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Glimepiride (original trade name Amaryl ) is an orally available medium-to-long-acting sulfonylurea antidiabetic drug. It is sometimes classified as either the first third-generation sulfonylurea,
1 Indications
2 Contraindications
3 Adverse effects
4 Pharmacokinetics
5 Mechanism of action
6 Interactions
7 References
8 External links
Main article: Sulfonylurea
Glimepiride is indicated to treat type 2 diabetes mellitus ; its mode of action is to increase insulin secretion by the pancreas. However it requires adequate insulin synthesis as prerequisite to treat appropriately. It is not used for type 1 diabetes because in type 1 diabetes the pancreas is not able to produce insulin.
Its use is contraindicated in patients with hypersensitivity to glimepiride or other sulfonylureas.
Adverse effects
Side effects from taking glimepiride include gastrointestinal tract (GI) disturbances, occasional allergic reactions, and rarely blood production disorders including thrombocytopenia, leukopenia, and hemolytic anemia. In the initial weeks of treatment, the risk of hypoglycemia may be increased. Alcohol consumption and exposure to sunlight should be restricted because they can worsen side effects.
Two generic oral tablets of glimepiride, 2 mg each
Gastrointestinal absorption is complete, with no interference from meals. Significant absorption can occur within one hour, and distribution is throughout the body, 99.5% bound to plasma protein. Metabolism is by oxidative biotransformation, it is hepatic and complete. First, the medication is metabolized to M 1 metabolite by CYP2C9. M 1 possesses about ​ 1 ⁄ 3 of pharmacological activity of glimepiride, yet it is unknown if this results in clinically meaningful effect on blood glucose. M 1 is further metabolized to M 2 metabolite by cytosolic enzymes. M 2 is pharmacologically inactive. Excretion in the urine is about 65%, and the remainder is excreted in the feces.
Mechanism of action
Main article: Sulfonylurea
Like all sulfonylureas, glimepiride acts as an insulin secretagogue. It lowers blood sugar by stimulating the release of insulin by pancreatic beta cells and by inducing increased activity of intracellular insulin receptors.
Not all secondary sufonylureas have the same risk of hypoglycemia. Glibenclamide (glyburide) is associated with an incidence of hypoglycemia of up to 20–30%, compared to as low as 2% to 4% with glimepiride. Glibenclamide also interferes with the normal homeostatic suppression of insulin secretion in reaction to hypoglycemia, whereas glimepiride does not. Also, glibenclamide diminishes glucagon secretion in reaction to hypoglycemia, whereas glimepiride does not.
Nonsteroidal anti-inflammatory drugs (such as salicylates ), sulfonamides, chloramphenicol, coumadin and probenecid may potentiate the hypoglycemic action of glimepiride. Thiazides, other diuretics, phothiazides, thyroid products, oral contraceptives, and phenytoin tend to produce hyperglycemia.

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