Glimepiride is used along with diet and exercise, and sometimes with other medications, to treat type 2 diabetes (condition in which the body does not use insulin normally and, therefore, cannot control the amount of sugar in the blood). Glimepiride lowers blood sugar by causing the pancreas to produce insulin (a natural substance that is needed to break down sugar in the body) and helping the body use insulin efficiently. This medication will only help lower blood sugar in people whose bodies produce insulin naturally. Glimepiride is not used to treat type 1 diabetes (condition in which the body does not produce insulin and, therefore, cannot control the amount of sugar in the blood) or diabetic ketoacidosis (a serious condition that may occur if high blood sugar is not treated).
Indications and Usage
Glimepiride is an oral drug that belongs to a class of drugs called sulfonylureas. It helps to control blood sugar, along with a healthy diet and exercise. Taking glimepiride as directed, eating healthily, and exercising regularly can help to reduce your risk of complications from type 2 diabetes. It increases insulin secretion from beta cells; may also decrease rate of hepatic glucose production and increase insulin receptor sensitivity. It works by causing the pancreas to release insulin, which helps to lower blood sugar.
Mechanism of Action
In healthy subjects, the time to reach maximal effect (minimum blood glucose concentrations) was approximately 2-3 hours after single oral doses of glimepiride.
Glimepiride does not accumulate in serum following multiple dosing. The pharmacokinetics of glimepiride does not differ between healthy subjects and patients with type 2 diabetes. Clearance of glimepiride after oral administration does not change over the 1 mg to 8 mg dose range, indicating linear pharmacokinetics. In healthy subjects, the intra- and inter-individual variabilities of glimepiride pharmacokinetic parameters were 15-23% and 24-29%, respectively.
Distribution: After intravenous (IV) dosing in healthy subjects, the volume of distribution (Vd) was 8.8 l (113 ml/Kg), and the total body clearance (CL) was 47.8 ml/min. Protein binding was greater than 99.5%.
Metabolism: Glimepiride is completely metabolized by oxidative biotransformation after either an intravenous (IV) or oral dose. The major metabolites are the cyclohexyl hydroxy methyl derivative (M1) and the carboxyl derivative (M2). Cytochrome P450 C9 is involved in the biotransformation of glimepiride to M1. M1 is further metabolized to M2 by one or several cytosolic enzymes. M2 is inactive. In animals, M1 possesses about one-third of the pharmacological activity of glimepiride, but it is unclear whether M1 results in clinically meaningful effects on blood glucose in humans.
EExcretion: When 14 C-glimepiride was given orally to 3 healthy male subjects, approximately 60% of the total radioactivity was recovered in the urine in 7 days and M1 and M2 accounted for 80-90% of the radioactivity recovered in the urine. The ratio of M1 to M2 in the urine was approximately 3:2 in two subjects and 4:1 in one subject. Approximately 40% of the total radioactivity was recovered in feces and M1 and M2 (predominant) accounted for about 70% of that recovered in feces. M1 and M2 accounted for approximately 70% (ratio of M1 to M2 was 1:3) of the radioactivity recovered in feces. No parent drug was recovered from urine or feces. After IV dosing in patients, no significant biliary excretion of glimepiride or its M1 metabolite has been observed.
Hypoglycemia, dizziness, asthenia, headache, and nausea
Fertility, Pregnancy And Lactation
Category C: There are no adequate and well-controlled studies of glimepiride in pregnant women. Glimepiride should be used during pregnancy only if the potential benefit justifies the potential risk to the fetus. Because data suggest that abnormal blood glucose during pregnancy is associated with a higher incidence of congenital abnormalities, diabetes treatment during pregnancy should maintain the blood glucose levels as close to normal as possible.
Nonteratogenic effects: Prolonged severe hypoglycemia (4-10 days) has been reported in neonates born to mothers receiving a sulfonylurea at the time of delivery.
It is not known whether glimepiride is excreted in human milk. Based on these animal data and the potential for hypoglycemia in a nursing infant, a decision should be made whether to discontinue nursing or discontinue glimepiride, taking into account the importance of glimepiride to the mother.
Thiazides and other diuretics, corticosteroids, phenothiazines, thyroid products, oestrogens, phenytoin, nicotinic acid, sympathomimetics and CYP2C9 inducers may reduce hypoglycaemic effect of glimepiride. Reduced plasma concentration with colesevelam.
● Patient exposed to stress (e.g. fever, trauma, infection, surgery).
● Mild to moderate hepatic or renal impairment.
● Elderly, debilitated and malnourished patients.
Severe hypoglycemia with coma, seizure, or neurological impairment can be treated with glucagon or intravenous glucose. Continued observation and additional carbohydrate intake may be necessary because hypoglycemia may recur after apparent clinical recovery.