Indications
Pharmacology
An acute attack of gout seems to come from an inflammatory reaction to crystals of monosodium urate. These crystals form in the joint tissue when body fluids carry too much uric acid. The reaction gets worse as more urate crystals build up. White blood cells (leukocytes) move to the spots where the crystals have collected and try to engulf them by phagocytosis. This releases lactic acid and proinflammatory enzymes, which cause the inflammation behind the severe pain, redness and swelling in the affected joint. The lactic acid also lowers the pH locally, and that makes more uric acid deposit in the joint. Colchicine stops leukocytes from taking up uric acid by phagocytosis, and it also directly reduces the amount of lactic acid produced. In this way it breaks the cycle of crystal deposition and inflammation that keeps an acute gout attack going.
Colchicine is absorbed well when taken by mouth. After a single dose on an empty stomach, the mean Cmax is 2.5 ng/mL (range 1.1 to 4.4 ng/mL), reached within 1 to 2 hours. Its mean apparent volume of distribution is about 5 to 8 L/kg. Colchicine binds only weakly to serum protein, 39 ± 5%, and it binds mainly to albumin whatever the concentration. CYP3A4 helps metabolise colchicine into 2-O-demethylcolchicine and 3-O-demethylcolchicine. These metabolites are present in very small amounts, less than 5% of the parent drug in plasma. After multiple oral doses of 0.6 mg twice daily, the mean elimination half-life is 26.6 to 31.2 hours.
Pregnancy & Breastfeeding
Pregnancy Category C. There have been no adequate, well-controlled studies of colchicine in pregnant women. Colchicine passes into breast milk, so nursing mothers should use it only with caution.
⚠️ Talk to your doctor before taking any medicine during pregnancy or while breastfeeding.
Dosage Reference
⚠️ Reference ranges from official sources only. Consult your doctor for personalized dosing.
Side Effects & Interactions
Side Effects
No side-effect data recorded yet.