Colchicine is specifically used for acute attack of gout. It is not analgesic and relieves pain by controlling inflammation. But has very narrow therapeutic index so fallen out of favor and is hardly available.
Alkaloid obtained from Colchicum autumnale
Mechanism of Action
In acute inflammation for migration and macrophage functions microtubules are required. Polymerization of tubulin occurs. When colchicine binds tubulin, it prevents polymerization. Both chemotactic and phagocytic functions of macrophages are lost, thus
- Controls inflammation and
- Rapid proliferation of these inflammatory cells
For cell division, microtubules are required, as are inhibited, thus cell proliferation does not take place.
Colchicine also inhibits leukotrines B4 by unknown mechanism. Thus used for treatment of acute gout.
Well absorbed orally. Also used I/V.
Dose 0.6 mg initially. 0.6 mg after every two hours, till acute attack subsides. As little as 8 mg can be fatal.
Metabolites are partly excreted through liver, and partly through kidneys.
- GIT intolerance –where cells are rapidly dividing, nausea, vomiting, diarrhea, abdominal pain are1st sign of acute toxicity.
- Bone marrow suppression
- Hair loss
- Peripheral neuritis
- Burning throat pain
- Oliguria leading to hematuria
- Ascending CNS paralysis occurs because of respiratory paralysis