Patients with lab reports showing hyperuricemia without symptoms, usually worried about reports.
observe till symptomatic and strict dietary restrictions are to be followed and the dietary Smith should be removed.Read about hyperurecemic effects due to various individual products
Baseline recommendation (ACR guideline): Patient education with diet and life style modification, rule out secondary causes.
Indication for treatment: Presence of tophus or tophi by clinically or imaging, more than 2 attacks/year, CKD stage2, past h/o urolithiasis.
Target serum Uric acid < 6mg/dl.
There is no proof of any clinical benefit to treat asymptomatic patients with hyperuricemia. Uricemia raises generally in parallel to serum creatinin.
The presence of hyperuricemia is rarely an indication for specific antihyperuricemic drug therapy. Rather, the finding of hyperuricemia should cause the following questions to be addressed:
1. What is the cause of the hyperuricemia?
2. Are associated findings present?
3. Has damage to tissues or organs occurred as a result?
4. What, if anything, should be done?
Hyperuricemia may be the initial clue to the presence of a previously unsuspected disorder. In 70% of hyperuricemic patients, an underlying cause can be readily defined by history and physical examination. The nature of the underlying cause may be useful in predicting the potential consequences, if any, of the elevated serum urate concentration. Therefore, an underlying cause should be sought in every patient with hyperuricemia.
Whether to treat hyperuricemia uncomplicated by articular gout, urolithiasis, or nephropathy is an exercise in clinical judgment, and universal agreement is lacking. When considering whether to treat asymptomatic hyperuricemia with urate-lowering agents, the following data are pertinent:
• Although there is intriguing data from animal models to the contrary, there is no good evidence that renal function is adversely affected by elevated serum urate concentrations.
• The renal disease that accompanies hyperuricemia is most often related to inadequately controlled hypertension.
Although debate exists regarding whether hyperuricemia is an independent risk factor for coronary artery disease, there is no evidence that correction of hyperuricemia has an effect on the development of heart disease.
Thus, it seems prudent not to treat hyperuricemia with specific antihyperuricemic agents until symptoms develop. Rare exceptions include individuals with a known hereditary cause of uric acid overproduction or patients at risk for acute uric acid nephropathy.
It is, however, strongly recommended that the cause of hyperuricemia be determined and any associated factors related to the process, such as obesity, hyperlipidemia, alcoholism, and, especially, hypertension, be addressed. Fenofibrate and losartan might be appropriate agents for the treatment of hypertriglyceridemia and hypertension, respectively, in hyperuricemic individuals, because each has modest uricosuric effects.
Referrence: Firestein: Kelley's Textbook of Rheumatology, 8th ed.
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