Antiinflammatory effects of Colchicine compared with phenylbutazone and indomethacin
Colchicine suppresses the development of carrageenan-induced edema in the rat with a minimum effective oral dose of 6.0 mg/kg. The slope of the dose-response regression line for Colchicine differs significantly from that of indomethacin and phenylbutazone. Based on the dosages required to achieve a 50% suppression of this inflammation, Colchicine is 0.6 and 1.5 times as potent as indomethacin and phenylbutazone, respectively. In the reversed passive Arthus reaction in the rat, the suppressive activity of Colchicine is at least 50 times that of indomethacin and 100 times that of phenylbutazone. The possible significance of these results with regard to the unique effectiveness of Colchicine in the treatment of gout is discussed.

Treatment of Gout
Preventing acute gout attacks is equally as important as treating the acute arthritis. Prevention of acute gout involves maintaining adequate fluid intake, weight reduction, dietary changes, reduction in alcohol consumption, and medications to reduce hyperuricemia. Maintaining adequate fluid intake helps prevent acute gout attacks. Adequate fluid intake also decreases the risk of kidney stone formation in patients with gout.

Alcohol is known to have diuretic effects which can contribute to dehydration and precipitate acute gout attacks. Alcohol can also affect uric acid metabolism and cause hyperuricemia. It causes gout by impeding (slowing down) the excretion of uric acid from the kidneys as well as by causing dehydration, which precipitates the crystals in the joints.

There are three aspects to the medication treatment of gout. First, pain relievers such as acetaminophen/Tylenol or other more potent analgesics are used to manage pain. Secondly, anti-inflammatory agents such as nonsteroidal anti-inflammatory drugs (NSAIDS), colchicine, and corticosteroids are used to decrease joint inflammation. Finally, medications are considered for managing the underlying metabolic derangement that causes hyperuricemia and gout. This means treating the elevated levels of uric acid in the blood with medications that reduce these levels.

Biliary excretion of Colchicine in newborn rats
In an attempt to determine the mechanism of the increased sensitivity of the newborn rat to the toxic action of Colchicine, the distribution of 3H after the administration of 3H-Colchicine (0.1 mg/kg) was measured in 10- and 35-day-old rats. The concentration of 3H was higher in all tissues of the newborn than the adult after ip administration, suggesting an immaturity in the pathway for Colchicine elimination. The results suggest that Colchicine is more toxic in the newborn because the drug remains in the body for a longer time due to immaturity of the liver excretory process.

Gout : Treatment by lowering Uric Acid Levels
In addition to medications for acute gout attacks, other drugs can be taken over prolonged periods to lower blood uric acid levels. Lowering blood uric acid levels reduces the risk of recurrent attacks of arthritis, kidney stones, and kidney disease, and also dissolves hard tophi deposits. Medicines used to lower blood uric acid level work either by increasing the kidney excretion of uric acid, or by decreasing the body's production of uric acid from the purine in foods. These medicines are generally not started until after the inflammation from acute gouty arthritis has subsided because they can worsen the attack. If they are already being taken prior to the attack, they are continued and only adjusted after the attack has resolved. Since many patients with elevated blood uric acid levels may not develop gouty attacks or kidney stones, the decision for prolonged treatment with uric acid-lowering drugs should be individualized.