Prevalence And Treatment Of Gout Among Patients With Chronic Kidney Disease In The Irish Health System

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• Health Alert:
• How Can I Manage My Gout And Improve My Quality Of Life?
• More Health News + Info

Merck & Co., Inc., Kenilworth, NJ, USA is a global healthcare leader working to help the world be well. From developing new therapies that treat and prevent disease to helping people in need, we are committed to improving health and well-being around the world. The Merck Manual was first published in 1899 as a service to the community. The legacy of this great resource continues as the Merck Manual in the US and Canada and the MSD Manual outside of North America.Learn more about our commitment to Global Medical Knowledge. Suspect gout in patients with sudden, unexplained acute monoarticular or oligoarticular arthritis, particularly if the great toe or midfoot is affected or there is a prior history of sudden, unexplained acute arthritis with spontaneous remission. (about 0.5 mg/kg once/day), IM or IV corticosteroids, or single-dose adrenocorticotropic hormone 80 U IM is also very effective, particularly if multiple joints are involved.

Gout attacks can be managed with a medical treatment plan combined with making lifestyle choices to lower uric acid levels. Gouty arthritis attacks can be prevented by avoiding foods and alcohol that raise uric acid levels. Gout treatment plans provide ways to lower uric acid levels and promote joint health. Gout attacks have multiple risk factors that cause uric acid levels to rise.

Health Alert:

During acute exacerbations the physical therapist should focus on reinforcement of management program and splinting, orthotics, or other assistive devices to protect the affected joint. When refering to evidence in academic writing, you should always try to reference the primary source. That is usually the journal article where the information was first stated.

How Can I Manage My Gout And Improve My Quality Of Life?

Newer treatment options are being extensively studied especially interleukin-1 (IL-1) inhibitors but their approval is still pending. The quest for an optimally designed drug with desirable efficacy and acceptable safety profile is still on. 16-23 suggests, there continues to be a strong interest in the development of new medications for the treatment of gout. The pending medication approvals include both oral medications with existing mechanisms of action, and new mechanisms of action and an injectable medication.

The explanatory variables included age modelled as 5-year intervals, sex, comorbid medical conditions, laboratory values recorded prior to clinic visit, and prescribed medications. A final multivariate model was constructed to identify the relative contributions of demographic, clinical and treatment factors with the presence of gout. Model performance was assessed using the c-statistic and the adequacy of the logistic models was tested using the Hosmer and Lemeshow goodness-of-fit test. Associations were expressed as odds ratios and 95% confidence intervals and all analyses were performed using R statistical software .

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Uricases also generate 1 mole of the oxidant hydrogen peroxide for each mole of uric acid degraded . Uricase expression was lost in humans and higher primates during the course of evolution . Illustrating the huge role uricase plays in uric acid homeostasis in mammals, normal serum urate in rodents is approximately 1 mg/dL, whereas it is approximately 10 mg/dL in uricase knockout mice.

Because allopurinol, febuxostat, and probenecid change serum and tissue uric acid levels, they may precipitate acute attacks of gout. To reduce this undesired effect, colchicine or low-dose NSAID treatment is provided for at least 6 months. In patients who cannot take colchicine or NSAIDs, low doses of prednisone can be considered. When used prophylactically, colchicine can reduce such flares by 85%. Patients with gout may be able to abort an attack by taking a single colchicine tablet at the first twinge of an attack.

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In addition, the advent of both new urate-lowering and anti-inflammatory drugs, also reviewed here, promises for improved management of refractory gout, including in subjects with co-morbidities such as chronic kidney disease. Gout is a disease in which the metabolic condition hyperuricemia leads to the formation of monosodium urate crystals, which provoke acute and chronic inflammatory responses through activation of the innate immune system. These, and other advances, have shaped our current strategies for managing gout. Here, we review the most current, evidence-based gout management approaches, including treating acute flares, addressing gout through the long-term regulation of serum urate, and prophylaxis against gouty flares during urate lowering. Dietary modification is typically the initial treatment for patients with gout. For patients who do not reach target serum uric acid goals with diet changes alone, pharmacologic therapy is required to reduce the production or increase the excretion of serum uric acid.

In addition to the strategies described above, a doctor will usually recommend taking a prescription medication, such as allopurinol, that is proven effective in preventing gout attacks. You may be at high risk for another attack if you haven’t made any changes to your diet, lifestyle, or medication regimen. Taking precautions against future attacks can spare you from gout pain and limit long-term damage to your joints. While gout is no longer thought to be a disease of the wealthy, it is more common in men and people with weight-related health problems including high blood pressure and type 2 diabetes.

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It still is not fully clear whether CHF, anemia, hyperlipidemia, CKD, and other comorbidities influence uricase. As an “induction therapy,” uricase ultimately could be replaced by less intensive maintenance oral SUA-lowering therapy with other agents, once resolution of clinically detectable tophi and gross synovitis is achieved. Pegloticase is awaiting FDA approval, and although there may be long-term safety issues, its potential for rapidly eliminating the tophus burden and reducing morbidity is indisputable. Most rheumatologists prescribe about 40 mg/d of prednisone with a slow taper to avoid rebound attacks after corticosteroid withdrawal.

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Gout is caused by a condition known as hyperuricemia, where there is too much uric acid in the body. The body makes uric acid when it breaks down purines, which are found in your body and the foods you eat.

Febuxostat is a novel non-purine selective inhibitor of xanthine oxidase for the management of hyperuricemia in patients with gout. The ability of febuxostat to decrease serum uric acid production through selective inhibition of enzyme xanthine oxidase has been established in short-term Phase II and III clinical trials and long-term open-label studies. Clinical studies have revealed that febuxostat lowers serum uric acid levels more potently than allopurinol while having minimal effects on other enzymes associated with purine and pyrimide metabolism. The most frequent adverse events reported in clinical trials with febuxostat were liver function abnormalities, nausea, arthralgias, and rash. More cardiovascular thromboembolic events occurred in randomized trials in patients treated with febuxostat. Although a causal relationship has not been established, patients should be monitored for signs and symptoms of myocardial infarction and stroke.

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The safety of this particular 'biologic' approach, especially beyond a term of 6 to 12 months, will require further investigation. Limited reports and pilot studies have evaluated off-label use of the non-PEGylated recombinant fungal enzyme rasburicase36,37-which is FDA-approved for single-course therapy in tumor lysis syndrome-in severe, chronic gout. However, rasburicase is not practical for long-term use because it is highly antigenic and has a short half-life.36 Also, at about $8000 per dose, the cost of rasburicase is prohibitive. SUA-lowering agents frequently used to manage chronic gout include purine and nonpurine inhibitors of xanthine oxidase and uricosuric agents . Also, new medications on the horizon may be used instead of or in addition to those already approved for use in chronic gout.

But both gout and tophi can disappear if they are properly treated. Many doctors and patients are, however, unsure of the best treatment. It has become the most common cause of inflammatory arthritis in men, and its prevalence in postmenopausal women continues to rise. This increase is due to changes in diet and lifestyle, increased use of certain diuretics and increasing obesity.