomi / Radvanski, Diane C / Young, Tina C / McCoy, Jonathan V / Eisenstein, Robert / Moore, Dirk F. ·Division of Rheumatology, Department of Medicine, Rutgers Robert Wood Johnson Medical School, New Brunswick, NJ, USA. · Department of Biostatistics, Rutgers School of Public Health Piscataway, NJ, USA. · Department of Emergency Medicine, Rutgers Robert Wood Johnson Medical School, New Brunswick, NJ, USA. ·Open Rheumatol J · Pubmed #26106456.

ABSTRACT: BACKGROUND: Acute gout attacks account for a substantial number of visits to the emergency department (ED). Our aim was to evaluate acute gout diagnosis and treatment at a University Hospital ED. METHODS: Our study was a retrospective chart review of consecutive patients with a diagnosis of acute gout seen in the ED 1/01/2004 - 12/31/2010. We documented: demographics, clinical characteristics, medications given, diagnostic tests, consultations and whether patients were hospitalized. Descriptive and summary statistics were performed on all variables. RESULTS: We found 541 unique ED visit records of patients whose discharge diagnosis was acute gout over a 7 year period. 0.13% of ED visits were due to acute gout. The mean patient age was 54; 79% were men. For 118 (22%) this was their first attack. Attack duration was ≤ 3 days in 75%. Lower extremity joints were most commonly affected. Arthrocentesis was performed in 42 (8%) of acute gout ED visits. During 355 (66%) of ED visits, medications were given in the ED and/or prescribed. An anti-inflammatory drug was given during the ED visit during 239 (44%) visits. Medications given during the ED visit included: NSAIDs: 198 (56%): opiates 190 (54%); colchicine 32 (9%) and prednisone 32 (9%). During 154 (28%) visits an anti-inflammatory drug was prescribed. Thirty two (6%) were given no medications during the ED visit nor did they receive a prescription. Acute gout rarely (5%) led to hospitalizations. CONCLUSION: The diagnosis of acute gout in the ED is commonly clinical and not crystal proven. Anti-inflammatory drugs are the mainstay of treatment in acute gout; yet, during more than 50% of ED visits, anti-inflammatory drugs were not given during the visit. Thus, improvement in the diagnosis and treatment of acute gout in the ED may be required.

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