Gout, colchicine toxic effects

Other approaches to induce gastrointestinal discomfort have far more serious toxic effects. The chemical colchicine stops cell division (an antimitotic), producing severe nausea, vomiting, and dehydration, which can lead to delirium, neuropathy, and kidney failure. On the other hand, colchicine is used in the treatment of gout and has been studied as an anticancer agent because it stops cell division. Most toxic of all are plants that produce lectins, and the most toxic of these is the chemical ricin produced by castor beans. Only 5 to 6 seeds are necessary to kill a small child. Fortunately, following oral consumption much of the ricin is destroyed in the stomach. Ricin is extremely effective at stopping protein synthesis, so much so that direct exposure to only 0.1 pg/kg can be fatal. 

Colchicine dramatically relieves acute attacks of gout. It is effective in roughly two-thirds of patients if given within 24 hours of the onset of the attack. Pain, swelling, and redness abate within 12 hours and are completely gone within 48-72 hours. The typical oral dose is 0.6 mg each hour for a total of three doses. This dose should not be exceeded. Treatment with colchicine should not be repeated within 7 days to avoid cumulative toxicity. 

Colchicine interferes with cell division and gastrointestinal toxicity limits the amounts which can be given for the control of acute gout. It also has toxic effects on the blood and peripheral nerves. In overdosage, colchicine is a very dangerous drug. 

Colchicine is an antimitotic drug that is highly effective in relieving acute gout attacks but has a low benefit-toxicity ratio. When colchicine is started within the first 24 hours of an acute attack, about two-thirds of patients respond within several hours. The likelihood of success decreases substantially if treatment is delayed longer than 48 hours after symptom onset. 

Although colchicine is more specific in gout than the NSAIDs, NSAIDs (eg, indomethacin and other NSAIDs [except aspirin]) have replaced it in the treatment of acute gout because of the troublesome diarrhea sometimes associated with colchicine therapy. Colchicine is now used for the prophylaxis of recurrent episodes of gouty arthritis, is effective in preventing attacks of acute Mediterranean fever, and may have a mild beneficial effect in sarcoid arthritis and in hepatic cirrhosis. Although it can be given intravenously, this route should be used cautiously because of increased bone marrow toxicity. 

Colchicine is a poisonous tricyclic tropane alkaloid from the autumn crocus (Colchicum autumnale) and gloriosa lily (Gloriosa superba). This alkaloid is a potent spindle fiber poison, preventing tubulin polymerization.25 Colchicine has been used as an effective anti-inflammatory drug in the treatment of gout and chronic myelocytic leukemia, but therapeutic effects are attainable at toxic or near toxic dosages. For this reason, colchicine and its analogs are primarily used as biochemical tools in the mechanistic study of new mitotic inhibitors. 

Colchicine (23) is a toxic substance occurring in Colchicum autumnale, it contains the nucleus of pyrogallol trimethyl ether. Colchicine has been used in the treatment of acute gout, and in plant genetics research to effect doubling of chromosomes. 

Colchicine provides dramatic relief from acute attacks of gout. The effect is sufficiently selective that the drug has been used for diagnostic purposes, but the test is not infallible. Colchicine also has an established role in preventing and aborting acute attacks of gout. However, its toxicity and the availability of alternative agents that are less toxic have substantially lessened its usefulness. 

Colchicine is an antimitotic agent, highly effective in the treatment of gout, but associated with considerable toxicity. Diarrhea is used as a criterion for adequate dosage. Accidental overdosage occurs relatively often and can be dangerous. For these reasons, NSAIDs (except aspirin) are often used in acute gout instead of colchicine. 

Acute reversible ciclosporin toxicity occurred in a renal transplant patient a few days after colchicine was administered for an acute attack of gout (SEDA-16, 115). Other potential adverse effects of combining colchicine with ciclosporin include diarrhea, increases in serum liver enzymes, bilirubin, and creatinine, and less often severe myalgia (SEDA-19, 101). Acute myopathy, associated with neuropathy in one case, has been observed in two young renal transplant recipients (SEDA-22, 119). 

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