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1212 Colchicine
Abbot
0.6mg
100
50.88
out of stock
1213 Colgout tabs (Colchicine)
Generic
500mcg
100 tabs
50.88
ma211 Colchicum Dispert (Generic Colchicine)
Dr Frik
Turkey
0.5mg
50 tabs
49.00

General Description & Use
Treats gout attacks, gouty arthritis, and other medical problems.

Buy Colchicine Colgout tabs Colchicum Dispert and Generic ColchicineColchicine (Colgout tabs, Colchicum Dispert and Generic Colchicine) is originally extracted from plants of the genus Colchicum (Autumn crocus, Colchicum autumnale, also known as the "Meadow saffron"). Originally used to treat rheumatic complaints and especially gout, it was also prescribed for its cathartic and emetic effects. Its present medicinal use is mainly in the treatment of gout; as well, it is being investigated for its potential use as an anti-cancer drug. It can also be used as initial treatment for pericarditis and preventing recurrences of the condition. In neurons, axoplasmic transport is disrupted by colchicine.

Colchicine is Food and Drug Administration (FDA)-approved for the treatment of gout and also for familial Mediterranean fever, secondary amyloidosis(AA), and scleroderma. It is also used as an anti-inflammatory agent for long-term treatment of Behçet's disease. The Australian biotechnology company Giaconda has developed a combination therapy to treat constipation-predominant irritable bowel syndrome which combines colchicine with the anti-inflammatory drug olsalazine.

A British drug development company is developing a prodrug of colchicine, ZD6126 (also known as ANG453) as a treatment for cancer. Colchicine has a relatively low therapeutic index. Colchicine is "used widely" off-label by naturopaths for a number of treatments, including the treatment of back pain.

News in 2008
Sometimes during surgery to remove a tumor, cells become detached from the bulk of the tumor. In a small number of cases, these tumor cells stick to cells at the site of the surgical wound and go on to form a secondary tumor, having an enormous negative impact on the survival and quality of life of the patient.

New data, generated at the John D. Dingell VA Medical Center and Wayne State University, Detroit, using a mouse model of surgery to remove a colon cancer tumor, suggest that perioperative treatment with colchicine might decrease the incidence of tumor formation at the site of the surgical wound. When colon cancer tumor cells are exposed to high pressure they exhibit an increased ability to stick to other cells. In the study, to mimic the conditions of surgery, the authors removed colon cancer cells from one mouse, exposed them to high pressure in vitro, and then transplanted them into a second mouse that they monitored for the development of tumors at the site of the surgical wound.

The most important observation made was that if the mice from which the colon cancer cells came from were treated perioperatively with colchicine there was a dramatic decrease in the number of tumors that formed at the site of the surgical wound in the second mouse.

As in vitro exposure of tumor cells from breast and head and neck cancers to high pressure also increases their ability to stick to other cells it is possible that these data might have implications in several clinical settings.

Colchicine inhibits microtubule polymerization by binding to tubulin, one of the main constituents of microtubules. Availability of tubulin is essential to mitosis, and therefore colchicine effectively functions as a "mitotic poison" or spindle poison. Since one of the defining characteristics of cancer cells is a significantly increased rate of mitosis, this means that cancer cells are significantly more vulnerable to colchicine poisoning than are normal cells. However, the therapeutic value of colchicine against cancer is (as is typical with chemotherapy agents) limited by its toxicity against normal cells.

Apart from inhibiting mitosis, a process heavily dependent on cytoskeletal changes, colchicine also inhibits neutrophil motility and activity, leading to a net anti-inflammatory effect. Colchicine also inhibits urate crystal deposition, which is enhanced by a low pH in the tissues, probably by inhibiting oxidation of glucose and subsequent lactic acid production in leukocytes. The inhibition of uric acid crystals is a vital aspect on the mechanism of gout treatment.

Side effects
Side effects include gastro-intestinal upset and neutropenia. High doses can also damage bone marrow and lead to anaemia. Note that all of these side effects can result from hyper-inhibition of mitosis.

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