Key Points About
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 (Colcrys) is used to alleviate attacks. This drug can cause serious side effects and toxicity and even death in high doses.
Side Effects: 80% of people who take colchicine in doses that are high enough to be effective develop stomach problems, such as cramping, nausea, diarrhea, or vomiting. Serious side effects of colchicine include bone marrow problems, muscle inflammation, severe anemia, and extremely low white blood counts that can increase the risk of infection developing. Colchicine is usually avoided or the dose adjusted in people who have reduced kidney function.
Colchicine is not like any other pain reliever or anti-inflammatory. This drug literally binds to the proteins of our white blood cells known as neutrophils. This halts the cells from migrating to the 'infected' area to do their normal job of trying to heal the area. By stopping this migration, you are avoiding the inflammatory reaction that comes with the healing process. This can work wonders, but should we really be unnaturally altering our immune system in this manner? We think not! This is precisely why the dangers of its immunosuppressive side effects should not be taken lightly.
Colchicine cannot cure Gout
The problem with this medication, aside from it's scary side effects, is that it doesn't actually do a single thing to address the root problem, the building uric acid deposits. It can truly be a magical drug for someone under a current attack and bring a false sense of reality when it comes to future Gout control.
Couple Colchicine with a pain killer and that relief is all anyone can see at that moment of desperation. This temporary fix will do nothing to remove the uric acid crystals that triggered the attack, and so the cycle begins.
The uric acid crystal deposits continue to build, as does the intensity, frequency, and length of the future attacks. More medication is usually needed than before, and often additional medications are necessary to bring you the relief you previously experienced. This vicious cycle will continue unless you address the real problem. If you don't believe us, talk to anyone suffering with Chronic Gout and living with tophi deformities. Ask them directly about their history of Gout medications and the progression of those medications. Ask them about their liver and kidney tests after years on these medications. The truth may be hard to swallow, but let it be your guide and the determining factor for obtaining REAL Gout Control.
Colchicine is difficult to get a hold of now and extremely expensive. This medicine has been around for a very long time, some 200 years, but is no longer under a patent and wasn't available as a generic medication for quite a while. When the monopoly on this drug ended 9 years ago the price went up 5000%. A few years later a generic brand was introduced, but remained extremely expensive. This problem is yet another reason to avoid relying on these drugs to save you in a desperate situation. Not only will they never address the real problem, but they may be completely unattainable when you need them the most. A good maintenance plan will help you avoid ever having to rely on these quick fixes again -- an invaluable peace of mind AND a real solution to your Gout control is possible with our product(s) and program.
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: 10.3109/15563650.2010.495348.
(Finkelstein Y1, Aks SE, Hutson JR, Juurlink DN, Nguyen P, Dubnov-Raz G, Pollak U, Koren G, Bentur Y.)
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.
MECHANISMS OF TOXICITY:
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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