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The acute gout initiates an inflammatory response and releases a glycoprotein. The release of glycoprotein aggravates the inflammation by increasing lactic acid production from inflammatory cells and by releasing lysosomal enzymes. The increased lactic acid production decreases the local pH and cause more precipitation of urate crystals in the joint. The release of lysosomal enzymes causes joint destruction. Colcrys inhibits the synthesis of glycoprotein and subsequent events by binding to protein tubulin. Colcrys inhibits granulocyte migration into the inflamed joint.

The common side effects reported with Colcrys are bone marrow depression, aplastic anemia, agranulocytosis, thrombocytopenia, peripheral neuritis, purpura, myopathy, loss of hair, reversible azoospermia, vomiting, diarrhea, nausea , dermatoses and hypersensitivity reactions.

Colcrys should be administered with caution along with acidifying and alkalinizing agents. The action of acidifying agents is inhibited by Colchicine and action of alkalinizing agents is potentiated by Colchicine. Colchicine and CNS depressants should not be administered together as Colcrys increases the sensitivity of CNS depressants. The response to sympathomimetic agents is enhanced by Colcrys. Colcrys should be administered with caution in elderly patients and in patients with gastrointestinal, renal, hepatic, cardiac, or hematological disorders. Colchicine should not be administered in pregnant women and in nursing mothers. If it is an absolute must to take Colcrys during pregnancy and lactation, it should be administered under the supervision of a medical practitioner.

The recommended starting dosage of Colcrys to relieve or abort an attack is 1 to 1.2 mg (two 0.5 mg granules or two 0.6 mg tablets). This dose may be followed by one unit of either granule or tablet preparation every hour, or two units every two hours, until pain is relieved.