Uric acid serum

Hyperuricemia is defined as serum uric acid concentration >416 p mol/L or 7.0 mg/dL. With increasing serum uric acid concentration, the risk of acute gouty arthritis increases, but asymptomatic hyperuricemia does not have to be treated pharmacologically. 

Allopurinol (Zyloprim) reduces the production of uric acid, thus decreasing serum uric acid levels and the deposit of urate crystals in joints. The exact mechanism of action of colchicine is unknown, but it does reduce the inflammation associated with the deposit of urate crystals in the joints. This probably accounts for its ability to relieve the severe pain of acute gout. Colchicine has no effect on uric acid metabolism. 

In those with gout, the serum uric acid level is usually elevated. Sulfinpyrazone increases the excretion of uric acid by the kidneys, which lowers serum uric acid levels and consequently retards the deposit of urate crystals in the joints. Probenecid (Benemid) works in the same manner and may be given alone or with colchicine as combination therapy when there are frequent, recurrent attacks of gout. Probenecid also has been used to prolong the plasma levels of the penicillins and cephalosporins. 

Agamah, E.S., Srinivasan, S.R., Webber, L.S. and Berenson, G.S. (1991). Serum uric acid and its relation to cardiovascular disease risk factors in children and young adults from a biorac-ical community The Bogalusa Heart Study. J. Lab. Clin. Med. 113, 241-249. 

Ellerbe P, Cohen A, Welch MJ, and White V E (1990) Determination of serum uric acid by isotope dilution mass spectrometry as a candidate definitive method. Anal. Chem 62 2173-2177. 

All patients with major patterns are monitored for rhabdomyolysis and renal failure. An early sign of rhabdomyolysis is an elevated serum uric acid, associated with an increase in serum CK. Within 8 to 12 hours, the serum tests are repeated. If the uric acid falls and the CK rises, rhabdomyolysis is likely. Renal function tests may also be increased at this time. When the diagnosis of rhabdomyolysis is made, the patient is treated with 40 mg furose-mide IV once, and IV fluids. Urine myoglobin concentrations are obtained. If the patient develops renal failure, hemodialysis or peritoneal dialysis may be necessary. In all cases, multiple drug intoxication, trauma, and rhabdomyolysis are ruled out or treated. All patients are kept under observation until they are asymptomatic. 

Select an appropriate drug to reduce serum uric acid levels in patients with gout, and outline a plan for monitoring efficacy and toxicity. 

The increased serum uric acid involves either the underexcretion of uric acid (80% of patients) or its overproduction. The cause of overproduction or underexcretion of uric acid in... 

The risk of gout increases as the serum uric acid concentration increases, and approximately 30% of patients with levels greater than 10 mg/dL (greater than 595 pmol/L) develop symptoms of gout within 5 years. However, most patients with hyperuricemia are asymptomatic. Other risk factors for gout include obesity, ethanol use, and dyslipidemia. Gout is seen frequently in patients with type 2 diabetes mellitus and coronary artery disease, but a causal relationship has not been established. 

The serum uric acid level often is elevated but may be normal during an acute attack. 

Most patients in the United States are treated with allopurinol, which usually is effective if the dosage is titrated appropriately. The drug and its primary active metabolite, oxypurinol, reduce serum uric acid concentrations by inhibiting the enzyme xanthine oxidase, thereby blocking the oxidation of hypoxanthine and xanthine to uric acid. 

Allopurinol is well absorbed with a short half-life of 2 to 3 hours. The half-life of oxypurinol approaches 24 hours, allowing allopurinol to be dosed once daily. Oxypurinol is cleared primarily renally and can accumulate in patients with reduced kidney function. Allopurinol should not be started during an acute gout attack because sudden shifts in serum uric acid levels may precipitate or exacerbate gouty arthritis. Rapid shifts in serum uric acid can change the concentration of monosodium urate crystals in synovial fluid, causing more crystals to precipitate. Thus some clinicians advocate a prophylactic dose of colchicine (0.6 mg/day) during initiation of antihyperuricemic therapy. Acute episodes should be treated appropriately before maintenance treatment is started. 

Serum uric acid levels must be monitored periodically, with the first follow-up level obtained 6 months (or sooner) after starting therapy. The target serum uric acid level is less than 6 mg/dL (less than 357 ptmol/L). The dose should be titrated upward (to a maximum of 800 mg/day) or downward as these levels dictate. 

Obtain the first follow-up serum uric acid level within 6 months of starting therapy. Then monitor levels at least every 6 to 12 months, and adjust the dose to achieve a target serum uric acid level of less than 6 mg/dL (less than 357 pmol/L). 

Pyrazinamide Adults Based on IBW 40-55 kg 1000 mg 56-75 kg 1500 mg 76-90 kg 2000 mg Children 15-30 mg/kg Hepatotoxicity, gastrointestinal symptoms (nausea, vomiting), non-gouty polyarthralgia, asymptomatic hyperuricemia, acute gouty arthritis, transient morbilliform rash, dermatitis Serum uric acid can serve as a surrogate marker for compliance FFTs in patients with underlying liver disease... 

What risk factors does HT have for tumor lysis syndrome Why is the serum uric acid elevated and renal function decreased ... 

Serum uric acid level greater than 8 mg/dL (476 pmol/L)... 

Hyperuricemia Elevated serum uric acid concentration, defined as a level greater than 7.0 mg/dL. 

Uric acid A by-product of purine metabolism in mammals, including humans. A high serum uric acid concentration is a major risk factor for gout. 

A study of 55 adolescents who had been treated for lead intoxication in early childhood (11-17 years earlier) revealed no evidence of chronic nephropathy, as evidenced by endogenous creatinine clearance, BUN, serum uric acid, and routine urinalysis (Chisolm et al. 1976). PbB levels during the acute poisoning episode ranged from 100 to 650 pg/dL all patients received immediate chelation therapy. At the time of the study, their PbB levels had decreased to less than 40 pg/dL. 

Administration of urate oxidase to humans suffering from hyperuricaemia results in the reduction of serum uric acid levels through its conversion to allantoin. Urate oxidase purified directly... 

Fed diets containing 50 mg/kg for 10 weeks with no effect on serum uric acid levels... 

Karring, M., R. Pohjanvirta, T. Rahko, and H. Korpela. 1981. The influence of dietary molybdenum and copper supplementation on the contents of serum uric acid and some trace elements in cocks. Acta Vet. Scand. 22 289-295. 

Hyperuricemia may be an asymptomatic condition, with an increased serum uric acid concentration as the only apparent abnormality. A urate concentration greater than 7.0 mg/dL is abnormal and associated with an increased risk for gout. 

If the patient had a severe attack of gouty arthritis, a complicated course of uric acid lithiasis, a substantially elevated serum uric acid (greater than 10 mg/dL), or a 24-hour urinary excretion of uric acid of more than 1,000 mg, then prophylactic treatment should be instituted immediately after resolution of the acute episode. 

Prophylactic therapy is cost-effective for patients with frequent attacks of gouty arthritis (i.e., two or more attacks per year) even if the serum uric acid concentration is normal or only minimally elevated. 

Patients with a history of recurrent acute gouty arthritis and a significantly elevated serum uric acid concentration are probably best managed with uric acid-lowering therapy. 

The therapeutic objective of antihyperuricemic therapy is to achieve and maintain a serum uric acid concentration less than 6 mg/dL, and preferably below 5 mg/dL. 

Allopurinol and its major metabolite, oxypurinol, are xanthine oxidase inhibitors and impair the conversion of hypoxanthine to xanthine and xanthine to uric acid. Allopurinol also lowers the intracellular concentration of PRPP. Because of the long half-life of its metabolite, allopurinol can be given once daily orally. It is typically initiated at a dose of 100 mg/day and increased by 100 mg/day at 1-week intervals to achieve a serum uric acid level of 6 mg/dL or less. Serum levels can be checked about 1 week after starting therapy or modifying the dose. Although typical doses are 100 to 300 mg daily, occasionally doses of 600 to 800 mg/day are necessary. The dose should be reduced in patients with renal insufficiency (200 mg/day for CLcr 60 mL/min or less, and 100 mg/day for CLcr 30 mL/min or less). 

Because of comorbidity with diabetes, dyslipidemia, hypertension, and stroke, the presence of increased serum uric acid levels or gout should prompt evaluation for cardiovascular disease and the need for appropriate risk reduction measures. Clinicians should also look for possible correctable causes of hyperuricemia (e.g., medications, obesity, and alcohol abuse). 

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