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Gout: HELP
Articles by Dr. Naomi Schlesinger
Based on 41 articles published since 2008
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Between 2008 and 2019, N. Schlesinger wrote the following 41 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 Review Imaging of gout: findings and utility. 2009

Perez-Ruiz, Fernando / Dalbeth, Nicola / Urresola, Aranzazu / de Miguel, Eugenio / Schlesinger, Naomi. ·Rheumatology Division, Hospital de Cruces, Baracaldo, Vizcaya, Spain. fernando.perezruiz@osakidetza.net ·Arthritis Res Ther · Pubmed #19591633.

ABSTRACT: Imaging is a helpful tool for clinicians to evaluate diseases that induce chronic joint inflammation. Chronic gout is associated with changes in joint structures that may be evaluated with diverse imaging techniques. Plain radiographs show typical changes only in advanced chronic gout. Computed tomography may best evaluate bone changes, whereas magnetic resonance imaging is suitable to evaluate soft tissues, synovial membrane thickness, and inflammatory changes. Ultrasonography is a tool that may be used in the clinical setting, allowing evaluation of cartilage, soft tissues, urate crystal deposition, and synovial membrane inflammation. Also ultrasound-guided puncture may be useful for obtaining samples for crystal observation. Any of these techniques deserve some consideration for feasibility and implementation both in clinical practice and as outcome measures for clinical trials. In clinical practice they may be considered mainly for evaluating the presence and extent of crystal deposition, and structural changes that may impair function or functional outcomes, and also to monitor the response to urate-lowering therapy.

17 Review Gout--what are the treatment options? 2009

Schlesinger, Naomi / Dalbeth, Nicola / Perez-Ruiz, Fernando. ·Division of Rheumatology Department of Medicine, UMDNJ-Robert Wood Johnson Medical School, New Brunswick, NJ 08903-0019, USA. schlesna@umdnj.edu ·Expert Opin Pharmacother · Pubmed #19463070.

ABSTRACT: There has been an increase in the incidence and prevalence of gout in the past several decades. A distinction needs to be made between the treatment of gout as an acute inflammatory disease and the lowering of the serum urate (SU) levels into a normal range. Treating acute gout attacks alone is not sufficient to prevent the disease from progressing. When treating gout one needs to treat acute attacks, and lower excess stores of uric acid to achieve dissolution of monosodium urate crystals through a long-term reduction of SU concentrations far beyond the threshold for saturation of urate and provide prophylaxis to prevent acute flares. The options available for the treatment of acute gout are NSAIDs, colchicine, corticosteroids, adrenocorticotropic hormone (ACTH) and intra-articular corticosteroids. The most important determinant of therapeutic success is not which anti-inflammatory agent is chosen, but rather how soon therapy is initiated and that the dose be appropriate. Prophylaxis should be considered an adjunct, rather than an alternative, to long-term urate-lowering therapy. For purposes of maintaining patient adherence to urate-lowering therapy, there is interest in improving prophylaxis of such treatment-induced attacks. The optimal agent, dose and duration for gout prophylaxis are unknown and require further investigation. The importance of long-term management of gout is the reduction and maintenance of SU in a goal range, usually defined as less than 6.0 mg/dL. Allopurinol and benzbromarone remain the cornerstone drugs for reducing SU levels lower than the saturation threshold to dissolve urate deposits effectively. Febuxostat and pegloticase help to optimize control of SU levels, especially in those patients with the most severe gout. Other agents, such as fenofibrate and losartan may be helpful as adjuvant drugs. Treatment for gout has advanced little in the last 40 years, until recently. The recent development of new therapeutic options promises to provide much needed alternatives for the many patients with gout who are intolerant of or refractory to available therapies. It is important to note that inappropriate use of medications as opposed to an apparent refractoriness to available therapies is not uncommon.

18 Review Management of gout. 2008

Perez-Ruiz, F / Schlesinger, N. ·Division of Rheumatology, Hospital de Cruces, País Vasco, Baracaldo, Spain. fernando.perezruiz@osakidetza.net ·Scand J Rheumatol · Pubmed #18415763.

ABSTRACT: -- No abstract --

19 Review Overview of the management of acute gout and the role of adrenocorticotropic hormone. 2008

Schlesinger, Naomi. ·Department of Medicine, UMDNJ-Robert Wood Johnson Medical School, New Brunswick, New Jersey 08903-0019, USA. schlesna@umdnj.edu ·Drugs · Pubmed #18318560.

ABSTRACT: It is important to distinguish between therapy used to reduce acute inflammation in gout and therapy used to manage hyperuricaemia in patients with chronic gouty arthritis. This article discusses treatments for acute gout, emphasizing the use of corticotrophin (adrenocorticotropic hormone; ACTH) and the evidence on which we base our treatment of acute gout. There are no formal guidelines for the treatment of acute gout and only a few randomized controlled trials have been conducted to evaluate the efficacy of the various treatments for acute gout. The options available for the treatment of acute attacks of gout are NSAIDs, colchicine, corticosteroids, corticotropin and intra-articular corticosteroids. Most rheumatologists practicing in the US use combination therapy to treat acute gout, a practice that merits study. In a patient without complications, NSAIDs are the preferred therapy. The most important determinant of therapeutic success is not which NSAID is chosen, but rather how soon NSAID therapy is initiated. Exciting new research shows that corticotropin acts peripherally by activation of the melanocortin type 3 receptor, and this could be responsible, at least in part, for its efficacy in acute gout. Hopefully, this will lead to renewed interest in corticotropin as a treatment for acute gout.

20 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.

21 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.

22 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.

23 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.

24 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.

25 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.

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