Voltend M

Voltend M Uses, Dosage, Side Effects, Food Interaction and all others data.

Metformin is an antihyperglycemic agent which improves glucose tolerance in patients with type 2 diabetes, lowering both basal and postprandial plasma glucose. Metformin reduces hepatic glucose production by inhibiting gluconeogenesis and glycogenolysis, and stimulates intracellular glycogen synthesis by acting on glycogen synthase. In muscle, it increases insulin sensitivity, improving peripheral glucose uptake and utilization. Metformin also delays intestinal glucose absorption. Metformin increases the transport capacity of all types of membrane glucose transporters (GLUTs) known to date.

In humans, independently of its action on glycemia, metformin has favorable effects on lipid metabolism. This has been shown at therapeutic doses in controlled, medium-term or long-term clinical studies: Metformin reduces total cholesterol, LDL, cholesterol and triglycerides levels. Unlike sulfonylureas, metformin does not produce hypoglycemia in either patients with type 2 diabetes or normal subjects and does not cause hyperinsulinemia. With metformin therapy, insulin secretion remains unchanged while fasting insulin levels and daylong plasma insulin response may actually decrease.

General effects

Insulin is an important hormone that regulates blood glucose levels . Type II diabetes is characterized by a decrease in sensitivity to insulin, resulting in eventual elevations in blood glucose when the pancreas can no longer compensate. In patients diagnosed with type 2 diabetes, insulin no longer exerts adequate effects on tissues and cells (called insulin resistance) and insulin deficiency may also be present .

Metformin reduces liver (hepatic) production of glucose, decreases the intestinal absorption of glucose, and enhances insulin sensitivity by increasing both peripheral glucose uptake and utilization. In contrast with drugs of the sulfonylurea class, which lead to hyperinsulinemia, the secretion of insulin is unchanged with metformin use .

Alpha-glucosidase inhibitors are saccharides that act as competitive inhibitors of enzymes needed to digest carbohydrates: specifically alpha-glucosidase enzymes in the brush border of the small intestines. The membrane-bound intestinal alpha-glucosidases hydrolyze oligosaccharides, trisaccharides, and disaccharides to glucose and other monosaccharides in the small intestine. Acarbose also blocks pancreatic alpha-amylase in addition to inhibiting membrane-bound alpha-glucosidases. Pancreatic alpha-amylase hydrolyzes complex starches to oligosaccharides in the lumen of the small intestine. Inhibition of these enzyme systems reduces the rate of digestion of complex carbohydrates. Less glucose is absorbed because the carbohydrates are not broken down into glucose molecules. In diabetic patients, the short-term effect of these drugs therapies is to decrease current blood glucose levels: the long term effect is a small reduction in hemoglobin-A1c level.

Voglibose, an alpha-glucosidase inhibitor, is a synthetic compound with potent and enduring therapeutic efficacies against disorders of sensory, motor and autonomic nerve systems due to diabetes mellitus. The drug was approved in Japan in 1994 for the treatment of diabetes, and it is under further investigation by Takeda for the treatment of impaired glucose tolerance. Alpha-glucosidase inhibitors are oral anti-diabetic drugs used for diabetes mellitus type 2 that work by preventing the digestion of complex carbohydrates (such as starch). Complex carbohydrates are normally converted into simple sugars (monosaccharides) which can be absorbed through the intestine. Hence, alpha-glucosidase inhibitors reduce the impact of complex carbohydrates on blood sugar.

Trade Name Voltend M
Generic Voglibose + Metformin
Weight 0.2mg
Type Tablet
Therapeutic Class
Manufacturer Ajanta Pharma Ltd
Available Country India
Last Updated: September 19, 2023 at 7:00 am
Voltend M
Voltend M

Uses

Metformin Hydrochloride, as monotherapy, is used for an adjunct to diet to lower blood glucose especially in overweight patients with non-insulin-dependent diabetes mellitus (NIDDM) or type 2 diabetes mellitus whose hyperglycemia cannot be satisfactorily managed on diet alone. Metformin Hydrochloride may be used concomitantly with a sulfonylurea when diet and metformin hydrochloride or sulfonylureas alone do not result in adequate glycemic control.

Voglibose is used in diabetes mellitus (DM) for reduction in Post-Prandial Hyperglycaemia (PPHG), only when diet and/or exercise with lifestyle modification or Oral Hypoglycaemic Agents (OHAs) or insulin preparations, in addition to diet and/or exercise, do not result in an adequate glycaemic control.Thus, Voglibose is used for:

  • In non-insulin-dependent diabetes mellitus (NIDDM) patients as immunotherapy
  • In combination with other OHAs
  • In addition to insulin in diabetes mellitus patients
  • In prevention of onset of type 2 diabetes mellitus in impaired glucose tolerance (only for Voglibose 0.2 mg Tablets) (However, Voglibose Tablets should be used only when impaired glucose tolerance has not been improved in patients already undergoing appropriate dietary treatment and/or exercise therapy.)
  • In elderly patients and in those with hepatic dysfunction or mild to moderate renal impairments in whom other OHAs are contraused or they need to be used with caution, Voglibose will be helpful.
  • In glycogen storage disease: Voglibose is helpful in prevention of hypoglycaemia in patients with type lb glycogen storage disease, it being an amylase (a glucosidase) inhibitor.
  • In non-diabetic Hyperinsulinemia, Voglibose is helpful in preventing hypoglycaemic attacks.
  • In steroid induced diabetes mellitus also, Voglibose is helpful. However, clinical data in this setting are limited.

Voligbose has general properties similar to acarbose and selectively inhibits α-glucosidase in the enteric canal, delaying the digestion and absorption of carbohydrate, thereby suppressing sharp increase in post-prandial plasma glucose.

Voltend M is also used to associated treatment for these conditions: Polycystic Ovaries Syndrome, Type 2 Diabetes Mellitus, Glycemic ControlPost Prandial Hyperglycemia, Type 1 Diabetes Mellitus, Type 2 Diabetes Mellitus, Glycemic Control

How Voltend M works

Metformin's mechanisms of action are unique from other classes of oral antihyperglycemic drugs. Metformin decreases blood glucose levels by decreasing hepatic glucose production (gluconeogenesis), decreasing the intestinal absorption of glucose, and increasing insulin sensitivity by increasing peripheral glucose uptake and utilization . It is well established that metformin inhibits mitochondrial complex I activity, and it has since been generally postulated that its potent antidiabetic effects occur through this mechanism . The above processes lead to a decrease in blood glucose, managing type II diabetes and exerting positive effects on glycemic control.

After ingestion, the organic cation transporter-1 (OCT1) is responsible for the uptake of metformin into hepatocytes (liver cells). As this drug is positively charged, it accumulates in cells and in the mitochondria because of the membrane potentials across the plasma membrane as well as the mitochondrial inner membrane. Metformin inhibits mitochondrial complex I, preventing the production of mitochondrial ATP leading to increased cytoplasmic ADP:ATP and AMP:ATP ratios . These changes activate AMP-activated protein kinase (AMPK), an enzyme that plays an important role in the regulation of glucose metabolism . Aside from this mechanism, AMPK can be activated by a lysosomal mechanism involving other activators. Following this process, increases in AMP:ATP ratio also inhibit fructose-1,6-bisphosphatase enzyme, resulting in the inhibition of gluconeogenesis, while also inhibiting adenylate cyclase and decreasing the production of cyclic adenosine monophosphate (cAMP) , a derivative of ATP used for cell signaling . Activated AMPK phosphorylates two isoforms of acetyl-CoA carboxylase enzyme, thereby inhibiting fat synthesis and leading to fat oxidation, reducing hepatic lipid stores and increasing liver sensitivity to insulin .

In the intestines, metformin increases anaerobic glucose metabolism in enterocytes (intestinal cells), leading to reduced net glucose uptake and increased delivery of lactate to the liver. Recent studies have also implicated the gut as a primary site of action of metformin and suggest that the liver may not be as important for metformin action in patients with type 2 diabetes. Some of the ways metformin may play a role on the intestines is by promoting the metabolism of glucose by increasing glucagon-like peptide I (GLP-1) as well as increasing gut utilization of glucose .

In addition to the above pathway, the mechanism of action of metformin may be explained by other ways, and its exact mechanism of action has been under extensive study in recent years .

Alpha-glucosidase inhibitors are saccharides that act as competitive inhibitors of enzymes needed to digest carbohydrates: specifically alpha-glucosidase enzymes in the brush border of the small intestines. The membrane-bound intestinal alpha-glucosidases hydrolyze oligosaccharides, trisaccharides, and disaccharides to glucose and other monosaccharides in the small intestine. Acarbose also blocks pancreatic alpha-amylase in addition to inhibiting membrane-bound alpha-glucosidases. Pancreatic alpha-amylase hydrolyzes complex starches to oligosaccharides in the lumen of the small intestine. Inhibition of these enzyme systems reduces the rate of digestion of complex carbohydrates. Less glucose is absorbed because the carbohydrates are not broken down into glucose molecules. In diabetic patients, the short-term effect of these drugs therapies is to decrease current blood glucose levels: the long term effect is a small reduction in hemoglobin-A1c level. (From Drug Therapy in Nursing, 2nd ed)

Dosage

Voltend M dosage

Adult-

Metformin 500 mg tablet: Initial dosage is 500 mg tablet 2-3 times daily with or after meals, gradually increased if necessary to 2 to 3 gm daily.

Metformin 850 mg tablet: Initial dosage is 850 mg tablet once or twice daily with or after meals, gradually increased if necessary to 2 to 3 gm daily.

Metformin extended release orlong acting tablet: The usual starting dose of Metformin extended release tabletis 500 mg once daily with the 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. If glycemic control is not achieved on Metformin extended release tablet 2000 mg once daily, a trial of Metformin extended release tablet 1000 mg twice daily should be considered. The maximum recommended dose of metformin is 3 gm daily.

Transfer from other antidiabetic therapy: When transferring patients from standard oral hypoglycemic agents other than Chlorpropamide to Metformin HCl, no transition period generally is necessary. When transferring patients fromChlorpropamide, care should be exercised during the first two weeks because of the prolonged retention of Chlorpropamide in the body, leading to overlapping drug effects and possible hypoglycemia.

Children and adolescents-

Monotherapy and combination with insulin

  • Metformin tablets can be used in children from 10 years of age and adolescents.
  • The usual starting dose is one tablet of 500 mg or 850 mg once daily, given during meals or after meals.

After 10 to 15 days the should be adjusted on the basis of blood glucose measurements. A slow increase of dose may improve gastrointestinal tolerability. The maximum recommended dose of metformin is 2 g daily, taken as 2 or 3 divided doses.

Elderly-

Due to the potential for decreased renal function in elderly subjects, the metformin dosage should be adjusted based on renal function. Regular assessment of renal function is necessary.

Normal Adult Dose: Usually, Voglibose tablets are orally administered in a single dose of 0.2 mg, 3 times a day, before each meal. If the effect is not sufficient, the quantity of a single dose may be increased up to 0.3 mg.

Pediatrics: The safety and effectiveness of Voglibose in children has not been established.

Geriatrics: Since elderly patients generally have a physiological hypofunction, it is desirable that such caution be taken as starting the administration at a lower dose (eg, 0.1 mg at a time). Furthermore, this drug should be carefully administered under close observation, through the course of the disease condition, with careful attention to the blood sugar level and the onset of gastrointestinal symptoms.

Side Effects

Metformin may cause gastro-intestinal adverse effects like diarrhoea, anorexia, nausea & vomiting. Lactic acidosis and malabsorption of vitamin B12 may be occurred. Patients may experience a metallic taste and there may be weight loss, which in some diabetics could be an advantage.

Diarrhoea, loose stools, abdominal pain, constipation, loss of appetite, urge to vomit (nausea), vomiting, heartburn, increased gas, and intestinal obstruction like symptoms due to increased intestinal gas. OHAs plus voglibose may cause hypoglycaemia (0.1% to <5%), delay in digestion and absorption of disaccharides, fulminant hepatitis, serious liver dysfunction with increased liver enzymes, jaundice, anaemia, numbness, edema, blurred vision, hot flushes, malaise, weakness, hyperkalemia, increased pancreatic enzyme (serum amylase).

Toxicity

Metformin (hydrochloride) toxicity data:

Oral LD50 (rat): 1 g/kg; Intraperitoneal LD50 (rat): 500 mg/kg; Subcutaneous LD50 (rat): 300 mg/kg; Oral LD50 (mouse): 1450 mg/kg; Intraperitoneal LD50 (mouse): 420 mg/kg; Subcutaneous LD50 (mouse): 225 mg/kg .

A note on lactic acidosis

Metformin decreases liver uptake of lactate, thereby increasing lactate blood levels which may increase the risk of lactic acidosis . There have been reported postmarketing cases of metformin-associated lactic acidosis, including some fatal cases. Such cases had a subtle onset and were accompanied by nonspecific symptoms including malaise, myalgias, abdominal pain, respiratory distress, or increased somnolence. In certain cases, hypotension and resistant bradyarrhythmias have occurred with severe lactic acidosis . Metformin-associated lactic acidosis was characterized by elevated blood lactate concentrations (>5 mmol/L), anion gap acidosis (without evidence of ketonuria or ketonemia), as well as an increased lactate:pyruvate ratio; metformin plasma levels were generally >5 mcg/mL.

Risk factors for metformin-associated lactic acidosis include renal impairment, concomitant use of certain drugs (e.g. carbonic anhydrase inhibitors such as topiramate), age 65 years old or greater, having a radiological study with contrast, surgery and other procedures, hypoxic states (e.g., acute congestive heart failure), excessive alcohol intake, and hepatic impairment .

A note on renal function

In patients with decreased renal function, the plasma and blood half-life of metformin is prolonged and the renal clearance is decreased .

Metformin should be avoided in those with severely compromised renal function (creatinine clearance < 30 ml/min), acute/decompensated heart failure, severe liver disease and for 48 hours after the use of iodinated contrast dyes due to the risk of lactic acidosis . Lower doses should be used in the elderly and those with decreased renal function. Metformin decreases fasting plasma glucose, postprandial blood glucose and glycosolated hemoglobin (HbA1c) levels, which are reflective of the last 8-10 weeks of glucose control. Metformin may also have a positive effect on lipid levels.

A note on hypoglycemia

When used alone, metformin does not cause hypoglycemia, however, it may potentiate the hypoglycemic effects of sulfonylureas and insulin when they are used together .

Use in pregnancy

Available data from post-marketing studies have not indicated a clear association of metformin with major birth defects, miscarriage, or adverse maternal or fetal outcomes when metformin was ingested during pregnancy. Despite this, the abovementioned studies cannot definitively establish the absence of any metformin-associated risk due to methodological limitations, including small sample size and inconsistent study groups .

Use in nursing

A limited number of published studies indicate that metformin is present in human milk. There is insufficient information to confirm the effects of metformin on the nursing infant and no available data on the effects of metformin on the production of milk. The developmental and health benefits of breastfeeding should be considered as well as the mother’s clinical need for metformin and any possible adverse effects on the nursing child .

Precaution

Lactic acidosis is a rare, but serious (high mortality in the absence of prompt treatment), metabolic complication that can occur due to metformin accumulation. Reported cases of lactic acidosis in patients on metformin have occurred primarily in diabetic patients with significant renal failure. The incidence of lactic acidosis can and should be reduced by assessing also other associated risk factors such as poorly controlled diabetes, ketosis, prolonged fasting, excessive alcohol intake, hepatic insufficiency and any condition associated with hypoxia. Lactic acidosis is characterized by acidotic dyspnea, abdominal pain and hypothermia followed by coma. Diagnostic laboratory findings are decreased blood pH, plasma lactate levels above 5 mmol/L, and an increased anion gap and lactate/pyruvate ratio. If metabolic acidosis is suspected, metformin should be discontinued and the patient should be hospitalized immediately.

Renal function: As metformin is excreted by the kidney, serum creatinine levels should be determined before initiating treatment and regularly thereafter: at least annually in patients with normal renal function, at least two to four times a year in patients with serum creatinine levels at the upper limit of normal and in elderly subjects. Decreased renal function in elderly subjects is frequent and asymptomatic. Special caution should be exercised in situations where renal function may become impaired, for example when initiating antihypertensive therapy or diuretic therapy and when starting therapy with an NSAID.

Administration of iodinated contrast agent: As the intravascular administration of iodinated contrast materials in radiologic studies can lead to renal failure, metformin should be discontinued prior to, or at the time of the test and not reinstituted until 48 hours afterwards, and only after renal function has been re-evaluated and found to be normal.

Surgery: Metformin hydrochloride should be discontinued 48 hours before elective surgery with general anesthesia and should not be usually resumed earlier than 48 hours afterwards.

Children and adolescents: The diagnosis of type 2 diabetes mellitus should be confirmed before treatment with metformin is initiated. No effect of metformin on growth and puberty has been detected during controlled clinical studies of one-year duration but no long-term data on these specific points are available. Therefore, a careful follow-up of the effect of metformin on these parameters in metformin-treated children, especially pre-pubescent children, is recommended.

Children aged between 10 and 12 years: Only 15 subjects aged between 10 and 12 years were included in the controlled clinical studies conducted in children and adolescents. Although metformin efficacy and safety in children below 12 did not differ from efficacy and safety in older children, particular caution is recommended when prescribing to children aged between 10 and 12 years.

Other precautions: All patients should continue their diet with a regular distribution of carbohydrate intake during the day. Overweight patients should continue their energy-restricted diet. The usual laboratory tests for diabetes monitoring should be performed regularly. Metformin alone never causes hypoglycemia, although caution is advised when it is used in combination with insulin or sulphonylureas.

Careful Administration (should be administered with care in following patients):

  • Patients who are receiving other antidiabetic drugs as hypoglycaemia may occur
  • Patients with a history of laparotomy or ileus (intestinal obstruction-like symptoms are liable to develop due to an increase in intestinal gas, etc.)
  • Patients with chronic intestinal disease accompanied by a disturbance in digestion and absorption (the action of this drug may aggravate the pathologic conditions)
  • Patients with Roemheld’s Syndrome, severe hernia, Stenosis or ulceration of the large intestine, etc. (Symptoms may worsen due to an increase in the intestinal gas, etc.)
  • Patients with serious hepatic dysfunction (Because of possible changes in metabolic condition, the status of plasma glucose control may greatly vary. In patients with severe liver cirrhosis, hyperammonemia may worsen, followed by disturbance of consciousness.)
  • Patients with serious renal dysfunction (Because of possible changes in metabolic conditions, the status of plasma glucose control may greatly vary.)
  • Elderly patients

Interaction

Concomitant use not recommended-

Alcohol: Increased risk of lactic acidosis in acute alcohol intoxication, particularly in case of: fasting or malnutrition, hepatic insufficiency. Avoid consumption of alcohol and alcohol-containing medications.

Iodinated contrast agents: Intravascular administration of iodinated contrast agents may lead to renal failure, resulting in metformin accumulation and a risk of lactic acidosis. Metformin should be discontinued prior to, or at the time of the test and not reinstituted until 48 hours afterwards, and only after renal function has been re-evaluated and found to be normal.

Combinations requiring precautions for use-

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. When such drugs are administered to a patient receiving Metformin HCl, the patient should be closely observed to maintain adequate glycemic control. Inform the patient and perform more frequent blood glucose monitoring, especially at the beginning of treatment. If necessary, adjust the dosage of the antidiabetic drug during therapy with the other drug and upon its discontinuation.

Nifedipine appears to enhance the absorption of Metformin. Metformin has minimal effects on nifedipine. ACE-inhibitors may decrease the blood glucose levels. If necessary, adjust the dosage of the antidiabetic drug during therapy with the other drug and upon its discontinuation.

Voglibose should be administered with care when co-administered with the following drugs:

Antidiabetic drugs: Derivative(s) of sulfonylamide and sulfonylurea, biguanide derivatives, insulin preparations and improving agents for insulin resistance.

For the concomitant use of antldlabetlc drugs and the drugs which enhance or diminish the hypoglycaemic action of antldlabetlc drugs:

  • Drugs enhancing the hypoglycaemic action of antidiabetic drugs: β-blockers, salicylic acid preparations, monoamine oxidase inhibitors, fibrate derivatives for the treatment of hyperlipemia, warfarin, etc.
  • Drugs diminishing the hypoglycemic actton of antidiabetic drugs: Adrenaline, adrenocortical hormone, thyroid hormone, etc.

Volume of Distribution

The apparent volume of distribution (V/F) of metformin after one oral dose of metformin 850 mg averaged at 654 ± 358 L .

Elimination Route

Regular tablet absorption

The absolute bioavailability of a metformin 500 mg tablet administered in the fasting state is about 50%-60%. Single-dose clinical studies using oral doses of metformin 500 to 1500 mg and 850 to 2550 mg show that there is a lack of dose proportionality with an increase in metformin dose, attributed to decreased absorption rather than changes in elimination .

At usual clinical doses and dosing schedules of metformin, steady-state plasma concentrations of metformin are achieved within 24-48 hours and are normally measured at Label.

Extended-release tablet absorption

After a single oral dose of metformin extended-release, Cmax is reached with a median value of 7 hours and a range of between 4 and 8 hours. Peak plasma levels are measured to be about 20% lower compared to the same dose of regular metformin, however, the extent of absorption of both forms (as measured by area under the curve - AUC), are similar .

Effect of food

Food reduces the absorption of metformin, as demonstrated by about a 40% lower mean peak plasma concentration (Cmax), a 25% lower area under the plasma concentration versus time curve (AUC), and a 35-minute increase in time to peak plasma concentration (Tmax) after ingestion of an 850 mg tablet of metformin taken with food, compared to the same dose administered during fasting .

Though the extent of metformin absorption (measured by the area under the curve - AUC) from the metformin extended-release tablet is increased by about 50% when given with food, no effect of food on Cmax and Tmax of metformin is observed. High and low-fat meals exert similar effects on the pharmacokinetics of extended-release metformin .

Slowly and poorly absorbed. The reported pharmacokinetic parameters of voglibose with metformin are Cmax corresponds to 1.38 mcg/ml while AUC is 8.17 mcg.h/ml and tmax is of 2.5 hours.

Half Life

Approximately 6.2 hours in the plasma and in the blood, the elimination half-life is approximately 17.6 hours, suggesting that the erythrocyte mass may be a compartment of distribution .

The half-life of voglibose is very similar to the one found for metformin and it is reported to be of 4.08 hours.

Clearance

Renal clearance is about 3.5 times greater than creatinine clearance, which indicates that tubular secretion is the major route of metformin elimination. Following oral administration, approximately 90% of the absorbed drug is eliminated via the renal route within the first 24 hours .

Elimination Route

This drug is substantially excreted by the kidney .

Renal clearance of metformin is about 3.5 times higher than creatinine clearance, which shows that renal tubular secretion is the major route of metformin elimination. After oral administration, about 90% of absorbed metformin is eliminated by the kidneys within the first 24 hours post-ingestion .

Pregnancy & Breastfeeding use

Pregnancy Category B. Animal studies do not indicate harmful effects with respect to pregnancy, embryonic or fetal development, parturition or postnatal development. There are no adequate and well-controlled studies in pregnant women. Can be used in pregnancy for both preexisting and gestational diabetes. Women with gestational diabetes should discontinue treatment after giving birth.

Lactation: Metformin is excreted into milk in lactating rats. Similar data is not available in humans and a decision should be made whether to discontinue nursing or to discontinue metformin, taking into account the importance of the drug to the mother. May be used during breast-feeding in women with pre existing diabetes.

Pregnancy: The safety of Voglibose in pregnancy has not been established. However, no adequate and well controlled studies have been done on pregnant women.

Lactation and Nursing Mothers: Although the levels of Voglibose reached in human milk are exceedingly low, it is recommended that Voglibose may not be administered to such women.

Contraindication

  • Hypersensitivity to metformin hydrochloride or to any of the excipients of the medication.
  • Diabetic ketoacidosis, diabetic pre-coma
  • Renal failure or renal dysfunction (creatinine clearance < 60 mL/min)
  • Acute conditions with the potential to alter renal function such as: dehydration, severe infection, shock, intravascular
  • administration of iodinated contrast agents.
  • Acute or chronic disease which may cause tissue hypoxia such as: cardiac or respiratory failure, recent myocardial
  • infarction, shock
  • Hepatic insufficiency, acute alcohol intoxication, alcoholism
  • Lactation

Contraindicated in patients with Hypersensitivity to Voglibose or to any of the excipients; Diabetic ketoacidosis, diabetic pre-coma; Severe infection, before and after operation or with serious trauma; Gastrointestinal obstruction or predisposed to it.

Special Warning

Renal Impairment: Metformin is contraindicated in patients with an eGFR < 30 mL/minute/1.73 m2 . Starting metformin in patients with an eGFR between 30-45 mL/minute/1.73 m2 is not recommended. In patients taking metformin whose eGFR later falls below 45 mL/minute/1.73 m2 , assess the benefits and risks of continuing treatment. Discontinue metformin if the patient’s eGFR later falls below 30 mL/minute/1.73 m2 .

Dosage in Renal Failure: Voglibose is poorly absorbed after oral doses and renal excretion is negligible, suggesting that no dose adjustment is required. However, pharmacokinetic studies in patients with renal insufficiency are not available.

Acute Overdose

Hypoglycemia has not been seen with metformin doses up to 85g, although lactic acidosis has occurred in such circumstances. High overdose or concomitant risks of metformin may lead to lactic acidosis. Lactic acidosis is a medical emergency and must be treated in hospital. The most effective method to remove lactate and metformin is hemodialysis.

Unlike sulfonylureas or insulin, an overdose of Voglibose tablets will not result in hypoglycaemia. An overdose may result is transient increase in flatulence, diarrhoea and abdominal discomfort. Because of lack of extra-intestinal effects soon with Voglibose, no serious systemic reactions are expected in the event of an overdose.

Storage Condition

Keep out of the reach of children. Do not store above 25°C. Keep in the original package in a cool & dry place in order to protect from light and moisture.

Keep in a cool and dry place. Keep out of the reach of children. Protect from light.

Innovators Monograph

You find simplified version here Voltend M


*** Taking medicines without doctor's advice can cause long-term problems.
Share