Colcrys (Colchicine) 0.5mg

Last updated on April 30, 2024

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Colcrys may be marketed under different names in various countries. All of them contain Colchicine as main ingredient. Some of them are the following: Artrichine, Cochic, Colchicina, Colchicindon, Colchicinum, Colchicum, Colchidrint, Colchimedio, Colchiquim, Colchis, Colchisol, Colchysat, Colcitrat, Colcout, Colcrys, Colgout, Conicine, Cp-colchi, Dochicin, Goutichine, Goutnil, Kolsin, Lengout, Sixol, Tolchicine, Xuric.

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ColchicineWhat Is Colcrys (Colchicine)?

Colcrys, also known as Colchicine, is a medication commonly prescribed to treat gout, a type of arthritis caused by the buildup of uric acid crystals in the joints. It works by reducing inflammation and inhibiting the movement of white blood cells to the affected areas, thus alleviating pain and discomfort associated with gout attacks. Typically administered orally, Colcrys is often prescribed in a low dose, such as 0.5mg, to manage acute gout flares or as a preventive measure to reduce the frequency of recurrent attacks. Following the prescribed dosage and consulting a healthcare professional to monitor potential side effects or interactions with other medications is essential. Individual responses may vary with any medication, and discussing any concerns or medical history with your healthcare provider is crucial.


Peak plasma concentrations of Colchicine are reached within 2 hours of oral use. Colchicine is partially deacetylated in the liver, and the unchanged drug and its metabolites are excreted in the bile and undergo intestinal reabsorption. Colchicine is found in high concentrations in leucocytes, kidneys, the liver, and spleen. Most of the drug is excreted in the feces, but 10 to 20% is excreted in the urine, and this proportion rises in patients with liver disorders. Colchicine is distributed into breast milk.

Uses and Administration

Colchicine relieves acute gout and prevents acute attacks, particularly during the first few months of treatment with allopurinol or uricosurics. Colchicine produces a dramatic response in acute gout, probably by reducing the inflammatory reaction to urate crystals; this effect might be due to several actions, including decreased leucocyte mobility. It is not an analgesic and does not affect blood concentrations of uric acid or the excretion of uric acid. Colchicine also has an antimitotic action. Colchicine has also been used in several other conditions, including amyloidosis, Behcet’s syndrome, familial Mediterranean fever, idiopathic thrombocytopenic purpura, pericarditis, primary biliary cirrhosis, and pyoderma gangrenosum.

If Colchicine is used for acute attacks of gout, then treatment should be started as soon as possible, and an effect may be expected within 12 hours. The recommended oral dose in the UK is 1 mg initially, then 500 micrograms every 2 to 3 hours until pain relief or gastrointestinal adverse effects occur (see also Administration section). Although some licensed products allow doses up to a maximum of 10 mg, the BNF considers that the total dose should not exceed 6 mg. At least three days should elapse before another course is given. In the USA, the oral dose is 1 to 1.2 mg initially; this may be repeated every 2 hours or 500 or 600 micrograms may be taken every hour (or even every 2 or 3 hours if sufficient) until the pain is relieved or gastrointestinal adverse effects occur. The maximum total dose for an acute attack should not exceed 8 mg.

Colchicine has sometimes been given intravenously in a dose of 1 or 2 mg over 2 to 5 minutes with additional dosesof0.5 or 1 mg every 6 hours as required to a total dose of not more than 4 mg in 24 hours; once this amount of Colchicine has been given further doses should not then be given by any route for at least seven days. For the view that the intravenous route should be avoided, see the Administration section. When used to prevent gout, oral doses are 500 or 600 micrograms once daily; some patients may require doses up to 1.8 mg daily.

Consideration should be given to using reduced dosages in patients with renal impairment.


Although colchicine 1 mg orally, followed by 500 micrograms every 2 to 3 hours, is recommended in the UK for the treatment of acute gout, many rheumatologists consider this excessive; a low-dose regimen of 500 micrograms no more than three times daily has been advocated in preference. It has also been suggested that intravenous Colchicine, although undoubtedly effective, should not be used because of the risk of severe or fatal adverse effects. For reports of fatalities with intravenous Colchicine during unlicensed use, see the Inappropriate Administration section.

Administration in Renal Impairment

Some licensed product information in the UK recommends that the dose of oral Colchicine should be reduced by up to 50% in patients with mild to moderate renal impairment and that it should not be used in those with severe impairment. Various sources in the USA have made similar recommendations; for example, the American Hospital Formulary Service notes that some recommend the prophylactic oral dose should not exceed 600 micrograms daily in patients with a serum creatinine of 1.6 mg per lOOmL or greater or with a creatinine clearance (CC) of 50mL/minute or less. Some patients may only need 600 micrograms every alternate day. The intravenous dose should be reduced by 50% in patients with a CC of between 10 and 50 mL/minute, and it is contra-indicated in those patients with a CC of less than 10 mL/minute.


Colchicine is well known to have a helpful role in amyloidosis secondary to familial Mediterranean fever, where results have suggested the possibility of reversing nephropathic changes due to renal amyloid deposition (see below). However, combination therapy with melphalan and prednisone was found to be more effective than Colchicine alone in primary amyloidosis, and a later study found no benefit in adding Colchicine to the standard therapy. The mechanism of the anti-amyloid effect of Colchicine is not precise.

Behcet’s Syndrome

Behcet’s syndrome has been treated with numerous drugs. Where possible, topical treatment of local lesions should be tried before starting systemic therapy. Corticosteroids are favored for systemic treatment in many countries, but Colchicine has also been widely used. Beneficial responses have been described for most of the symptoms, including the arthritic, ocular, and cutaneous manifestations, although a systematic review has questioned Colchicine’s efficacy. The mechanism of action in this condition is believed to be based on the effect on polymorphonuclear leucocytes and other cellular effects. Colchicine has also been used with corticosteroids for acute exacerbations, followed by colchicine maintenance; Colchicine with aspirin has also been recommended in acute disease, and Colchicine with benzathine benzylpenicillin has been tried.

Diffuse Parenchymal Lung Disease

Colchicine is a potential alternative to corticosteroid therapy in patients with cryptogenic fibrosing alveolitis (see Diffuse Parenchymal Lung Disease). However, the degree of benefit, if any, is unclear, although Colchicine does appear to be safer and better tolerated than corticosteroid therapy.

Familial Mediterranean Fever

Familial Mediterranean fever (recurrent or paroxysmal polyserositis; periodic disease) is an inherited disorder that primarily affects Sephardic Jews or persons of Arab, Armenian, or Turkish ancestry. It is characterized by attacks of acute abdominal pain, fever, and signs of peritonitis, which resolve spontaneously, usually in 24 to 48 hours. Pleuritic chest pain, arthritis, skin rash, pericarditis, and headache may occur. The most dangerous complication, however, is type AA amyloidosis, which can lead to nephrotic syndrome, renal failure, and death.

Familial Mediterranean fever is managed with Colchicine. Colchicine cannot stop an established attack, but, given prophylactically in oral adult doses of 1 to 3 mg daily, it reduces the frequency of attacks, prevents amyloidosis, and reverses proteinuria. An initial daily dose of 500 micrograms or less has been suggested for children younger than five years of age, 1 mg for those aged 5 to 10 years, and 1.5 mg for children aged over ten years; doses may be increased in a stepwise fashion to a maximum of 2 mg daily if needed. Attacks are usually treated with NSAIDs or, in severe cases, opioids. Anecdotal evidence has suggested that prazosin may also be of benefit, but initial reports of improvement with interferon alfa have not been borne out. Anakinra has also been investigated.

Idiopathic Thrombocytopenic Purpura

In idiopathic thrombocytopenic purpura, refractory to standard therapy, a few patients have had a partial or complete response to Colchicine, and further studies have been suggested.


Mild cases of recurrent pericarditis may be treated with Colchicine as an adjunct to NSAID therapy. It may also provide effective prevention, allowing the tapering of corticosteroids, usually reserved for treating severe acute attacks. The drug has also been used successfully in children. In an open-label study, Colchicine added to conventional therapy with aspirin or prednisone significantly decreased the recurrence rate in patients with a first episode of recurrent pericarditis compared with conventional therapy alone. Another open-label study had similar results using adjunctive Colchicine for the first episode of acute pericarditis. Colchicine was found to be highly effective in preventing recurrence in patients with two or more relapses of acute pericarditis. The proportion of patients with relapses during or after colchicine therapy was significantly higher, and the duration of colchicine therapy was significantly longer in those who had pre-treatment with corticosteroids.

Peyronie’s Disease

Beneficial effects of Colchicine have been reported in men with Peyronie’s disease. Small studies show Colchicine to be most effective in reducing pain during penile erection. A combination of vitamin E and Colchicine has also been suggested as an alternative to treat early disease.

Primary Biliary Cirrhosis

Primary biliary cirrhosis is a chronic progressive liver disease with no specific treatment, and in general, drug therapy has been poor or largely ineffective. Reviewers have noted that several studies have been conducted with Colchicine, and although biochemical parameters were improved, a beneficial effect on clinical symptoms or liver histology was not found. A comparative study of Colchicine and methotrexate showed that while both drugs improved biochemical test results and symptoms, the response to methotrexate was more significant. Some consider that combination therapy with Colchicine, methotrexate, and ursodeoxycholic acid may be more promising than monotherapy.

Pyoderma Gangrenosum

Pyoderma gangrenosum associated with inflammatory bowel disease has been successfully treated with Colchicine in 2 patients. Colchicine was also beneficial in 3 patients with pyoderma associated with familial Mediterranean fever. Other isolated reports include the use of low-dose Colchicine in idiopathic pyoderma gangrenosum.

Adverse Effects and Treatment

The most frequent adverse effects of oral Colchicine are those involving the gastrointestinal tract and may be associated with its antimitotic action. Diarrhea, nausea, vomiting, and abdominal pain are often the first signs of toxicity and are usually an indication that colchicine therapy should be stopped or the dose reduced. Larger doses may cause profuse diarrhea, gastrointestinal bleeding, skin rashes, and renal and hepatic damage.

Rarely, bone marrow depression with agranulocytosis, thrombocytopenia, and aplastic anemia have occurred on prolonged treatment, as have peripheral neuropathy, myopathy, rashes, and alopecia. Adverse effects after intravenous use include cardiac arrhythmias and local reactions such as thrombophlebitis and neuritis. Extravasation may cause tissue necrosis.

Symptoms of acute overdosage with oral Colchicine often do not appear for 2 to 12 hours. The first signs of toxicity are nausea, vomiting, and diarrhea; a burning sensation in the throat, stomach, and skin may also occur. The diarrhea may be severe and hemorrhagic and, coupled with vascular damage or paralytic ileus, can lead to dehydration, hypotension, and shock. Multiple organ failure may occur, manifesting as CNS toxicity (confusion, delirium, sometimes coma), bone marrow depression, hepatocellular damage, muscle damage, neuropathy, respiratory distress, myocardial depression, and renal damage. A toxic epidermal necrolysis-like reaction has also been reported. Death may be due to respiratory depression, cardiovascular collapse, or sepsis after pancytopenia. In surviving patients, alopecia, rebound leucocytosis, and stomatitis may occur about ten days after the acute overdose. The lethal dose varies: 7 mg of Colchicine has caused death, yet recovery has occurred after much larger doses.

When treating colchicine overdosage or acute poisoning, patients should be carefully monitored for some time to take account of the delayed onset of symptoms. The stomach may be emptied by lavage in adults within 1 hour of acute poisoning; multiple doses of activated charcoal should be given to adults and children who have ingested more than 300 micrograms/kg of Colchicine, provided vomiting has not started. Treatment is primarily symptomatic and supportive, focusing on respiration control, blood pressure and circulation maintenance, and fluid and electrolyte imbalance correction.

ColchicineEffects on the Neuromuscular System

Colchicine-induced myoneuropathy may be a common but unrecognized condition in patients with reduced renal function who receive usual doses of Colchicine. Although skeletal muscles and peripheral nerves are affected, myopathy is most prominent and associated axonal neuropathy is mild. The condition usually presents with proximal muscle weakness and is accompanied by elevated serum creatine kinase concentrations. Withdrawal of Colchicine leads to spontaneous remission of these symptoms within a few weeks, but resolution of the polyneuropathy is slow. Examination of proximal muscles shows marked abnormal spontaneous activity, and because of the features of the condition, it is often misdiagnosed as probable polymyositis or uraemic myopathy. A literature review identified renal impairment as the primary risk factor for the development of colchicine-induced myopathy; dosage adjustment is advised in these patients.

There have been reports suggesting colchicine-induced myopathy may develop in patients who have normal renal function. A patient with normal renal function but chronic alcohol-induced liver disease developed an unusual form of myoneuropathy after receiving only a short course of Colchicine. This patient was also taking tolbutamide, the microsomal enzyme-inhibiting activity of which may have exacerbated the toxicity of Colchicine. A teenager with familial Mediterranean fever who had normal renal and hepatic function developed toxic myopathy due to colchicine use. Myopathy improved after Colchicine was stopped and recurred when it was restarted at a lower dose. Rhabdomyolysis has also been reported.

Effects on the Reproductive System

UK licensing information states that Colchicine may adversely affect spermatogenesis under certain conditions of therapy. Animal data has shown that Colchicine in high doses may arrest spermatogenesis and lead to azoospermia. However, in clinical practice, male infertility is not expected in patients given Colchicine. It may be related in some cases to the underlying disease rather than the drug. Similarly, although Colchicine is not recommended in the first trimester of pregnancy, it may improve fertility in women with familial Mediterranean fever, and results in women who have been taking Colchicine at conception and during pregnancy have been relatively reassuring (see also under the Pregnancy section).

Inappropriate Administration

Intravenous use of Colchicine is associated with a risk of severe or fatal adverse effects (see Administration section). Although unlicensed either orally or parenterally for use in back pain, intravenous Colchicine has been used in alternative medicine for this indication. As of February 2008, the FDA had received reports of 50 adverse events, including 23 deaths, associated with the unapproved use of intravenous Colchicine. Three of the reported deaths were associated with compounded Colchicine that, due to preparation errors, was 8 times more potent than the amount stated on the label. Potentially fatal effects include neutropenia, thrombocytopenia, pancytopenia, acute renal failure, and congestive heart failure.


Colchicine should be given with great care to elderly or debilitated patients who may be particularly susceptible to cumulative toxicity. It should also be used cautiously in patients with cardiac, hepatic, renal, or gastrointestinal disease. Colchicine should be avoided in patients with blood disorders. It should also generally be avoided in pregnancy since it is known to be teratogenic in animals, and there have also been some suggestions of a risk of fetal chromosome damage in humans.

Colchicine should not be given by subcutaneous or intramuscular injection as it causes severe local irritation.


Colchicine is distributed into breast milk, and some have recommended waiting 8 hours or 12 hours after a dose before breastfeeding to minimize the infant’s exposure. However, since no adverse effects on the infant have been noted in these reports, the American Academy of Pediatrics considered its use to be usually compatible with breastfeeding.


Colchicine is contra-indicated in pregnancy because of animal teratogenicity. However, it has been used during pregnancy in women with familial Mediterranean fever. There was no increase in the abnormality rate of the newborns, and no problems were detected in 130 offspring.


Colchicine toxicity may result from its use with clarithromycin, erythromycin, or tolbutamide. Thiazide diuretics may increase serum uric acid and interfere with its activity. Muscle disorders have been reported when Colchicine is used with ciclosporin. Colchicine may also impair the absorption of vitamin B12.

Cardiovascular Drugs

An acute myopathy has been reported in patients with chronic renal impairment given Colchicine with simvastatin. Similar effects have been seen in patients with renal impairment given Colchicine with fluvastatin or pravastatin. Since many statins are metabolized by the cytochrome P450 isoenzyme CYP3A4, as is Colchicine, this has been proposed as one possible mechanism. However, fluvastatin and pravastatin are cleared through different isoenzymes. Alternative proposed mechanisms are synergistic myopathy or interference with transport mediated by P-glycoprotein. Tetraparesis developed in a patient who took Colchicine with verapamil; this was considered to be due to a pharmacokinetic interaction that increased serum and CSF concentrations of Colchicine.


There is a need for caution if Colchicine is used with ciclosporin. Myopathies or rhabdomyolysis may be a problem, especially in transplant patients or those with renal impairment. In addition, increased blood-ciclosporin concentrations and nephrotoxicity developed in a renal transplant patient after the introduction of colchicine therapy.


Life-threatening colchicine toxicity has been described after use for two weeks with erythromycin in a patient with hepatic and renal impairment. In a patient with end-stage renal disease but no hepatic impairment, fatal colchicine toxicity developed after four days of clarithromycin therapy. A patient with moderate chronic renal impairment developed acute but non-fatal colchicine intoxication on day 4 of a 7-day Helicobacter pylori treatment course containing clarithromycin. A retrospective study of 116 patients given both drugs concluded that clarithromycin increased the risk of colchicine toxicity, especially in those patients with renal impairment, and that the two drugs should not be used together.


For a suggestion that tolbutamide may have exacerbated the toxicity of Colchicine in a patient with liver disease, see Effects on the Neuromuscular System section.

Colcrys is a vital drug for the treatment of gout since it relieves the severe pain and inflammation that come with the disease. Colcrys has established itself as a mainstay in the gout patient’s treatment regimen thanks to its capacity to lower uric acid levels and lessen the likelihood of acute attacks. As with any drug, speaking with a healthcare provider is essential to ascertain suitability and ensure it is used correctly for the best possible therapeutic results.  

Drug Nomenclature

Synonyms: Colchicine; Colchicinum; Kolchicin; Kolchicinas; Kolkicin; Kolkisiini

Chemical name: (S)-N-(5,6,7,9-Tetrahydro-1,2,3,10-tetramethoxy-9-oxobenzo[α]heptalen-7-yl)acetamide

Molecular formula: C22H25NO6 =399.4

CAS: 64-86-8

ATC code: M04AC01

Read code: y031L

Description. Colchicine is an alkaloid obtained from various Colchicum spp.

Pharmacopoeias. In China, Europe, Japan, and the US. China also has a monograph for colchicine amide.

European Pharmacopoeia, 6th ed., 2008, and Supplements 6.1 and 6.2 (Colchicine). It is a yellowish-white amorphous or crystalline powder. It is very soluble in water and rapidly recrystallizes from concentrated solutions as a sesquihydrate; it is freely soluble in alcohol and chloroform. Protect from light.

The United States Pharmacopeia 31, 2008, and Supplements 1 and 2 (Colchicine). Colchicine is an alkaloid obtained from various Colchicum spp. and other genera. It is pale yellow to pale greenish-yellow amorphous scales, powder, or crystalline powder. It is odorless or nearly so and darkens on exposure to light. It is soluble in 1 in 25 of water and 1 in 220 of ether; it is freely soluble in alcohol and chloroform. Store in airtight containers. Protect from light.

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