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Uric acid displays lactam–lactim tautomerism. [4] Uric acid crystallizes in the lactam form, [5] with computational chemistry also indicating that tautomer to be the most stable. [6] Uric acid is a diprotic acid with pK a1 = 5.4 and pK a2 = 10.3. [7] At physiological pH, urate predominates in solution. [medical citation needed]
Unless high blood levels of uric acid are determined in a clinical laboratory, hyperuricemia may not cause noticeable symptoms in most people. [4] 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 ...
Hypouricemia or hypouricaemia is a level of uric acid in blood serum that is below normal. In humans, the normal range of this blood component has a lower threshold set variously in the range of 2 mg/dL to 4 mg/dL, while the upper threshold is 530 μmol/L (6 mg/dL) for women and 619 μmol/L (7 mg/dL) for men. [1]
Aspartic acid: Amino acid 0-3 × 10 −6: In WBCs 2.5-4.0 × 10 −4: 9-12 × 10 −6: Bicarbonate: Buffer in blood 5-5.7 × 10 −4: Bile acids Digestive function, bilirubin excretion 2-30 × 10 −6: 3-30 × 10 −6: Bilirubin: Hemoglobin metabolite 2-14 × 10 −6: 1-10 × 10 −6: Biotin (Vitamin H) Gluconeogenesis, metabolize leucine ...
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]
Acid–base and blood gases are among the few blood constituents that exhibit substantial difference between arterial and venous values. [6] Still, pH, bicarbonate and base excess show a high level of inter-method reliability between arterial and venous tests, so arterial and venous values are roughly equivalent for these. [44]