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Uric acid : an almost insoluble compound that is a breakdown product of nitrogenous metabolism. It is the main excretory product in birds, reptiles, and insects. Also important to blood uric acid levels are purines. Purines are nitrogen-containing compounds, which are made inside the cells of the body (endogenous), or come from outside of the body, from foods containing purine (exogenous). Purine breaks down into uric acid.

Purines are nitrogenous heterocyclic bases, e.g. adenine, guanine, hypoxanthine and xanthine. The degradation of purines leads to uric acid, which is excreted in primates, birds and some other animals. In many other vertebrates uric acid is degraded further to the excretory product allantoin.

Most of it is excreted (removed from your body) in your urine, or passes through your intestines to regulate "normal" levels.

Normal Uric acid levels are 2.4-6.0 mg/dL (female) and 3.4-7.0 mg/dL (male). Normal values will vary from laboratory to laboratory

Hyperuricemia refers to an excessive amount of uric acid in the blood. The term originated from the words "ouron" which means urine and "haima" which means blood.
Problems, such as kidney stones, and gout (collection of uric acid crystals in the joints, especially in your toes and fingers), may occur.

(1) An increase in the consumption of exogenous purins. (2) Increased destruction of the cells in the body. (3) Diminished oxidation of uric acid in the body. (4) Increased washing out of stores retained in the body. There is, however, no proof of the retention of uric acid in the body excepting temporarily in gout, although exogenous purins may remain for days in the body. (5) The possibility of a synthetic formation of uric acid in the body from substances other than nuclein or purins.

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Hyperuricemia is generally divided into 3 pathophysiologic categories, ie, uric acid underexcretion, uric acid overproduction, and combined causes.

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Idiopathic Renal insufficiency: Renal failure is one of the more common causes of hyperuricemia. Drugs: Causative drugs include diuretics, low-dose salicylate, cyclosporine, pyrazinamide, ethambutol, levodopa, nicotinic acid, and methoxyflurane. Hypertension.

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Acidosis: Types that cause hyperuricemia include lactic acidosis, diabetic ketoacidosis, alcoholic ketoacidosis, and starvation ketoacidosis. Hypothyroidism. Hyperparathyroidism. Sarcoidosis Obesity.

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Purine-rich diet: A diet rich in meats, organ foods, alcohol.... Increased nucleic acid turnover: This may be observed in persons with hemolytic anemia and hematologic malignancies such as lymphoma, myeloma, or leukemia. Tumor lysis syndrome: This may produce the most serious complications of hyperuricemia. Glycogenoses III, V, and VII

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Alcohol : Ethanol increases the production of uric acid by causing increased turnover of adenine nucleotides. Exercise: Exercise may result in enhanced tissue breakdown and decreased renal excretion due to mild volume depletion. Deficiency of aldolase B (fructose-1-phosphate aldolase): This is a fairly common inherited disorder, often resulting in gout. Glucose-6-phosphatase deficiency (glycogenosis type I, von Gierke disease)

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is a medical condition usually characterized by recurrent attacks of acute inflammatory arthritis a red, tender, hot, swollen joint. The metatarsalphalangeal joint at the base of the big toe is the most commonly affected (approximately 50% of cases). However, it may also present as tophi, kidney stones, or urate nephropathy. It is caused by elevated levels of uric acid in the blood. The uric acid crystallizes, and the crystals deposit in joints, tendons, and surrounding tissues.

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hyperuricemia presence of uric acid crystals in joint fluid more than one attack of acute arthritis arthritis that develops in a day, producing a swollen, red, and warm joint attack of arthritis in only one joint, often the toe, ankle, or knee.

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To stop a gout attack, your doctor can give you a shot of corticosteroids, or prescribe a large daily dose of one or more medicines. The doses will get smaller as your symptoms go away. Relief from a gout attack often begins within 24 hours if you start treatment right away. To ease the pain during a gout attack, rest the joint that hurts. Taking ibuprofen or another antiinflammatory medicine can also help you feel better. But don't take aspirin. It can make gout worse by raising the uric acid level in the blood.

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Diet treatment Disease Treatment

Drug Treatments

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Elevated uric-acid levels can be caused by diet, and can be treated by altering the diet in certain cases. When a person eats certain foods that contain purines, such as mackerel, liver and sardines, the body produces uric acid as a result of breaking down the food. Eating these foods in excess can cause elevated uric-acid levels, so eliminating these foods can help reduce uric acid

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Diet therapy can also help those who have elevated uric acid caused by conditions unrelated to diet. For example, drinking black cherry juice and eating lots of fruit (especially strawberries) can help reduce uric-acid levels in the body.

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Often, elevated uric-acid levels are caused by an underlying condition. For example, renal failure, diabetes, chemotherapy (administered in the treatment of cancer), toxic pregnancy, alcoholism, acidosis, lead poisoning and hypoparathyroidism can all cause elevated uric-acid levels.

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Whenever possible, the best method of treating the high uric-acid levels is to treat the underlying condition. If the underlying condition cannot be treated, the high levels of uric acid may be a persistent and chronic problem that can be treated with medication, but not eliminated or cured.

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If the underlying cause of the elevated uric acid can't be resolved, the best method of treatment may be to treat the hyperuricemia as a chronic condition and medicate the condition. This involves prescribing medications that either encourage the body to excrete more uric acid, or prevent the body from making or absorbing uric acid.

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One drug, Probenecid, prevents the body from absorbing urates. Allupurinol, febuxostate and sulfinpyrazone all work to prevent the body form producing uric acid and/or to encourage the body to excrete uric acid.

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