Molecular Mechanism of Action
The pharmacological effects of colchicine are based on its ability to penetrate blood cells and concentrate there in high volumes.
- The substance interacts with $\alpha$- and $\beta$-tubulin.
- Complete blockade of microtubule formation occurs.
Disruption of this intracellular structure leads to a cascade of cellular changes that ultimately halts the development of the inflammatory response.
Cellular Effects
The loss of microtubules disrupts normal leukocyte function:
- Antimitotic effect: cell division and overall leukopoiesis are inhibited.
- Impaired motility: migration of cellular components is blocked, and exocytosis of biologically active substances ceases.
- Chemotaxis blockade: leukocytes lose the ability to directionally migrate to the site of inflammation.
- Impaired phagocytosis: cells cannot engulf urate crystals.
As a result, the release of inflammatory mediators is reduced, leading to rapid resolution of the attack.
Pharmacokinetics and Elimination
Upon oral administration, the drug is characterized by rapid absorption in the gastrointestinal tract.
- The half-life ($t_{1/2}$) is approximately 1 hour.
- Elimination occurs predominantly via bile.
- The compound is also characterized by pronounced enterohepatic recirculation.
Adverse Reactions
The use of colchicine is accompanied by several adverse effects that are important to consider in clinical practice:
- Gastrointestinal: the most frequent manifestations include loss of appetite, nausea, vomiting, and diarrhea.
- With prolonged use: bone marrow suppression may occur, driven by the antimitotic effect of the drug.