Medications and Lifestyle Adjustments to Lower Uric Acid. Acute Gout Attack. The goal of treatment during an acute. It is important to note, that if a patient is not on uric acid lowering therapy at the time of an acute attack – then this is not the time to initiate such therapy. However, if a patient is on uric acid lowering therapy at the time of an acute attack, it should not be discontinued. Treatment of pain and inflammation can be achieved with NSAIDs, colchicine, or corticosteroids (systemic or intra- articular).
Anti-hypertension diet could also help gout patients. They found the effect on uric acid levels of a diet rich in fruits. HYPERTENSION CAUSED WITH URIC ACID. Hypertension caused with uric acid. It is important to note that whenever starting a uric acid. Eating a healthy balanced diet. Diagnosis, Treatment, and Prevention of Gout. Although febuxostat is superior to 300 mg allopurinol at lowering serum uric acid levels. The choice of which treatment is the right one for a particular patient should be made on the basis of the patient’s co- morbid medical conditions, other medications, and side effect profile. NSAIDS: Commonly used NSAIDs during an acute gout attack include. Treatment should be discontinued when symptoms resolve. Colchicine. High dose oral colchicine (1. GI side effects. Lower doses are much better received and may be used in combination with NSAIDs. Corticosteroids: In patients with contraindications to NSAID use, corticosteroids are the next choice. Corticosteroids can be administered as an injection into the effected joint (intra- articular steroids) or given systemically (orally, such as prednisone or medrol). Intra- articular steriods are useful if only one or two joints are affected and the treating physician is proficient in injecting those joints. Use of uric acid lowering agents will reduce the frequency of gout attacks and over time, reduce tophi formation, and diminish the risk of joint destruction. The following are indications for uric acid lowering therapy: tophi or chronic arthritis on examfailure of colchicine prophylaxis of acute gouty arthritisrenal stones. Prior to chemotherapy as prophylaxis of tumor lysis syndrome. Extremely high levels of serum uric acid (> 1. Uric acid is the end product of purine (nucleic acid component of DNA) metabolism and is produced normally by the body during tissue remodeling and breakdown. About 2. 0% of uric acid is derived from purines ingested in food. Causes of hyperuricemia can be divided into two major categories: decreased clearance of uric acid from the kidney and increased synthesis of uric acid. Decreased renal clearance – (9. Intrinsic kidney diseaseheart disease causing decreased blood flow to the kidneydrugs (loop diuretics, low dose aspirin, cyclosporin)genetic predispositionage related decrease in glomerulofiltration rate. Increased uric acid synthesis. Dietary indiscretions. Genetic predisposition. Increased tissue turnover–tumors, lymphoproliferative disorders. Stress induced increased turnover of ATPAlcohol induced turnover of ATPAll patients should be encouraged to modify their lifestyle including limiting alcohol intake, encouraging weight loss where appropriate and decreasing food rich in purines. Co- morbid medical conditions should also be controlled including hypertension, diabetes and hyperlipidemia. Foods High in Purines. Very High – Hearts, herring , mussels, yeast , smelt, sardines, sweetbreads. Moderately High – Anchovies, grouse,mutton, veal, bacon, liver salmon, turkey, kidneys, partridge, trout, goose, haddock, pheasant, scallops. Medication Options for Uric Acid Lowering. It is important to note that whenever starting a uric acid lowering treatment, there is a risk of precipitating a gout flare. A plan should be in place for management if this occurs. This generally can be avoided with the co- administration of prophylactic medications (steroids, colchicine, NSAIDs) along with the uric acid lowering therapy. Probenecid Probenecid may be given to patients with decreased clearance of uric acid by the kidney and normal renal function. In general its use should be limited to patients under the age of 6. Probenecid acts by inhibiting reabsorption of uric acid in the proximal tubules of the kidney. Starting dose is at 5. Occasionally higher doses are needed. Probenecid may precipitate renal stone formation and good oral hydration should be encouraged. Probenecid is contraindicated in patients with renal stones (including calcium and uric acid stones) and in patients with urate nephropathy. Probenecid given inappropriately to patients with hyperuricemia due to overproduction of uric acid can cause renal stones and urate nephropathy. Allopurinol Allopurinol is a well tolerated, inexpensive, and. Toxicites include rash, hepatoxicity, bone marrow suppression and severe hypersensitivity reactions. Allopurinol should be avoided in. Its efficacy has been demonstrated in patients with mild or moderate renal impairment and gout. However, it can cause abnormalities in liver function tests and routine monitoring of bloodwork is recommended. Similar to allopurinol, there are interactions of febuxostat with azathioprine, 6. MP, and theophylline. Uricase is present in most mammals, and these mammals with uricase do not develop gout. However, humans and some primates lack uricase (because of evoluationary gene inactivation) and lack the ability to make uric acid more soluable and hence, have gout. Pegloticase is a porcine uricase which was approved by the FDA. Patients should be treated prophylactically for allergic reations to the infusion with steroids and anti- histamines and monitored closely for the development of an infusion reaction. Caution should be used in prescribing this treatment in patients with a known cardiac history. Treatment: Lifestyle. Nutrition. Obesity and increased fat.
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May 2017
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