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Attacks
Acutely, first line treatment should be pain relief. Once the diagnosis has been confirmed, the drugs of choice are indomethacin, other nonsteroidal anti-inflammatory drugs (NSAIDs), or intra-articular glucocorticoids, administered via a joint injection.
Colchicine was previously the drug of choice in acute attacks of gout. It impairs the motility of granulocytes and can prevent the inflammatory phenomena that initiate an attack of gout. Colchicine should be taken within the first 12 hours of the attack and usually relieves the pain within 48 hours. Its main side-effects (gastrointestinal upset such as diarrhea and nausea) can complicate its use. The homeopathic preparation of the plant, Colchicum autumnale, from which Colchicine is derived, is a non-toxic alternative treatment. NSAIDs are the preferred form of analgesia for patients with gout.
Before medical help is available, some over the counter medication can provide temporary relief to the pain and swelling. NSAIDs such as ibuprofen can reduce the pain and inflammation slightly, although aspirin should not be used as it can worsen the condition. Preparation H hemorrhoidal ointment can be applied to the swollen skin to reduce the swelling temporarily. Professional medical care is needed for long term management of gout. Ice may be applied for 20–30 minutes several times a day. There are concerns that uric acid crystallization is accelerated by low temperature, but in a 2002 study in the Journal of Rheumatology patients who used ice packs had better relief of pain with no negative side effects. Keeping the affected area elevated above the level of the heart may help as well.
Due to swelling around affected joints for prolonged periods, shedding of skin may occur. This is particularly evident when small toes are affected and may promote fungal infection in the web region if dampness occurs; it is usually treated in a similar fashion to athlete's foot.
Prevention
Long term treatment (in frequent attacks) is antihyperuricemic therapy.
Because the body metabolizes purines into uric acid, a maintained, low-purine diet can help lower the plasma urate level. Avoiding alcohol, high-purine foods, such as meat, fish, dry beans (also lentils and peas), mushrooms, spinach, asparagus, and cauliflower can lower plasma urate levels. In addition, consuming purine-neutralizing foods, such as fresh fruits (especially cherries and strawberries) and most fresh vegetables, diluted celery juice, distilled water, and B-complex and C vitamins can also help lower plasma urate levels.
A possible "natural" cure is a berry extract supplement consisting of bilberry, blueberry or cherry extracts. The anthocyanins which give the berries their blue and purple hues, after entering the body, turn into powerful anti-inflammatories. These might be an especially preferable option to transplant patients, who frequently suffer gout due to increased toxicity and strain on the kidneys due to their immunosuppressant medication.
The mainstay of prevention is the drug allopurinol, a xanthine oxidase inhibitor, which directly reduces the production of uric acid. However, allopurinol treatment should not be initiated during an attack of gout, as it can then worsen the attack. If a patient is on allopurinol during an attack, it should be continued. However, if an attack occurs when the patient isn't on allopurinol yet, he has to wait until the end of the attack to start allopurinol.
The decision to use allopurinol is often a lifelong one. Patients have been known to relapse into acute arthritic gout when they stop taking their allopurinol, as the changing of their serum urate levels alone seems to cause crystal precipitation.
Allopurinol and uricosuric agents are contraindicated in patients with kidney stones and other renal conditions.
Additional measures
* Febuxostat ((2-[3-cyano-4-isobutoxyphenyl]-4-methylthiazole-5-carboxylic acid) - a novel non-purine inhibitor of xanthine oxidase seems to be an alternative that is superior to allopurinol; it is currently in Phase III trials.
* Probenecid, a uricosuric drug that promotes the excretion of uric acid in urine, is also commonly prescribed - often in conjunction with colchicine. Interestingly, the drug fenofibrate (which is used in treating hyperlipidemia) also exerts a beneficial uricosuric effect.
* As arterial hypertension quite often coexists with gout, treating it with losartan, an angiotensin II receptor antagonist, might have an additional beneficial effect on uric acid plasma levels. This way losartan can offset the negative side-effect of thiazides (a group of diuretics used for high blood pressure) on uric acid metabolism in patients with gout.
* It is suspected that in many cases gout may be secondary to untreated sleep apnea, when oxygen-starved cells break down and release purines as a by-product. Treatment for apnea can be effective in lessening incidence of acute gout attacks.
* A study in 2004 suggests that animal flesh sources of purine, such as beef and seafood, greatly increase the risk of developing gout. However, high-purine vegetable sources did not. Low fat dairy products such as skim milk significantly reduced the chances of gout. The study followed over 40 thousand men over a period of years, in which 1300 cases of gout were reported.
* PEG-uricase, a polyethylene glycol ("PEG") conjugate of recombinant porcine uricase (urate oxidase), which breaks down the uric acid deposits is being studied in Phase III clinical trials for the treatment of severe, treatment-refractory gout in the United States in 2006.Pipeline
Surgery
For extreme cases of gout, surgery may be necessary to remove large tophi and correct joint deformity.
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Important notice:
The content is not intended to be a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other
qualified health provider with any questions you may have regarding a medical condition.
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