Gout

2013 ◽  
Author(s):  
Nicola Dalbeth
Keyword(s):  
Disease Patient ◽  
Joint Damage ◽  
Serum Urate ◽  
Acute Attack ◽  
Dietary Factors ◽  
Acute Gout ◽  
Chronic Synovitis ◽  
Inflammatory Drugs ◽  
Renal Tubular

Gout is a common and treatable disorder of purine metabolism. Gout typically presents as recurrent self-limiting episodes of severe inflammatory arthritis affecting the foot. In the presence of persistent hyperuricaemia, tophi, chronic synovitis, and joint damage may develop. Diagnosis of gout is confirmed by identification of monosodium urate (MSU) crystals using polarizing light microscopy. Hyperuricaemia is the central biochemical cause of gout. Genetic variants in certain renal tubular urate transporters including SLC2A9 and ABCG2, and dietary factors including intake of high-purine meats and seafood, beer, and fructose, contribute to development of hyperuricaemia and gout. Gout treatment includes: (1) management of the acute attack using non-steroidal anti-inflammatory drugs (NSAIDs), corticosteroids, or low-dose colchicine; (2) prophylaxis against gout attacks when commencing urate-lowering therapy (ULT), with NSAIDs or colchicine; and (3) long-term ULT to achieve a target serum urate of less than 0.36 mmol/litre. Interleukin (IL)-1β‎ is a central mediator of acute gouty inflammation and anti-IL-1β‎ therapies show promise for treatment of acute attacks and prophylaxis. The mainstay of ULT remains allopurinol. However, old ULT agents such as probenecid and benzbromarone and newer agents such as febuxostat and pegloticase are also effective, and should be considered in patients in whom allopurinol is ineffective or poorly tolerated. Management of gout should be considered in the context of medical conditions that frequently coexist with gout, including type 2 diabetes, hypertension, dyslipidaemia, and chronic kidney disease. Patient education is essential to ensure that acute gout attacks are promptly and safely managed, and long-term ULT is maintained.

Gout

2016 ◽  
Author(s):  
Nicola Dalbeth
Keyword(s):  
Disease Patient ◽  
Joint Damage ◽  
Serum Urate ◽  
Acute Attack ◽  
Dietary Factors ◽  
Acute Gout ◽  
Chronic Synovitis ◽  
Inflammatory Drugs ◽  
Renal Tubular

Gout is a common and treatable disorder of purine metabolism. Gout typically presents as recurrent self-limiting episodes of severe inflammatory arthritis affecting the foot. In the presence of persistent hyperuricaemia, tophi, chronic synovitis, and joint damage may develop. Diagnosis of gout is confirmed by identification of monosodium urate (MSU) crystals using polarizing light microscopy. Hyperuricaemia is the central biochemical cause of gout. Genetic variants in certain renal tubular urate transporters including SLC2A9 and ABCG2, and dietary factors including intake of high-purine meats and seafood, beer, and fructose, contribute to development of hyperuricaemia and gout. Gout treatment includes: (1) management of the acute attack using non-steroidal anti-inflammatory drugs (NSAIDs), corticosteroids, or low-dose colchicine; (2) prophylaxis against gout attacks when commencing urate-lowering therapy (ULT), with NSAIDs or colchicine; and (3) long-term ULT to achieve a target serum urate of less than 0.36 mmol/litre. Interleukin (IL)-1β‎ is a central mediator of acute gouty inflammation and anti-IL-1β‎ therapies show promise for treatment of acute attacks and prophylaxis. The mainstay of ULT remains allopurinol. However, old ULT agents such as probenecid and benzbromarone and newer agents such as febuxostat and pegloticase are also effective, and should be considered in patients in whom allopurinol is ineffective or poorly tolerated. Management of gout should be considered in the context of medical conditions that frequently coexist with gout, including type 2 diabetes, hypertension, dyslipidaemia, and chronic kidney disease. Patient education is essential to ensure that acute gout attacks are promptly and safely managed, and long-term ULT is maintained.

Gout

2013 ◽  
pp. 1199-1210
Author(s):  
Nicola Dalbeth
Keyword(s):  
Disease Patient ◽  
Joint Damage ◽  
Serum Urate ◽  
Acute Attack ◽  
Dietary Factors ◽  
Acute Gout ◽  
Chronic Synovitis ◽  
Renal Tubular

Gout is a common and treatable disorder of purine metabolism. Gout typically presents as recurrent self-limiting episodes of severe inflammatory arthritis affecting the foot. In the presence of persistent hyperuricaemia, tophi, chronic synovitis, and joint damage may develop. Diagnosis of gout is confirmed by identification of monosodium urate (MSU) crystals using polarizing light microscopy. Hyperuricaemia is the central biochemical cause of gout. Genetic variants in certain renal tubular urate transporters including SLC2A9 and ABCG2, and dietary factors including intake of high-purine meats and seafood, beer, and fructose, contribute to development of hyperuricaemia and gout. Gout treatment includes: (1) management of the acute attack using non-steroidal anti-inflammatory drugs (NSAIDs), corticosteroids, or low-dose colchicine; (2) prophylaxis against gout attacks when commencing urate-lowering therapy (ULT), with NSAIDs or colchicine; and (3) long-term ULT to achieve a target serum urate of less than 0.36 mmol/litre. Interleukin (IL)-1β‎‎ is a central mediator of acute gouty inflammation and anti-IL-1β‎‎ therapies show promise for treatment of acute attacks and prophylaxis. The mainstay of ULT remains allopurinol. However, old ULT agents such as probenecid and benzbromarone and newer agents such as febuxostat and pegloticase are also effective, and should be considered in patients in whom allopurinol is ineffective or poorly tolerated. Management of gout should be considered in the context of medical conditions that frequently coexist with gout, including type 2 diabetes, hypertension, dyslipidaemia, and chronic kidney disease. Patient education is essential to ensure that acute gout attacks are promptly and safely managed, and long-term ULT is maintained.

scholarly journals Pharmacotherapy for gout

2021 ◽  
Vol 64 (11) ◽  
pp. 772-777
Author(s):  
Chang-Nam Son
Keyword(s):  
Uric Acid ◽  
Serum Uric Acid ◽  
Serum Urate ◽  
Treat To Target ◽  
Common Disease ◽  
Uric Acid Concentration ◽  
Acute Gout ◽  
Serum Uric Acid Concentration ◽  
Inflammatory Drugs

Background: Gout is a common disease that is mainly caused by hyperuricemia. Although it is relatively easy to treat, adherence to drug treatment and the rate at which treatment targets are met is low.Current Concepts: For the treatment of acute gout attack, colchicine, nonsteroidal anti-inflammatory drugs, and glucocorticoids can be used alone or in combination depending on the severity of symptoms. To prevent gout attacks, patients are started on colchicine prior to or concurrent with treatment with uric acid–lowering drugs. The treatment is maintained until serum uric acid levels have returned to normal, and the patient has had no acute attacks for three to six months. Ultimately, the symptoms of gout are controlled in the long term by treating the patient’s hyperuricemia. For this purpose, allopurinol, febuxostat, and benzbromarone are used, and the side effects and contraindications for each drug should be checked. The goal for the treatment of chronic gout is to maintain a serum uric acid concentration below 6.0 mg/dL.Discussion and Conclusion: Patients visit the emergency departments of hospitals for sudden gout attacks. However, gout is a chronic disease that requires the lifelong use of uric acid–lowering agents. Therefore, it is necessary to educate patients on a serum urate-based treat-to-target approach.

Serum Urate During Acute Gout

2009 ◽  
Vol 36 (6) ◽  
pp. 1287-1289 ◽  
Author(s):  
NAOMI SCHLESINGER ◽  
JOSEPHINE M. NORQUIST ◽  
DOUGLAS J. WATSON
Keyword(s):  
Uric Acid ◽  
Serum Urate ◽  
Acute Attack ◽  
Normal Serum ◽  
The Body ◽  
Acute Gout ◽  
Acid Pool ◽  
Randomized Controlled Clinical Trials ◽  
Acute Gout Treatment ◽  
The Relationship

Objective.To study the frequency of normal serum urate (SU) levels during acute gout in the largest studies of acute gout treatment to date.Methods.Data collected from 2 randomized controlled clinical trials assessing the efficacy of etoricoxib or indomethacin for 7 days in acute gout were used to assess SU levels during acute gouty attacks. Efficacy was similar with both agents, so both groups were combined for analysis.Results.A total of 339 patients were enrolled in the 2 studies; 94% were male; mean age was 50.5 years. At baseline, 14% of patients had a “true” normal SU (≤ 6 mg/dl) and 32% had SU ≤ 8 mg/dl during acute gout. Baseline mean SU was 7.1 versus 8.5 mg/dl (p < 0.001) in those taking allopurinol versus nonusers. Patients taking chronic allopurinol were more likely to have lower SU at baseline compared to those not taking chronic allopurinol (p < 0.001) during the acute attack.Conclusion.A normal SU level at presentation does not exclude an acute gouty attack. In the largest studies of acute gout to date, attacks still occurred despite SU levels being below 6.8 mg/dl, the saturation level for urate. This may be attributed to persistence of tophi and an increased body uric acid pool. Additional studies are needed to determine the correlation between SU and the body uric acid pool as well as the relationship to timing of changes during acute gout.

scholarly journals High-Protein Diet Induces Hyperuricemia in a New Animal Model for Studying Human Gout

2020 ◽  
Vol 21 (6) ◽  
pp. 2147 ◽  
Author(s):  
Fan Hong ◽  
Aijuan Zheng ◽  
Pengfei Xu ◽  
Jialin Wang ◽  
Tingting Xue ◽  
...  
Keyword(s):  
Animal Model ◽  
Metabolic Diseases ◽  
High Protein Diet ◽  
Serum Urate ◽  
Dietary Factors ◽  
High Protein ◽  
Protein Diet ◽  
Positive Effects ◽  
Biological Studies

Hyperuricemia is a central risk factor for gout and increases the risk for other chronic diseases, including cardiometabolic disease, kidney disease, and hypertension. Overproduction of urate is one of the main reasons for hyperuricemia, and dietary factors including seafoods, meats, and drinking are contributed to the development of it. However, the lack of a suitable animal model for urate metabolism is one of the main reasons for the delay and limitations of hyperuricemia research. Combining evolutionary biological studies and clinical studies, we conclude that chicken is a preferred animal model for hyperuricemia. Thus, we provided chickens a high-protein diet (HPD) to evaluate the changes in the serum urate levels in chickens. In our study, the HPD increased the serum urate level and maintained it at a long-term high level in chickens. Long-term high serum urate levels induced an abnormal chicken claw morphology and the precipitation of monosodium urate (MSU) in joint synovial fluid. In addition, a long-term HPD also decreased the glomerular filtration rate and induced mild renal injury. Most importantly, allopurinol and probenecid displayed the positive effects in decreasing serum urate and then attenuated hyperuricemia in chicken model. These findings provide a novel model for hyperuricemia and a new opportunity to further investigate the effects of long-term hyperuricemia on other metabolic diseases.

scholarly journals Facilitating equitable prevention and management of gout for Māori in Northland, New Zealand, through a collaborative primary care approach

2019 ◽  
Vol 11 (2) ◽  
pp. 117 ◽  
Author(s):  
Aniva Lawrence ◽  
Sharon Scott ◽  
Fabio Saparelli ◽  
Georgina Greville ◽  
Andrew Miller ◽  
...  
Keyword(s):  
Primary Care ◽  
New Zealand ◽  
Community Pharmacists ◽  
Community Support ◽  
Serum Urate ◽  
Acute Gout ◽  
Serum Urate Level ◽  
Diabetes Status ◽  
Urate Lowering Treatment

ABSTRACT INTRODUCTIONThe Gout Stop Programme was developed for primary care in Northland, New Zealand, to address inequitable health outcomes for Māori and Pacific people with gout. AIMThe aim of the programme was to make it easier for clinicians to prescribe urate-lowering treatment, facilitate patient adherence through education and support, and reduce barriers to gout prevention and long-term management. METHODSFrom 2015 to 2017, patients with acute gout who met inclusion criteria were prescribed treatment according to a ‘Gout Stop Pack’ option, based on renal function and diabetes status. Patients were monitored by community pharmacists. Gout educators and a Gout Kaiāwhina (community support worker) provided education and support to patients and whānau (families). Patient completion of the programme and outcomes, according to target serum urate level, were recorded. Patient experience was documented using a questionnaire and rating scale. RESULTSIn total, 160 clinicians prescribed therapy at 887 patient presentations; 71% were Māori and Pacific patients. The completion rate was 55% in this group and 84% for the non-Māori and non-Pacific group. In the Māori and Pacific group, 40% reached the target serum urate level (≤0.36 mmol L-1) in 91 days, and 26% required further titration. In the non-Māori/non-Pacific group, these rates were 51% and 19% respectively. Following programme completion, 68% of Māori and Pacific patients and 65% of non-Māori and non-Pacific patients continued to take allopurinol. The 21 patients interviewed rated the programme as excellent or very good. DISCUSSIONCulturally appropriate education and support for patients and the primary care team was essential. Collaboration between prescribers, community pharmacists and support workers reduced barriers to initiating prevention and long-term urate-lowering treatment and urate testing in this high-needs gout population.

Principles of gout management

2016 ◽  
Author(s):  
Nicola Dalbeth
Keyword(s):  
Disease Patient ◽  
Serum Urate ◽  
Physician Education ◽  
Effective Management ◽  
Long Term Outcomes ◽  
Sustained Reduction ◽  
Term Management ◽  
Adherence To Therapy

The main goal of therapy is to achieve ‘remission’—the absence of gout attacks and tophi. A sustained reduction in serum urate is critical to the long-term management of gout and will ultimately result in cessation of gout attacks and resolution of tophi. Target serum urate is <0.36 mmol/L for everyone, although a lower target of <0.30 mmol/L may be required for those with severe tophaceous disease. Patient and physician education about the causes and effective management of gout are required to improve adherence to therapy and thereby long-term outcomes.

scholarly journals POS1477-HPR GOUT PATIENTS IN REMISSION, AND THEIR PERSPECTIVES ON URATE LOWERING THERAPY TREATMENT STOP OR CONTINUATION STRATEGIES

2021 ◽  
Vol 80 (Suppl 1) ◽  
pp. 1023.2-1024
Author(s):  
I. R. Peeters ◽  
S. A. C. Wanten ◽  
L. M. Verhoef ◽  
A. Den Broeder ◽  
N. Van Herwaarden ◽  
...  
Keyword(s):  
General Practice ◽  
Side Effects ◽  
The Netherlands ◽  
Medication Use ◽  
Joint Damage ◽  
Treatment Strategies ◽  
Serum Urate ◽  
The Body ◽  
Treat To Target

Background:Urate lowering therapies (ULT) are used to reduce hyperuricemia in gout patients (1). When gout remission is reached, patients often ask if ULT should be continued lifelong (treat to target strategy, T2T), or if tapering or stopping (a treat to symptom approach, T2S) can be attempted. In fact, although current rheumatology guidelines (1,2) suggest continuation, conclusive evidence for this is absent. Since ULT therapy adherence also remains suboptimal, exploring gout patients’ beliefs on different long term ULT treatment strategies is of great value.Objectives:To identify cognitions and emotions on ULT treatment strategies (T2T continuation and T2S cessation) of gout patients in remission with current or previous ULT use.Methods:Purposive sampling (3) was used to recruit patients from a general practice and a rheumatology department (Nijmegen, the Netherlands), with a clinical diagnosis of gout, current or previous ULT use and remission according to adapted (without serum urate criterion) preliminary gout remission criteria(4). Semi-structured interviews were conducted by two interviewers and audio-records were fully transcribed. Inductive thematic analysis (5) was used to analyse and interpret our data using the ATLAS.ti. software.Results:From a total of 18 patients (16 male/2 female), 14 patients were treated by a rheumatologist (10 currently using ULT, 1 intermittent and 3 previously) and 4 were treated by a general practitioner (all currently using ULT). Patients were satisfied with a T2T strategy, due to the absence of flares, a feeling of certainty and the reassurance of serum urate monitoring. Reluctance towards medication was reported, the importance of indefinite ULT use was questioned and its chronic use was addressed as a drawback. Reducing medication use by a T2S strategy was assessed positively and this strategy was considered less burdensome. A wish for and the willingness to follow a T2S approach was expressed. Fear and concerns of flaring after ULT cessation were expressed and were deemed both acceptable and unacceptable. See Table 1 for a schematic overview of the results.Table 1.Overview of patients’ perspectives on ULT treatment strategiesMotivation for a T2T strategyDrawbacks of a T2T strategy1. Being free of flares2. Acceptance of and contentment with chronic ULT use3. Feels secure due to regular SU monitoring4. No desire for change1. Resistance to (any) medication use2. Side effects of ULT3. Possibly detrimental to healthcare costsMotivation for a T2S strategyDrawbacks of a T2S strategy1. Doubt if chronic ULT use is necessary a. Possible restorative capacity of the body b. Curious to effects of ULT cessation2. Being free of ULT side effects3. Long term damage ULT unknown4. Less burdensome for patient and body5. Wish for minimization of (any) medication use1. Fear and insecurities on a. Flaring and not being able to function b. Joint damage2. Feels uncontrolled3. Hassle with visits, blood tests and medication adjustments when a flare occurs.Conclusion:This study provides an overview of perspectives on ULT treatment strategies of gout patients in remission. These results must be considered in developing educational material for patients and in future research on gout management, particularly in designing randomised clinical trials on this subject.References:[1]Richette P et al. Ann Rheum Dis. 2017;76(1):29-42.[2]FitzGerald JD et al. Arthritis Care Res (Hoboken). 2020;72(6):744-60.[3]Pope C et al. Qual Saf Health Care. 2002;11(2):148-52.[4]de Lautour H et al. Arthritis Care Res (Hoboken). 2016;68(5):667-72.[5]Pope C et al. Bmj. 2000;320(7227):114-6.Acknowledgements:We would like to thank dr. Erik Bischoff for his cooperation and help in including primary care patients from his general practice UGC Heyendael, Nijmegen the Netherlands.Disclosure of Interests:None declared

Die Gicht und ihr Management in der Praxis

Praxis ◽  
2020 ◽  
Vol 109 (6) ◽  
pp. 439-445
Author(s):  
Thomas Langenegger ◽  
Andreas Krebs ◽  
Thomas Rosemann ◽  
Thomas Hügle ◽  
Johannes von Kempis
Keyword(s):  
Bildgebende Verfahren ◽  
Acute Attack ◽  
Acute Gout ◽  
Metabolic Complications ◽  
Xanthine Oxidase Inhibitors ◽  
First Choice ◽  
Prime Objective ◽  
Inflammatory Drugs ◽  
High Resolution Ultrasonography ◽  
Metabolische Komplikationen

Zusammenfassung. Bei Gicht steht im klinischen Alltag meist die akute Attacke im Vordergrund. Als diagnostischer Goldstandard gilt dabei der Kristallnachweis in der Gelenksflüssigkeit mittels Polarisationsmikroskopie. Auch bildgebende Verfahren wie der hochauflösende Ultraschall sind von Nutzen. Zur Behandlung der akuten Gichtattacke dienen nicht-steroidale Antirheumatika, Steroide und Colchizin (in der Schweiz nicht zugelassen, über Apotheken erhältlich). Ebenso wichtig wie Diagnose und Therapie der akuten Attacke ist aber die langfristige Behandlung der Hyperurikämie, um so weitere Gichtschübe sowie mögliche renale, kardiale oder metabolische Komplikationen zu verhindern. Daher sollte bei bestätigter Gichtdiagnose neben nicht-medikamentösen Massnahmen auch eine harnsäuresenkende Therapie, mit dem Zielwert von <360 µmol/l (<6 mg/dl), erfolgen. Mittel der ersten Wahl stellen dabei Xanthinoxidasehemmer dar. Das Erreichen des Therapieziels ist regelmässig zu überprüfen und die Therapie allenfalls anzupassen. Resolution of an acute attack is usually the prime objective in routine clinical management of gout. Crystal identification in synovial fluid by polarised light microscopy is considered the diagnostic gold standard. Imaging procedures such as high-resolution ultrasonography are also useful. Non-steroidal anti-inflammatory drugs, steroids and colchicine (not approved in Switzerland, available from pharmacies) are used to treat an acute gout attack. Just as important as the diagnosis and treatment of an acute attack is the long-term management of hyperuricaemia in order to prevent further gout attacks as well as possible renal, cardiac or metabolic complications. Therefore, patients with a confirmed diagnosis of gout should, apart from non-pharmacologic interventions, receive hypouricaemic therapy with a target uric acid level of <360 µmol/l (<6 mg/dl). Drugs of first choice are xanthine oxidase inhibitors. Achievement of the therapeutic objective should be periodically reviewed, adjusting therapy as necessary. Dans la pratique clinique, la crise aiguë figure le plus souvent au premier plan des cas de goutte. Le critère diagnostique de référence reste cependant la détection des cristaux dans le liquide synovial par microscopie à polarisation. Les techniques d’imagerie telles que l’échographie à haute résolution sont également utiles. Les anti-inflammatoires non stéroïdiens, les stéroïdes et la colchicine (non agréé en Suisse, mais disponible dans les pharmacies) sont utilisés pour traiter les crises de goutte aiguë. Le traitement au long cours de l’hyperuricémie est néanmoins tout aussi important que le diagnostic et le traitement des crises aiguës, ceci afin de prévenir d’autres crises de goutte et d’éventuelles complications rénales, cardiaques ou métaboliques. Par conséquent, si le diagnostic de goutte est confirmé, il convient d’instaurer, en plus des mesures non médicamenteuses, un traitement hypo-uricémiant avec la valeur cible de <360 µmol/l (<6 mg/dl), les médicaments de premier choix étant ici les inhibiteurs de la xanthine-oxydase. L’atteinte de l’objectif thérapeutique doit être régulièrement vérifiée et le traitement adapté si nécessaire.

scholarly journals Hyperuricaemia and gout

2020 ◽  
pp. 95-100
Author(s):  
A Kopke ◽  
OBW Greeff
Keyword(s):  
Uric Acid ◽  
Side Effects ◽  
Treatment Options ◽  
The Body ◽  
Acute Gout ◽  
Tophaceous Gout ◽  
Life Threatening ◽  
Inflammatory Drugs ◽  
Urate Crystals

Gout is a painful, inflammatory disease that affects more men than women. The incidence of gout has increased substantially over the past few decades, as evidenced by information from the Rochester project. Some of the risk factors for the development of gout include: increased ethanol intake, high dietary purine consumption, obesity and the use of certain drugs, such as diuretics. Another important risk factor for the development of gout is hyperuricaemia. Hyperuricaemia results from an imbalance between the rate of production and excretion of uric acid in the body. An excess of uric acid thus builds up in the body, supersaturating body fluids and leading to the formation of monosodium urate crystals. These crystals accumulate in tissue and around joints, leading to an acute gout attack. Gout can be divided into four phases, namely asymptomatic hyperuricaemia, acute gout attacks or recurrent gout, intercritical gout and chronic tophaceous gout. Various treatment options are available for gout, and the treatment for each gout patient is determined by the stage of the disease. Nonsteroidal anti-inflammatory drugs (NSAIDs), corticosteroids, corticotropin and colchicine are used for the treatment of acute gout attacks. Allopurinol and probenecid are used for long-term hypouricaemic therapy, while NSAIDs and colchicine are prescribed for the prophylaxis of future gout attacks. All of these treatments have side-effects, ranging from mild to life-threatening in nature. There is a need for novel gout therapies that have fewer side-effects but are still as effective.

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