Hyperuricemia asymptomatic

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. 

Asymptomatic hyperuricemia usually does not require treatment. 

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. 

Gout is an episodic disease, and the number of attacks varies widely from patient to patient. Thus the benefit of long-term prophylaxis against acute gout flares must be weighed against the cost and potential toxicity of therapy that may not be necessary in all patients. Asymptomatic hyperuricemia usually does not require treatment. 

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... 

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. 

Asymptomatic hyperuricemia Generally, do not use to treat asymptomatic hyperuricemia. Treatment should be considered with persitent hyperuricemia characterized by a serum urate concentration of greater than 13 mg/dL. High serum urate may be nephrotoxic. 

Hyperuricemia Pyrazinamide inhibits renal excretion of urates, frequently resulting in hyperuricemia that is usually asymptomatic. Patients started on pyrazinamide should have baseline serum uric acid determinations. Discontinue the drug and do not resume if signs of hyperuricemia accompanied by acute gouty arthritis appear. 

Sodium-restricted diets Each buffered tablet contains 264.5 mg sodium. Each single-dose packet of buffered powder for oral solution contains 1380 mg sodium. Hyperuricemia Didanosine has been associated with asymptomatic hyperuricemia consider suspending treatment if clinical measures aimed at reducing uric acid levels fail. 

Asymptomatic ventricular tachycardia, hyperuricemia not associated with gout, and nephrolithiasis occur rarely. 

Before starting chronic therapy for gout, patients in whom hyperuricemia is associated with gout and urate lithiasis must be clearly distinguished from those who have only hyperuricemia. In an asymptomatic person with hyperuricemia, the efficacy of long-term drug treatment is unproved. In some individuals, uric acid levels may be elevated up to 2 standard deviations above the mean for a lifetime without adverse consequences. 

The major dose-limiting toxicides of didanosine include peripheral neuropathy and pancreatitis. The neuropathy is typically symmetrical distal sensory neuropathy, which is reversible, and typically causes paresthesias, numbness and pain in lower extremities. Didanosine also causes retinal changes and optic neuritis. Other adverse effects include diarrhea, skin rash, headache, insomnia, seizures, hepatic toxicity, elevated hepatic transaminases and asymptomatic hyperuricemia. 

The term gout describes a disease spectrum including hyperuricemia, recurrent attacks of acute arthritis associated with monosodium urate crystals in leukocytes found in synovial fluid, deposits of monosodium urate crystals in tissues (tophi), interstitial renal disease, and uric acid nephrolithiasis. 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. 

Liang MH, Fries JF. Asymptomatic hyperuricemia the case for conservative management. Ann Intern Med 1978 88 666-670. 

FesselWJ,SiegelaubAB, Johnson ES. Correlation and consequences of asymptomatic hyperuricemia. Arch Intern Med 1973 132 44-54. 

Klinenberg JR, Gonick FIC, Dornfeld L. Renal function abnormalities in patient with asymptomatic hyperuricemia. Arthritis Rheum 1975 10(supp) 725-730. 

Asymptomatic hyperuricemia discovered incidentally requires no therapy. 

Gout is a disease diagnosed by symptoms rather than laboratory tests of uric acid. In fact, asymptomatic hyperuricemia discovered incidentally generally requires no therapy. 

Questions are often raised regarding the indications for drug therapy for asymptomatic hyperuricemia. The purported heneflts from treatment include prevention of acute gouty arthritis, tophi formation, nephrolithiasis, and chronic urate nephropathy. The first three complications are easily controlled shonld they develop therefore antihyperuricemic therapy is not warranted to prevent these conditions. 

The prevention of urate nephropathy might be a stronger indication because it is irreversible even with proper treatment. Available data indicate, however, that gouty nephropathy is extremely rare in the absence of clinical gout, and evidence that elevation of uric acid by itself may cause renal disease is weak and inconclusive. As discussed previously, renal impairment is very rare in the absence of concurrent hypertension and atherosclerosis. In addition, it is unclear whether uric acid-lowering therapy protects renal function in such individuals. Available data thus do not justify therapy for most patients with asymptomatic hyperuricemia. 

While asymptomatic hyperuricemia is not generally treated, some clinicians have begun recommending treatment to reduce the risk of coronary artery disease. Hyperuricemia is associated with both hypertension and coronary artery disease, and patients with elevated uric acid levels and hypertension are at increased risk of cardiovascular morbidity and mortality. 

Assuming no treatment of asymptomatic hyperuricemia, pharma-coeconomic considerations apply only to the management of the acute and chronic clinical manifestations of gout. 

Hyperuricemia may lead to acute arthritis, chronic gout, or kidney stones or remain asymptomatic. Asymptomatic hyperuricemia need not be treated, especially if the serum urate concentration remains below 10 mg/dL. 

---