Each extended release tablet contains Metformin Hydrochloride 500 mg.
Pharmacology: Pharmacodynamics: Metformin tablets are oral antihyperglycemic drugs used in the management of type 2 diabetes mellitus. It contains 500 mg of metformin hydrochloride as the active ingredient and the inactive ingredients are hydroxypropyl methyl cellulose, polyvinyl pyrrolidone, magnesium stearate, and talc. Metformin is an antihyperglycemic agent which improves glucose tolerance in patients with type 2 diabetes mellitus, lowering both basal and post prandial plasma glucose. Its pharmacologic mechanisms of action are different from other classes of oral antihyperglycemic agents. Metformin decreases hepatic glucose production, decreases intestinal absorption of glucose and improves insulin sensitivity by increasing peripheral glucose uptake and utilization. Metformin do not cause the body to make more insulin. Because of this, when taken alone, they rarely cause hypoglycemia (low blood sugar). Following oral administration, approximately 90% of the absorbed drug is eliminated via the renal route within the first 24 hours, with a plasma elimination half-life of approximately 6.2 hours.
For the management of Type II diabetes mellitus.
The usual starting dose of metformin is 500 mg once daily with evening meal. Dosage increases should be made in increments of 500 mg weekly, up to a maximum of 2000 mg once daily with the evening meal.
Metformin is contraindicated in patients with: Renal disease or renal dysfunction (e.g. as suggested by serum creatinine levels 1.5 mg/ dL [male], 1.4 mg/dL [female] or abnormal creatinine clearance) which may also result from conditions such as cardiovascular collapse (shock), acute myocardial infarction and septicemia.
Congestive heart failure requiring pharmacologic treatment.
Known hypersensitivity to metformin hydrochloride.
Acute or chronic metabolic acidosis, including diabetic ketoacidosis with or without coma. Diabetic ketoacidosis should be treated with insulin.
Monitoring renal function-metformin is known to be substantially excreted by the kidney and the risk of metformin accumulation and lactic acidosis increases with the degree of impairment of renal function. Intravascular contrast studies with iodinated materials can lead to acute alteration of renal function and have been associated with lactic acidosis in patients receiving metformin. Hypoxic states-cardiovascular collapse from acute congestive heart failure, acute myocardial infarction and other conditions characterized by hypoxemia have been associated with lactic acidosis and may also cause prerenal azotemia. Surgical procedures-metformin therapy should be temporarily suspended for any surgical procedure and should not be restarted until the patient's oral intake has resumed and renal function has been evaluated as normal. Alcohol is also known to potentiate the effect of metformin on lactate metabolism. Patients therefore should be warned against excessive alcohol intake. Since impaired hepatic function has been associated with some cases of lactic acidosis, metformin should generally be avoided in patients with clinical or laboratory evidence of hepatic disease. A patient with type 2 diabetes mellitus previously well controlled on metformin who develops laboratory abnormalities or clinical illness should be evaluated promptly for evidence of ketoacidosis or lactic acidosis. Hypoglycemia-it occurs when calorie intake is deficient, when exercise is not compensated by caloric supplementation, or during concomitant use with other glucose-lowering agents (such as sulfonylurea and insulin) or ethanol. Patients should be advised to discontinue metformin immediately and to promptly notify their health practitioner if unexplained hyperventilation, myalgia, malaise, unusual somnolence or other nonspecific symptoms occur. Metformin should not be used during pregnancy unless clearly needed. Because the potential for hyperglycemia in nursing infants may exist, a decision should be made whether to discontinue nursing or to discontinue the drug, taking into account the importance of the drug to the mother. Safety and effectiveness in pediatric patients have not been established. Because aging is associated with reduced renal function, care should be taken in dose selection and should be based on careful and regular monitoring of renal function.
In rare cases, metformin can cause a serious adverse effect called lactic acidosis. You should stop using metformin and call your doctor right away if you have signs of lactic acidosis.
Common effects of metformin include diarrhea, nausea and upset stomach. These effects generally go away after you take the medicine for a while.
In a single-dose interaction study in type 2 diabetes mellitus patients, co-administration of metformin and glyburide did not result in any changes in either metformin pharmacokinetics or pharmacodynamics.
A single-dose, metformin-furosemide drug interaction study in healthy subjects demonstrated that pharmacokinetic parameters of both compounds were affected by co-administration.
Nifedipine appears to enhance the absorption of metformin. Metformin had minimal effects on nifedipine.
Cationic drugs (e.g. amiloride, digoxin, morphine, procainamide, quinidine, quinine, ranitidine, triamterene, trimethoprim, or vancomycin) that are eliminated by renal tubular secretion theoretically have the potential for interaction with metformin by competing for common renal tubular transport systems.
Certain drugs tend to produce hyperglycemia and may lead to loss of glycemic control. These drugs include thiazide and other diuretics, corticosteroids, phenothiazines, thyroid products, estrogens, oral contraceptives, phenytoin, nicotinic acid, sympathomimetics, calcium channel blocking drugs and isoniazid.
Store at temperatures not exceeding 30°C.
A10BA02 - metformin ; Belongs to the class of biguanides. Used in the treatment of diabetes.