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Key Points About
Colchicine (Colcrys):

  • Colchicine is prescribed to
    treat or prevent Gout flares

  • Colchicine is not a pain
    medication and should not be
    used as such

  • Colchicine may reduce your
    body's ability to fight infection

  • Patients with liver or kidney
    disease, diabetes, HBP, or
    other serious health conditions
    should consider other
    Gout treatment options

  • Colchicine can cause serious
    side effects that should be
    discussed with your doctor

  • Is Colchicine (Colcrys) a Safe and Effective Gout Treatment?

    colchicine for gout

    COLCHICINE (Colcrys) is used to alleviate attacks. This drug can cause serious side effects and toxicity and even death in high doses.

    The side effects associated with colchicine highlight the potential risks of using this medication to treat gout. While it can effectively alleviate symptoms during acute attacks, it also carries significant risks, especially when used at higher doses.

    Gastrointestinal issues such as cramping, nausea, diarrhea, and vomiting are common among individuals taking colchicine, particularly at higher doses. However, more serious side effects, including bone marrow problems, muscle inflammation, severe anemia, and lowered white blood cell counts, can occur, posing a risk of infection.

    One of the unique mechanisms of colchicine involves binding to white blood cell proteins called neutrophils, inhibiting their migration to inflamed areas and suppressing the inflammatory response. While this action can provide relief from gout symptoms, it also interferes with the body's natural immune response and healing processes.

    Colchicine cannot cure Gout

    There are major limitations of medications like prednisone and colchicine in addressing the underlying cause of gout. While these medications can provide temporary relief from pain and inflammation during acute attacks, they do not address the root issue of uric acid crystal deposition.

    As we've pointed out, relying solely on symptomatic relief medications without addressing the underlying cause can lead to a vicious cycle of escalating pain, increasing medication use, and potential long-term health complications.

    To achieve lasting control over gout, it's essential to address the factors contributing to uric acid buildup and crystal formation. This often involves dietary and lifestyle changes aimed at reducing purine intake, maintaining a healthy weight, staying hydrated, and promoting kidney function. Additionally, incorporating natural remedies and supplements that support uric acid metabolism, inflammation reduction, and overall joint health can complement these lifestyle modifications.

    By taking a comprehensive approach to gout management that addresses both symptom relief and underlying causes, individuals can work towards achieving long-term control over their condition and minimizing the risk of recurrent attacks and associated complications.

    Expensive and Difficult to Obtain

    The accessibility and affordability issues surrounding colchicine highlight the challenges that individuals with gout face when seeking effective treatment options. Despite being a medication with a long history of use, the cost of colchicine has skyrocketed in recent years, making it prohibitively expensive for many patients.

    The lack of affordability and availability of colchicine underscores the importance of exploring alternative treatment approaches for managing gout. Relying solely on medications like colchicine, which may be both costly and difficult to obtain, is not a sustainable long-term solution. Instead, focusing on preventive measures and holistic treatment strategies can offer individuals with gout a more comprehensive approach to managing their condition.

    Study: NCBI- US National Library of Medicine Study: Colchicine poisoning- the dark side of an ancient drug

    {Clin Toxicol (Phila). 2010 Jun;48(5):407-14. doi:}


    Colchicine is used mainly for the treatment and prevention of gout and for familial Mediterranean fever (FMF). It has a narrow therapeutic index, with no clear-cut distinction between nontoxic, toxic, and lethal doses, causing substantial confusion among clinicians. Although colchicine poisoning is sometimes intentional, unintentional toxicity is common and often associated with a poor outcome.


    We performed a systematic review by searching OVID MEDLINE between 1966 and January 2010. The search strategy included "colchicine" and "poisoning" or "overdose" or "toxicity" or "intoxication."


    Colchicine is readily absorbed after oral administration, but undergoes extensive first-pass metabolism. It is widely distributed and binds to intracellular elements. Colchicine is primarily metabolized by the liver, undergoes significant enterohepatic re-circulation, and is also excreted by the kidneys. THERAPEUTIC AND TOXIC DOSES: The usual adult oral doses for FMF is 1.2-2.4 mg/day; in acute gout 1.2 mg/day and for gout prophylaxis 0.5-0.6 mg/day three to four times a week. High fatality rate was reported after acute ingestions exceeding 0.5 mg/kg. The lowest reported lethal doses of oral colchicine are 7-26 mg.


    CYP 3A4 and P-glycoprotein inhibitors, such as clarithromycin, erythromycin, ketoconazole, ciclosporin, and natural grapefruit juice can increase colchicine concentrations. Co-administration with statins may increase the risk of myopathy.


    Colchicine's toxicity is an extension of its mechanism of action - binding to tubulin and disrupting the microtubular network. As a result, affected cells experience impaired protein assembly, decreased endocytosis and exocytosis, altered cell morphology, decreased cellular motility, arrest of mitosis, and interrupted cardiac myocyte conduction and contractility. The culmination of these mechanisms leads to multi-organ dysfunction and failure. REPRODUCTIVE TOXICOLOGY AND LACTATION: Colchicine was not shown to adversely affect reproductive potential in males or females. It crosses the placenta but there is no evidence of fetal toxicity. Colchicine is excreted into breast milk and considered compatible with lactation.


    Colchicine poisoning presents in three sequential and usually overlapping phases: 1) 10-24 h after ingestion - gastrointestinal phase mimicking gastroenteritis may be absent after intravenous administration; 2) 24 h to 7 days after ingestion - multi-organ dysfunction. Death results from rapidly progressive multi-organ failure and sepsis. Delayed presentation, pre-existing renal or liver impairment are associated with poor prognosis. 3) Recovery typically occurs within a few weeks of ingestion, and is generally a complete recovery barring complications of the acute illness.


    History of ingestion of tablets, parenteral administration, or consumption of colchicine-containing plants suggest the diagnosis. Colchicine poisoning should be suspected in patients with access to the drug and the typical toxidrome (gastroenteritis, hypotension, lactic acidosis, and prerenal azotemia).


    Timely gastrointestinal decontamination should be considered with activated charcoal, and very large, recent (<60 min) ingestions may warrant gastric lavage. Supportive treatments including administration of granulocyte colony-stimulating factor are the mainstay of treatment. Although a specific experimental treatment (Fab fragment antibodies) for colchicine poisoning has been used, it is not commercially available.


    Although colchicine poisoning is relatively uncommon, it is imperative to recognize its features as it is associated with a high mortality rate when missed. PMID: 20586571 DOI: 10.3109/15563650.2010.495348 [Indexed for MEDLINE]

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