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Uric acid is a heterocyclic compound of carbon, nitrogen, oxygen, and hydrogen with the Chemical formula C5H4N4O3. It forms ions and salts known as urates and acid urates, such as ammonium acid urate. Uric acid is a product of the metabolic breakdown of purine , and it is a normal component of urine. Hyperuricemia can lead to gout and are associated with other medical conditions, including diabetes and the formation of ammonium acid urate kidney stones.
Uric acid displays lactam–lactim tautomerism. Uric acid crystallizes in the lactam form, with computational chemistry also indicating that tautomer to be the most stable. Uric acid is a diprotic acid with pKa = 5.4 and p Ka2 = 10.3. At physiological pH, urate predominates in solution.
| + Solubility of urate salts (grams of water per gram of compound) ! data-sort-type="text" | Compound ! data-sort-type="number" | Cold water ! data-sort-type="number" | Boiling water |
| Uric acid | 15,000 | 2,000 | |
| Ammonium hydrogen urate | — | 1,600 | |
| Lithium hydrogen urate | 370 | 39 | |
| Sodium hydrogen urate | 1,175 | 124 | |
| Potassium hydrogen urate | 790 | 75 | |
| Magnesium dihydrogen diurate | 3,750 | 160 | |
| Calcium dihydrogen diurate | 603 | 276 | |
| Disodium urate | 77 | — | |
| Dipotassium urate | 44 | 35 | |
| Calcium urate | 1,500 | 1,440 | |
| Strontium urate | 4,300 | 1,790 | |
| Barium urate | 7,900 | 2,700 |
The figures given indicate what mass of water is required to dissolve a unit mass of compound indicated. The lower the number, the more soluble the substance in the said solvent. (1976). 9780911910261, Merck. ISBN 9780911910261
Myogenic hyperuricemia, as a result of the purine nucleotide cycle running when ATP reservoirs in muscle cells are low, is a common pathophysiologic feature of glycogenoses, such as GSD-III, which is a metabolic myopathy impairing the ability of ATP (energy) production for muscle cells. In these metabolic myopathies, myogenic hyperuricemia is exercise-induced; inosine, hypoxanthine and uric acid increase in plasma after exercise and decrease over hours with rest. Excess AMP (adenosine monophosphate) is converted into uric acid.
AMP → IMP → Inosine → Hypoxanthine → Xanthine → Uric Acid
Excess blood uric acid (serum urate) can induce gout, a painful condition resulting from needle-like crystals of uric acid termed monosodium urate crystals precipitating in , Capillary, skin, and other tissues. Gout can occur where serum uric acid levels are as low as 6 mg per 100 mL (357 μmol/L), but an individual can have serum values as high as 9.6 mg per 100 mL (565 μmol/L) and not have gout.
In humans, purines are metabolized into uric acid, which is then excreted in the urine. Consumption of large amounts of some types of purine-rich foods, particularly meat and seafood, increases gout risk. Purine-rich foods include liver, kidney, and Sweetbread, and certain types of seafood, including anchovies, herring, sardines, mussels, scallops, trout, haddock, mackerel, and tuna. Moderate intake of purine-rich vegetables, however, is not associated with an increased risk of gout.
One treatment for gout in the 19th century was administration of lithium salts; lithium urate is more soluble. Today, inflammation during attacks is more commonly treated with , colchicine, or , and urate levels are managed with allopurinol. Allopurinol, which weakly inhibits xanthine oxidase, is an analog of hypoxanthine that is hydroxylated by Xanthine oxidase at the 2-position to give oxipurinol.
Saturation levels of uric acid in blood may result in one form of when the urate crystallizes in the kidney. These uric acid stones are radiodensity, so do not appear on an abdominal plain X-ray. Uric acid crystals can also promote the formation of calcium oxalate stones, acting as "seed crystals".
Tumor lysis syndrome
Tumor lysis syndrome, an emergency condition that may result from , produces high uric acid levels in blood when tumor cells release their contents into the blood, either spontaneously or following chemotherapy. Tumor lysis syndrome may lead to acute kidney injury when uric acid crystals are deposited in the kidneys. Treatment includes hyperhydration to dilute and excrete uric acid via urine, rasburicase to reduce levels of poorly soluble uric acid in blood, or allopurinol to inhibit purine catabolism from adding to uric acid levels.
Lesch–Nyhan syndrome
Lesch–Nyhan syndrome, a rare inherited disorder, is also associated with high serum uric acid levels. Spasticity, involuntary movement, and cognitive retardation as well as manifestations of gout are seen in this syndrome.
Cardiovascular disease
Hyperuricemia is associated with an increase in risk factors for cardiovascular disease. It is also possible that high levels of uric acid may have a causal role in the development of atherosclerotic cardiovascular disease, but this is controversial and the data are conflicting.
Uric acid stone formation
can form through deposits of sodium urate microcrystals.
Diabetes
Hyperuricemia is associated with components of metabolic syndrome, including in children.
Low uric acid
Low uric acid (hypouricemia) can have numerous causes. Low dietary zinc intakes cause lower uric acid levels. This effect can be even more pronounced in women taking oral contraceptive medication. Sevelamer, a drug indicated for prevention of hyperphosphataemia in people with chronic kidney failure, can significantly reduce serum uric acid.
Multiple sclerosis
Meta-analysis of 10 case-control studies found that the serum uric acid levels of patients with multiple sclerosis were significantly lower compared to those of healthy controls, possibly indicating a diagnostic biomarker for multiple sclerosis.
Normalizing low uric acid
Correcting low or deficient zinc levels can help elevate blood serum uric acid.
See also
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