Hella
Well I did some reserch and I hope this helps. So I also found out that its a diease of uric acid buildup. Here are some treatments.
The first line of treatment should be pain relief. Once the diagnosis has been confirmed, the drugs of choice are indomethacin, other nonsteroidal anti-inflammatory drugs (NSAIDs), oral glucocorticoids,[15] or intra-articular glucocorticoids administered via a joint injection.
Colchicine was previously the drug of choice in acute attacks of gout, as it impairs the motility of granulocytes and can prevent the inflammatory phenomena that initiate an attack. Colchicine should be taken within the first 12 hours of the attack and usually relieves the pain within 48 hours, although side effects (gastrointestinal upset such as diarrhea and nausea) can complicate its use. NSAIDs are the preferred form of analgesia for patients with gout.
A randomized controlled trial found similar benefit from nonsteroidal anti-inflammatory drugs and oral glucocorticoids; however, less adverse drug reactions occurred in the glucocorticoids group.[16] In the nonsteroidal anti-inflammatory drugs group, each patient initially received diclofenac (75 mg) intramuscularly, indomethacin 50 mg orally, and acetaminophen 1 g orally. The patient was received a 5-days of indomethacin (50 mg orally every 8 hours for 2 days, followed by indomethacin 25 mg every 8 hours for 3 days), and acetaminophen 1 g every 6 hours as needed. The glucocorticoids patients received prednisolone 30 mg orally, and acetaminophen 1 g orally. The patient was then given prednisolone 30 mg orally once per day for five days.
Before medical help is available, some over-the-counter medications can provide temporary relief from 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. This is because aspirin raises plasma uric acid levels even at low doses by inhibiting uric acid secretion in the renal tubules[citation needed]. Aspirin also reduces vasodilatation due to inhibition of prostaglandin PGE2 and PGI2 synthesis in the renal medulla and glomeruli respectively (see mechanism of action of aspirin). This may be a contra-indication for the use of aspirin for gout pain as well.
The anti-hemorrhoidal ointment Preparation H can reduce gout-induced skin swelling temporarily. Ice may be applied for 20 to 30 minutes several times a day, and a randomized controlled trial found that patients who used ice packs had better relief of pain without side effects.[17] Since gout is caused by crystals, it has been suggested that keeping very well hydrated and heating the affected joint in hot water (rather than cooling with ice) will promote the dissolution and clearance of the urate crytals.[18] Keeping the affected area elevated above the level of the heart also may help. Professional medical care is needed for long-term management of gout.
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, and treatment is similar to that for common athlete's foot.
Some sufferers of gout report an aggravation of the condition in the knees and toes associated with long periods of immobility, such as when sitting at a computer desk for long hours. Sufferers who notice early swelling or early pain may appear to be able to arrest the aggravation when medical treatment is applied before the condition gets worse. Where this is the case, a medically prescribed anti-inflammatory oral treatment taken with food and bed rest may provide relief within 6 to 8 hours.
Another possibility is acetazolamide, one of the first diuretics discovered. This drug inhibits the action of carbonic anhydrase on the proximal convoluted tubules within the kidneys, which effectively inhibits reabsorption of bicarbonate, thus alkalinizing the urine. After two to three days of usage, the diuretic effects of this drug decline because of increased downstream reabsorption of ions and water by the renal tubules; however, the alkalinization of urine persists, and this basic urine attracts weak acids such as uric acid and cystine into the urine, thus increasing their urinary excretion.
Orignal From: Is it true?? Help??
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