How To Treat Acute Gout Attack – Gout accounts for approximately 7 million outpatient visits in the United States each year at a cost of nearly $1 billion.
These factors can contribute to a high level of serum uric acid, which is currently defined as a value of at least 6.8 mg per dL (405 μmol per L).
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To prevent recurrent gout, patients should reduce consumption of soft drinks with high-fructose corn syrup, fruit and vegetable juices, and high-fructose fruits (eg, applesauce, agave). Reducing consumption of meat and seafood and increasing consumption of dairy products can help reduce the incidence of gout symptoms. Eating low-fat or fat-free dairy products can help reduce the frequency of flare-ups.
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Genetic mutations may be associated with excessive production, or often excessive excretion, of uric acid due to defects in the renal transport system.
The prevalence of gout increases with age and reaches a maximum of 12% in people over 80 years old.
Because female sex hormones increase urinary uric acid excretion, premenopausal women have a significantly lower incidence of gout compared to men (2.0% vs. 5.9%).
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Consumption of alcoholic beverages (especially beer), meat (especially red meat, wild game, and organic meat), some shellfish (eg, shellfish, some large saltwater fish), fruit juices, and beverages sweetened with high fructose corn syrup increases the risk. drop out
Gout is due to the precipitation of monosodium urate crystals in a joint space. Crystal deposition then triggers immune activation by releasing various inflammatory cytokines and recruiting neutrophils.
Over time, the joint space can be irreversibly damaged, leading to chronic pain and disability with severely deformed joints. Tophi (ie, subcutaneous nodules composed of monosodium urate crystals in a matrix of lipids, proteins, and mucopolysaccharides) can also be present in the joint space.
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(Figure 1). The first metatarsophalangeal joint is the most commonly affected. Other common sites include the midtarsal joints, ankles, knees, fingers (Figure 2), wrists, and elbows. Urate crystals can be deposited throughout the body (eg, vertebrae, skin, soft tissue), simulating other disease states.
Gout is usually diagnosed clinically based on the rapid development of monoarticular arthritis characterized by swelling and redness usually involving the first metatarsophalangeal joint. The American College of Rheumatology criteria are the most widely used for the diagnosis of gout (Table 2).
An online risk calculator is also available (http://www.gp-training.net/rheum/gout_calc.htm); uses gender, uric acid level, and five findings from the history and physical examination to predict the likelihood of acute gout flares.
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Complementary fluid microscopy is used less often, especially in symmetrical cases. In these situations, the diagnosis is established by joint aspiration or tophi and the identification of needle-shaped monosodium urate crystals, preferably intracellular, by including clear negative on compensated polarized light microscopy. Ultrasound, magnetic resonance imaging, and computed tomography are usually not necessary for diagnosis.
Differential diagnosis of acute monoarticular joint inflammation includes pseudogout, infection, and trauma. Pseudogout, or calcium pyrophosphate deposition disease, can mimic the clinical appearance of gout and may respond to nonsteroidal anti-inflammatory drugs (NSAIDs). Findings of calcium pyrophosphate crystals and normal serum uric acid levels on joint analysis can differentiate pseudogout from gout. Septic arthritis can present without fever or high white blood cell count; Arthrocentesis is necessary to differentiate this condition from acute gout. Gout and septic arthritis can occur at the same time, but this is rare.
Trauma-related inflammation is usually identified from the history; however, trauma can cause severe gout caused by increased synovial urate concentrations.
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Imaging studies may be needed to rule out a fracture in a patient with gout-like symptoms after a joint injury.
To achieve a rapid and complete resolution of symptoms, treatment of acute gout should begin within 24 hours of the onset of the symptom.
NSAIDs are the first line of treatment. Historically, indomethacin (Indocin) is the preferred choice; however, there is no evidence that it is more effective than any other NSAID. Intramuscular ketorolac appears to have similar efficacy.
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Any oral NSAID can be given at the maximum dose and continued for a day or two after relief of symptoms.
No analgesic properties; adverse gastrointestinal effects are common; avoid use in patients with renal and hepatic insufficiency; contraindicated in patients receiving clarithromycin (Biaxin)
Oral, intramuscular, or intra-articular route, variable dose (eg, prednisone, 40 mg for four days, then 20 mg for four days, then 10 mg for four days)
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The best treatment for patients in whom NSAIDs and colchicine are prohibited; when stopping oral corticosteroids, taper off gradually to avoid rebound flares
Patients with diabetes mellitus can receive corticosteroids for short-term use with adequate control of hyperglycemia. When gout is limited to one joint, intra-articular corticosteroid injections may be better than systemic corticosteroids because of the lower adverse effect profile.
Recurrent flares are common after discontinuation of corticosteroid therapy for acute gout. To reduce the risk of relapse, preventive treatment and initiation of a course of corticosteroids gradually over 10 to 14 days after resolution of symptoms is recommended.
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Colchicine is another treatment option for acute gout. Generic colchicine, which has been used for decades, was not formally reviewed by the US Food and Drug Administration (FDA) for this indication until 2009, when the brand name colchicine (Colcrys) was approved. However, Colcrys is expensive and generic colchicine is no longer available. In addition, colchicine has no analgesic properties and may be less effective in treating acute exacerbations when given more than 72 to 96 hours after symptom onset. Common side effects include nausea, vomiting, and diarrhea.
Treatment to lower serum urates should be started to prevent recurrence in people with a history of gout and any of the following: at least two flares per year (one per year in people with stage 2 or more kidney disease kidney), tophi, or a history of nephrolithiasis.
Serum urate should be reduced to a target of less than 5 to 6 mg per dL (297 to 357 μmol per L), depending on the crystal and tophaceous load.
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Normal serum urate levels do not exclude the diagnosis of gout. They should be monitored periodically to evaluate preventive therapy in patients with recurrent gout and a history of high urate levels.
Urate lowering therapy should be continued for three to six months after flare-up unless symptoms persist. Treatment should be continued indefinitely if there are persistent signs or symptoms (eg, one or more tophi on examination).
Patients with gout should limit the intake of high-purine animal proteins (eg, organic meat, beef, lamb, pork, shellfish) and avoid alcohol (especially beer).
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Although loop and thiazide diuretics have been recommended for patients with hypertension and gout because these agents can increase uric acid levels, a systematic review found that there was only a small increase in the risk of gout flare-ups.
Calcium channel blockers and the angiotensin receptor blocker losartan (Cozaar) are associated with a lower risk of incident gout.
100 mg per day initially, except in patients with kidney problems; A common effective dose is 300 mg per day, but higher doses may be required
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Genetic testing is recommended before starting treatment in patients at risk of severe skin reactions (those of Han Chinese or Thai descent, regardless of renal function, or Koreans with grade 3 or advanced chronic kidney disease).
40 mg once a day; May increase to 80 mg per day if serum uric acid level > 6 mg per dL (357 μmol per L) after 2 weeks
Historically, urate-lowering drugs were thought to worsen gout flares, but recent evidence suggests that allopurinol (Zyloprim) can be started during severe flares if used in conjunction with base with NSAID and colchicine.
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Patients receiving a urate-lowering drug should be treated concurrently with an NSAID, colchicine, or low-dose corticosteroids to prevent flare-ups. Treatment should be continued for at least three months after uric acid levels fall below target in those without tophi, or for six months in those with a history of tophi.
NSAIDs and corticosteroids should not be used for long periods without a urate-lowering drug because uric acid crystals continue to build up and damage the joint, despite the absence of pain or symptoms. clinical of inflammation.
If a patient has a gout flare while receiving a urate-lowering agent, the medication should be continued as long as the flare is treated aggressively.
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In patients with gout and chronic kidney disease or congestive heart failure, allopurinol has the added benefit of preventing the progression of chronic disease.
The starting dose is 100 mg daily and 300 mg daily is a common maintenance dose. Dosing is guided by the target serum uric acid level.
In patients with chronic kidney disease, low starting doses with slow titration to achieve the desired uric acid levels are recommended.
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Doses higher than 300 mg can be used, even in people with kidney problems, as long as patients are closely monitored for adverse effects.
Certain ethnic groups are at greater risk of severe skin reactions when starting allopurinol therapy. Screening for human leukocyte antigen-B*5801 genotyping is recommended before starting treatment in patients of Han Chinese or Thai descent, regardless of renal function, or in Koreans with stage 3 or renal disease higher kidney.
Febuxostat. Febuxostat (Uloric) is a xanthine oxidase inhibitor that was approved by the FDA in 2009. Although febuxostat is better than allopurinol 300 mg in reducing serum uric acid levels, it is not more effective in reducing the frequency of discounts.
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