Hyperuricemia treatment

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. 

Pharmaceutical therapy of acute arthritis of crystal-deposition disease is effective, in particular for gout and hyperuricemia. Treatment is directed towards termination of acute arthritis, prevention of recurring attacks and prophylaxis and reversal of complications of chronic gout. Such complications include tophi, urolithiasis, nephropathy and with hyperuricemia associated medical problems that can be prevented, inhibited, and sometimes reversed. 

Asymptomatic hyperuricemia usually does not require treatment. 

FIGURE 56-2. Treatment algorithm for gout and hyperuricemia. Renal insufficiency is defined as an estimated creatinine clearance (CrCI) of less than 30 mL/minute. IA, Intraarticular NSAID, nonsteroidal anti-inflammatory drug. 

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. 

Prophylaxis and treatment of hyperuricemia associated with tumor lysis syndrome. ALL, acute lymphoblastic leukemia AML, acute myelogenous leukemia IV, intravenous. (Data from refs. 32 and 33.)... 

The major adverse effect of niacin treatment is intense cutaneous flushing (vasodilation), which manifests as an uncomfortable burning sensation and itchiness of the face and upper body, thereby limiting patient compliance to therapy [13]. Moreover, a short half-life, dyspepsia, hyperuricemia, and modest hyperglycemia were also reported [14-16]. 

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. 

Its main adverse effect is hepatotoxicity which is dose dependent but still occurs in some 5% of the patients. Hyperuricemia is seen in almost all patients. When gout becomes manifest it does not respond to treatment with probenecid. 

Initial treatment of gout and its associated hyperuricemia must involve therapy directed toward terminating the painful inflammatory process that is a prominent feature of acute gouty arthritis. A variety of nonsteroidal antiinflammatory compounds (e.g., in-... 

The pyrazolo[3,4- pyrimidines 425 and 426 are claimed to be useful as pharmaceuticals for treatment of hyperuricemia and prevention of gout. 

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. 

MP is converted to an inactive metabolite (6-thiouric acid) by an oxidation reaction catalyzed by xanthine oxidase, whereas 6-TG undergoes deamination. This is an important issue because the purine analog allopurinol, a potent xanthine oxidase inhibitor, is frequently used as a supportive care measure in the treatment of acute leukemias to prevent the development of hyperuricemia that often occurs with tumor cell lysis. Because allopurinol inhibits xanthine oxidase, simultaneous therapy with allopurinol and 6-MP would result in increased levels of 6-MP, thereby leading to excessive toxicity. In this setting, the dose of mercaptopurine must be reduced by 50-75%. In contrast, such an interaction does not occur with 6-TG, which can be used in full doses with allopurinol. 

Tetrazolyl)- and 2- and 8-carboxylic acids derivatives of 11//-pyrido[2,l-h]quinazolin-ll-one were patented for the treatment of hyperuricemia (88GEP3704203) and hyperlipidemia (89EUP312076) and as cardioprotective agents (90GEP3902639). 

In long-term treatment, the thiazides may produce hypokalemia, hyperglycemia hyperuricemia, and a 5% increase in plasma cholesterol indapamide has been shown not to increase plasma cholesterol or lipids at therapeuLic doses. Thiazides can cause hyponatremia in patients with large Water intake while on the drug hyponatremia may be associated with nausea, vomiting, and headaches. 

Nicotinic acid is also a potent vasodilator, probably by a direct action on smooth muscle cells. It produces cutaneous vasodilatation, itching of the skin, facial flushing, a sensation of feeling hot, pounding in the head, gastric irritation, diarrhea, raised transaminases, hyperglycemia, and hyperuricemia. These unpleasant adverse effects limit its acceptability for many patients. Nicotinic acid as such is not used in the treatment of vascular disorders, but some of its derivatives are, albeit with poor evidence of clinical efficacy. 

The issues of whether hyperuricemia is an independent risk factor for cardiovascular disease and the clinical relevance of the rise in serum uric acid caused by diuretic treatment are controversial (SED-14, 660 351). In the Systolic Hypertension in the Elderly Program (SHEP), diuretic-based treatment in 4327 men and women, aged 60 years or more, with isolated systolic hypertension was associated with significant reduction in cardiovascular events (SED-14, 657). Serum uric acid independently... 

Mercaptopurine is used in the treatment of acute lymphoid leukemia. Maintenance therapy makes use of both methotrexate and 6-mercaptopurine. Mercaptopurine is absorbed well from the gastrointestinal tract. It is metabolized through (1) methylation of the sulfhydryl group and subsequent oxidation, and (2) conversion to 6-thiouric acid with the aid of xanthine oxidase, which is inhibited by allopurinol. Mercaptopurine may cause hyperuricemia. Its chief toxicities are hepatic damage and bone marrow depression. 

Allopurinol is used in the treatment of hyperuricemia, which is associated with chronic gout and in cancer chemotherapy. Allopurinol has been used in renal calculi caused by the deposition of calcium oxalate and of 2,8-dihydroxy-adenine. Allopurinol treatment does cause hypersensitivity reaction, which may be fatal. 

Adverse effects Thiazide diuretics induce hypokalemia and hyperuricemia in 70% of patients, and hyperglycemia in 10% of patients. Serum potassium levels should be monitored closely in patients who are predisposed to cardiac arrhythmias (particularly individuals with left ventricular hypertrophy, ischemic heart disease, or chronic congestive heart failure) and who are concurrently being treated with both thiazide diuretics and digitalis glycosides (see p. 160). Diuretics should be avoided in the treatment of hypertensive diabetics or patients with hyperlipidemia. 

Therapeutic uses Allopurinol is effective in the treatment of primary hyperuricemia of gout and hyperuricemia secondary to other conditions, such as that associated with certain malignancies (those in which large amounts of purines are produced) or in renal disease. 

The therapy of gout is twofold (1) treatment of the acute attack and (2) chronic lowering of hyperuricemia. 

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