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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]
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]
Hyperuricaemia or hyperuricemia is an abnormally high level of uric acid in the blood.In the pH conditions of body fluid, uric acid exists largely as urate, the ion form. [1] [2] Serum uric acid concentrations greater than 6 mg/dL for females, 7 mg/dL for males, and 5.5 mg/dL for youth (under 18 years old) are defined as hyperuricemia. [3]
Caesium in the body has a biological half-life of about one to four months. Mercury (as methylmercury) in the body has a half-life of about 65 days. Lead in the blood has a half life of 28–36 days. [29] [30] Lead in bone has a biological half-life of about ten years. Cadmium in bone has a biological half-life of about 30 years.
Allopurinol is a medication used to decrease high blood uric acid levels. [5] It is specifically used to prevent gout, prevent specific types of kidney stones and for the high uric acid levels that can occur with chemotherapy. [6] [7] It is taken orally (by mouth) or intravenously (injected into a vein). [7]
Throughout Drop Acid, Dr. Perlmutter offers suggestions and tips on maintaining lower uric values as well as a road map to addressing these hidden dangers. Per the description it also features ...
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]
In gout, probenecid competitively inhibits the reabsorption of uric acid through the organic anion transporter (OAT) at the proximal tubules. This leads to preferential reabsorption of probenecid back into plasma and excretion of uric acid in urine, [6] thus reducing blood uric acid levels and reducing its deposition in various tissues.
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