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Unless high blood levels of uric acid are determined in a clinical laboratory, hyperuricemia may not cause noticeable symptoms in most people. [5] Development of gout – which is a painful, short-term disorder – is the most common consequence of hyperuricemia, which causes deposition of uric acid crystals usually in joints of the extremities, but may also induce formation of kidney stones ...
Hyperuricemia (high levels of uric acid), which induces gout, has various potential origins: Diet may be a factor. High intake of dietary purine, high-fructose corn syrup, and sucrose can increase levels of uric acid. [36] [37] Serum uric acid can be elevated by reduced excretion via the kidneys. [38]
Gout is due to persistently elevated levels of uric acid (urate) in the blood (hyperuricemia). [2] [5] This occurs from a combination of diet, other health problems, and genetic factors. [1] [2] At high levels, uric acid crystallizes and the crystals deposit in joints, tendons, and surrounding tissues, resulting in an attack of gout. [1]
It is a biochemical intermediate in the formation of purine nucleotides via inosine-5-monophosphate, as well as in pyrimidine nucleotide formation. Hence it is a building block for DNA and RNA. [1] [2] [3] The vitamins thiamine [4] and cobalamin, [5] and the amino acid tryptophan also contain fragments derived from PRPP. [6]
Methotrexate also indirectly inhibits purine synthesis by blocking the metabolism of folic acid (it is an inhibitor of the dihydrofolate reductase). Allopurinol is a drug that inhibits the enzyme xanthine oxidoreductase and, thus, lowers the level of uric acid in the body. This may be useful in the treatment of gout, which is a disease caused ...
The starting material for the reaction sequence was uric acid (8), which had been isolated from kidney stones by Carl Wilhelm Scheele in 1776. [12] Uric acid was reacted with PCl 5 to give 2,6,8-trichloropurine, which was converted with HI and PH 4 I to give 2,6-diiodopurine. The product was reduced to purine using zinc dust.