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Tuesday, 5 May 2009

Hyperuricemia

Uric acid (an antioxidane) is a metabolite of purines (in food products as well as body cells going through their natural breakdown). Its continual supply is important for preventing damage to blood vessel linings. Uric acid is mostly excreted by the kidneys. But if too much uric acid is being produced or if the kidneys are not able to remove it, its level in the blood increases. Excessive uric acid is deposited in the tissues of the body. An increase in the level of Uric acid is referred to as hyperuricemia.

Because uric acid is formed from the breakdown of purines, low-purine diets are often considered in managing hyperuricemia. High-purine foods include: organ meats like kidney; fish like mackerel, herring, sardines and mussels; and yeast.
More information on the list of foods that contain high purines level [http://www.acumedico.com/purine.htm]

Drug treatment of hyperuricemia
There are two types of hyperuricemia, asymptomatic & symptomatic. Treatment for asymptomatic hyperuricemia is not considered cost-effective and generally, is not recommended. Treatment for symptomatic hyperuricemia is discussed under the treatment for gout, nephrolithiasis and uric acid nephropathy.

1) Drug treatment for gout: Drugs used for the treatment of acute attacks of gout are different from those used in long-term control of the disease.

Acute attacks of gout:
The main goal is to provide symptomatic relief from pain.
- The usual treatment is with high dose of NSAIDs (e.g. diclofenac, etorcoxib, indometacin and naproxen).
- Colchicine can be used alternatively (it has the risk of toxicity in higher dose, but as unlike NSAIDs it does not induce fluid retention, it can be used in patients with heart failure. It can also be given to patients on anticoagulants).
- Intra-articular injection of a corticosteroid may be used in acute monoarticular gout

Long term control of gout:
The main goal is to prevent further attacks of gout. The treatment for this phase is usually given 2-3 weeks after the acute attack has settled. The initiation of treatment may precipitate an attack of acute gout, hence prophylactic use of an anti-inflammatory analgesic or colchicine is recommended and it is continued for about three months.

The formation of uric acid can be reduced by
- uricosuric drugs (which promote uric acid excretion), probenecid, which is a uricosuric drug, inhibits the tubular reabsorption of filtered and secreted urate, thereby increasing urate excretion. But crystallisation of urate in the urine may occur, so adequate urine output must be ensured.
- xantine-oxidase inhibitors (which inhibit uric acid production).
Allopurinol is the most widely used antihyperuricemic agent. The major metabolite of allopurinol is oxypurinol, and both allopurinol and oxypurinol are competitive inhibitors of the enzyme xanthine oxidase.
Sulfinpyraone, can be used instead of allopurinol, or in conjunction with it.

2) Drug treatment for Uric acid nephrolithiasis (the process of forming a stone in the kidney or in the urinary tract).
Adequate hydration is recommended to maintain a high urine output, unless volume overload may be a concern. Allopurinol is the drug of choice in patients with hyperuricemia who develop uric acid stones. Patients with calcium stones who are hyperuricosuric may also benefit from allopurinol because urate crystals in the urine may act as a base for other stones to form.
Potassium citrate and occasionally sodium bicarbonate or acetazolamide may be required to alkalinize the urine and to decrease the solubility of uric acid.

3) Uric acid nephropathy (causing damaged to the kidney)
Xanthine is not very soluble in water; therefore, an increase in xanthine (could be induced by allopurinol) result in damage of the kidney.

Intravenous hydration with saline and the administration of furosemide or mannitol (to dilute the urine), and alkalinizing the urine with sodium bicarbonate or acetazolamide may be necessary.

If acute renal failure develops, then early hemodialysis is indicated.

Sourses:
In writing this piece the following articles were used:
- British National Formulary, March 2005
- WebMD, http://www.webmd.com/a-to-z-guides/uric-acid-in-blood, accessed on 5 May 2009
- emedicine, http://emedicine.medscape.com/article/241767-treatment, accessed on 5 May 2009
- The word’s healthiest foods, http://www.whfoods.com/genpage.php?tname=george&dbid=51, accessed on 5 May 2009



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Disclaimer: the main purpose of this blog is to assemble my notes for my Continuing Professional Development (CPD). The topic discussed here should not be referred to as the only source of information on the given topic. If there is anything with respect to this article that concerns you, please contact your doctor or pharmacist.
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