Colchicine mechanism of action hypertension

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A major alkaloid from Colchicum autumnale L. Its primary therapeutic use is in the treatment of gout, but it has here used also colchicine mechanism of action hypertension the wellbutrin alcohol abuse of familial Mediterranean fever periodic action hypertension. Colchicine is a highly poisonous alkaloid, originally extracted from plants of the genus Colchicum Autumn crocus, 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.

Colchicine - DrugBank

Its present medicinal use is mainly in the treatment action hypertension 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 read article of the condition.

The precise mechanism of action action hypertension not been here established. In patients with gout, colchicine apparently interrupts the cycle of monosodium urate crystal deposition in joint tissues colchicine mechanism the resultant inflammatory response that initiates and sustains an acute action hypertension. Colchicine decreases leukocyte chemotaxis and phagocytosis and inhibits colchicine mechanism formation and release of a chemotactic glycoprotein that is produced during phagocytosis of urate crystals.

Colchicine

Colchicine colchicine mechanism inhibits urate crystal deposition, which /diclofenac-sodium-gel-in-spanish.html enhanced by a low pH in colchicine mechanism tissues, probably by rosuvastatin calcium 10mg vs crestor oxidation of glucose and subsequent lactic acid production in leukocytes.

Colchicine has no analgesic or antihyperuricemic activity. Colchicine inhibits microtubule assembly in various cells, including leukocytes, probably by binding to action hypertension interfering with polymerization of the microtubule subunit tubulin. Although some studies have found that this action probably does not contribute significantly to colchicine's antigout action, a recent in vitro study has shown that it may be at least partially involved.

Colchicine is rapidly absorbed after oral administration, probably from action hypertension jejunum and ileum. However, the rate and extent of absorption are variable, depending on the tablet dissolution rate; colchicine mechanism of action hypertension in gastric emptying, intestinal motility, and pH at the absorption site; and the extent to which colchicine is bound to microtubules in gastrointestinal mucosal cells.

Although colchicine metabolites have not been identified in humans, metabolism by mammalian hepatic microsomes has been demonstrated in vitro.

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Enterohepatic recirculation and biliary excretion are also postulated to play a role in action hypertension elimination. Elimination half-life is approximately 1 hour in healthy subjects, although a study with an extended sampling time reported mean terminal elimination half-life values of approximately 9 to Other studies have reported half-life values of approximately 2 hours in patients with alcoholic cirrhosis and approximately 2.

The onset of toxic effects is usually delayed for several colchicine mechanism or more after the ingestion of an acute overdose. Nausea, colchicine mechanism of action hypertension, abdominal continue reading hypertension, and action hypertension occur first.

The diarrhea action hypertension be bloody due to hemorrhagic gastroenteritis. Burning sensations action hypertension the throat, stomach, and skin may be prominent symptoms.

Mechanism of action of colchicine in the treatment of gout.

Extensive vascular damage may result in shock. Kidney damage, evidenced by hematuria and oliguria, may occur.

Muscular weakness may be marked, and ascending paralysis of the central nervous system may develop; the patient action hypertension remains conscious.

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