Chemical formula: C₂₅H₄₃NO₁₈ Molecular mass: 645.608 g/mol PubChem compound: 41774
Acarbose interacts in the following cases:
Some drugs tend to cause hyperglycemia and may lead to loss of control of blood glucose. These drugs include thiazides and other diuretics, corticosteroids, phenothiazines, thyroid medications, estrogens, oral contraceptives, phenytoin, nicotinic acid, sympathomimetics, calcium channel blockers and isoniazide. When these drugs are administered to a patient receiving acarbose, the patient should be carefully monitored for inability to control blood glucose. When these drugs are stopped by a patient receiving acarbose in combination with a sulfonylurea or insulin, the patient should be carefully monitored for any evidence of hypoglycemia.
When administered alone, acarbose does not cause hypoglycaemia. It may, however, act to potentiate the hypoglycaemic effects of insulin, metformin and sulphonylurea drugs, and the dosages of these agents may need to be modified accordingly. In individual cases hypoglycaemic shock may occur (i.e. clinical sequelae of glucose levels <1 mmol/L such as altered conscious levels, confusion or convulsions).
Some drugs tend to cause hyperglycemia and may lead to loss of control of blood glucose. These drugs include thiazides and other diuretics, corticosteroids, phenothiazines, thyroid medications, estrogens, oral contraceptives, phenytoin, nicotinic acid, sympathomimetics, calcium channel blockers and isoniazide. When these drugs are administered to a patient receiving acarbose, the patient should be carefully monitored for inability to control blood glucose. When these drugs are stopped by a patient receiving acarbose in combination with a sulfonylurea or insulin, the patient should be carefully monitored for any evidence of hypoglycemia.
When administered alone, acarbose does not cause hypoglycaemia. It may, however, act to potentiate the hypoglycaemic effects of insulin, metformin and sulphonylurea drugs, and the dosages of these agents may need to be modified accordingly. In individual cases hypoglycaemic shock may occur (i.e. clinical sequelae of glucose levels <1 mmol/L such as altered conscious levels, confusion or convulsions).
Some drugs tend to cause hyperglycemia and may lead to loss of control of blood glucose. These drugs include thiazides and other diuretics, corticosteroids, phenothiazines, thyroid medications, estrogens, oral contraceptives, phenytoin, nicotinic acid, sympathomimetics, calcium channel blockers and isoniazide. When these drugs are administered to a patient receiving acarbose, the patient should be carefully monitored for inability to control blood glucose. When these drugs are stopped by a patient receiving acarbose in combination with a sulfonylurea or insulin, the patient should be carefully monitored for any evidence of hypoglycemia.
When administered alone, acarbose does not cause hypoglycaemia. It may, however, act to potentiate the hypoglycaemic effects of insulin, metformin and sulphonylurea drugs, and the dosages of these agents may need to be modified accordingly. In individual cases hypoglycaemic shock may occur (i.e. clinical sequelae of glucose levels <1 mmol/L such as altered conscious levels, confusion or convulsions).
Some drugs tend to cause hyperglycemia and may lead to loss of control of blood glucose. These drugs include thiazides and other diuretics, corticosteroids, phenothiazines, thyroid medications, estrogens, oral contraceptives, phenytoin, nicotinic acid, sympathomimetics, calcium channel blockers and isoniazide. When these drugs are administered to a patient receiving acarbose, the patient should be carefully monitored for inability to control blood glucose. When these drugs are stopped by a patient receiving acarbose in combination with a sulfonylurea or insulin, the patient should be carefully monitored for any evidence of hypoglycemia.
When administered alone, acarbose does not cause hypoglycaemia. It may, however, act to potentiate the hypoglycaemic effects of insulin, metformin and sulphonylurea drugs, and the dosages of these agents may need to be modified accordingly. In individual cases hypoglycaemic shock may occur (i.e. clinical sequelae of glucose levels <1 mmol/L such as altered conscious levels, confusion or convulsions).
Some drugs tend to cause hyperglycemia and may lead to loss of control of blood glucose. These drugs include thiazides and other diuretics, corticosteroids, phenothiazines, thyroid medications, estrogens, oral contraceptives, phenytoin, nicotinic acid, sympathomimetics, calcium channel blockers and isoniazide. When these drugs are administered to a patient receiving acarbose, the patient should be carefully monitored for inability to control blood glucose. When these drugs are stopped by a patient receiving acarbose in combination with a sulfonylurea or insulin, the patient should be carefully monitored for any evidence of hypoglycemia.
When administered alone, acarbose does not cause hypoglycaemia. It may, however, act to potentiate the hypoglycaemic effects of insulin, metformin and sulphonylurea drugs, and the dosages of these agents may need to be modified accordingly. In individual cases hypoglycaemic shock may occur (i.e. clinical sequelae of glucose levels <1 mmol/L such as altered conscious levels, confusion or convulsions).
Some drugs tend to cause hyperglycemia and may lead to loss of control of blood glucose. These drugs include thiazides and other diuretics, corticosteroids, phenothiazines, thyroid medications, estrogens, oral contraceptives, phenytoin, nicotinic acid, sympathomimetics, calcium channel blockers and isoniazide. When these drugs are administered to a patient receiving acarbose, the patient should be carefully monitored for inability to control blood glucose. When these drugs are stopped by a patient receiving acarbose in combination with a sulfonylurea or insulin, the patient should be carefully monitored for any evidence of hypoglycemia.
When administered alone, acarbose does not cause hypoglycaemia. It may, however, act to potentiate the hypoglycaemic effects of insulin, metformin and sulphonylurea drugs, and the dosages of these agents may need to be modified accordingly. In individual cases hypoglycaemic shock may occur (i.e. clinical sequelae of glucose levels <1 mmol/L such as altered conscious levels, confusion or convulsions).
Some drugs tend to cause hyperglycemia and may lead to loss of control of blood glucose. These drugs include thiazides and other diuretics, corticosteroids, phenothiazines, thyroid medications, estrogens, oral contraceptives, phenytoin, nicotinic acid, sympathomimetics, calcium channel blockers and isoniazide. When these drugs are administered to a patient receiving acarbose, the patient should be carefully monitored for inability to control blood glucose. When these drugs are stopped by a patient receiving acarbose in combination with a sulfonylurea or insulin, the patient should be carefully monitored for any evidence of hypoglycemia.
When administered alone, acarbose does not cause hypoglycaemia. It may, however, act to potentiate the hypoglycaemic effects of insulin, metformin and sulphonylurea drugs, and the dosages of these agents may need to be modified accordingly. In individual cases hypoglycaemic shock may occur (i.e. clinical sequelae of glucose levels <1 mmol/L such as altered conscious levels, confusion or convulsions).
Some drugs tend to cause hyperglycemia and may lead to loss of control of blood glucose. These drugs include thiazides and other diuretics, corticosteroids, phenothiazines, thyroid medications, estrogens, oral contraceptives, phenytoin, nicotinic acid, sympathomimetics, calcium channel blockers and isoniazide. When these drugs are administered to a patient receiving acarbose, the patient should be carefully monitored for inability to control blood glucose. When these drugs are stopped by a patient receiving acarbose in combination with a sulfonylurea or insulin, the patient should be carefully monitored for any evidence of hypoglycemia.
When administered alone, acarbose does not cause hypoglycaemia. It may, however, act to potentiate the hypoglycaemic effects of insulin, metformin and sulphonylurea drugs, and the dosages of these agents may need to be modified accordingly. In individual cases hypoglycaemic shock may occur (i.e. clinical sequelae of glucose levels <1 mmol/L such as altered conscious levels, confusion or convulsions).
Some drugs tend to cause hyperglycemia and may lead to loss of control of blood glucose. These drugs include thiazides and other diuretics, corticosteroids, phenothiazines, thyroid medications, estrogens, oral contraceptives, phenytoin, nicotinic acid, sympathomimetics, calcium channel blockers and isoniazide. When these drugs are administered to a patient receiving acarbose, the patient should be carefully monitored for inability to control blood glucose. When these drugs are stopped by a patient receiving acarbose in combination with a sulfonylurea or insulin, the patient should be carefully monitored for any evidence of hypoglycemia.
When administered alone, acarbose does not cause hypoglycaemia. It may, however, act to potentiate the hypoglycaemic effects of insulin, metformin and sulphonylurea drugs, and the dosages of these agents may need to be modified accordingly. In individual cases hypoglycaemic shock may occur (i.e. clinical sequelae of glucose levels <1 mmol/L such as altered conscious levels, confusion or convulsions).
The concomitant administration of acarbose with colestyramine may enhance the effects of acarbose , particularly with respect to reducing postprandial insulin levels. Simultaneous administration of acarbose and colestyramine should, therefore, be avoided. In the rare circumstance that both acarbose and colestyramine therapy are withdrawn simultaneously, care is needed as a rebound phenomenon has been observed with respect to insulin levels in non-diabetic subjects.
In individual cases, acarbose may affect digoxin bioavailability, which may require dose adjustment of digoxin. Monitoring of serum digoxin levels should be considered.
Some drugs tend to cause hyperglycemia and may lead to loss of control of blood glucose. These drugs include thiazides and other diuretics, corticosteroids, phenothiazines, thyroid medications, estrogens, oral contraceptives, phenytoin, nicotinic acid, sympathomimetics, calcium channel blockers and isoniazide. When these drugs are administered to a patient receiving acarbose, the patient should be carefully monitored for inability to control blood glucose. When these drugs are stopped by a patient receiving acarbose in combination with a sulfonylurea or insulin, the patient should be carefully monitored for any evidence of hypoglycemia.
When administered alone, acarbose does not cause hypoglycaemia. It may, however, act to potentiate the hypoglycaemic effects of insulin, metformin and sulphonylurea drugs, and the dosages of these agents may need to be modified accordingly. In individual cases hypoglycaemic shock may occur (i.e. clinical sequelae of glucose levels < 1 mmol/L such as altered conscious levels, confusion or convulsions).
The concomitant administration of acarbose with neomycin may lead to enhanced reductions of postprandial blood glucose and to an increase in the frequency and severity of gastro-intestinal side-effects. If the symptoms are severe, a temporary dose reduction of acarbose may be warranted.
Intestinal adsorbents (e.g. charcoal) and digestive enzyme preparations containing carbohydrate splitting enzymes (e.g. amylase, pancreatin) may reduce the effect of acarbose and should not therefore be taken concomitantly.
Some drugs tend to cause hyperglycemia and may lead to loss of control of blood glucose. These drugs include thiazides and other diuretics, corticosteroids, phenothiazines, thyroid medications, estrogens, oral contraceptives, phenytoin, nicotinic acid, sympathomimetics, calcium channel blockers and isoniazide. When these drugs are administered to a patient receiving acarbose, the patient should be carefully monitored for inability to control blood glucose. When these drugs are stopped by a patient receiving acarbose in combination with a sulfonylurea or insulin, the patient should be carefully monitored for any evidence of hypoglycemia.
When administered alone, acarbose does not cause hypoglycaemia. It may, however, act to potentiate the hypoglycaemic effects of insulin, metformin and sulphonylurea drugs, and the dosages of these agents may need to be modified accordingly. In individual cases hypoglycaemic shock may occur (i.e. clinical sequelae of glucose levels <1 mmol/L such as altered conscious levels, confusion or convulsions).
Some drugs tend to cause hyperglycemia and may lead to loss of control of blood glucose. These drugs include thiazides and other diuretics, corticosteroids, phenothiazines, thyroid medications, estrogens, oral contraceptives, phenytoin, nicotinic acid, sympathomimetics, calcium channel blockers and isoniazide. When these drugs are administered to a patient receiving acarbose, the patient should be carefully monitored for inability to control blood glucose. When these drugs are stopped by a patient receiving acarbose in combination with a sulfonylurea or insulin, the patient should be carefully monitored for any evidence of hypoglycemia.
When administered alone, acarbose does not cause hypoglycaemia. It may, however, act to potentiate the hypoglycaemic effects of insulin, metformin and sulphonylurea drugs, and the dosages of these agents may need to be modified accordingly. In individual cases hypoglycaemic shock may occur (i.e. clinical sequelae of glucose levels <1 mmol/L such as altered conscious levels, confusion or convulsions).
Sucrose (cane sugar) and foods containing sucrose often cause abdominal discomfort or even diarrhoea during treatment with acarbose tablets as a result of increased carbohydrate fermentation in the colon.
Acarbose should not be administered during pregnancy as no information is available from clinical studies on its use in pregnant women.
After the administration of radioactively marked acarbose to nursing rats, a small amount of radioactivity was recovered in the milk. To date there have been no similar findings in humans.
Nevertheless, as the possibility of drug induced effects on nursing infants can not be excluded, the prescription of acarbose is not recommended during breastfeeding.
None known.
The frequencies of adverse drug reactions (ADRs) reported with acarbose, based on placebo-controlled studies (acarbose N=8,595; placebo N=7,278), are summarised in the table below.
Within each frequency grouping, undesirable effects are presented in order of decreasing seriousness. Frequencies are defined as very common (≥1/10), common (≥1/100 to <1/10), uncommon (≥1/1,000 to <1/100) and rare (≥1/10,000 to <1/1,000).
The ADRs identified during postmarketing surveillance only and for which a frequency could not be estimated, are listed under “Not known”.
Not known: Thrombocytopenia
Not known: Drug hypersensivity and hypersensivity (rash, erythema, exanthema, urticaria) h3. Vascular disorders
Rare: Oedema
Very common: Flatulence
Common: Diarrhoea, Gastrointestinal and abdominal pains
Uncommon: Nausea, Vomiting, Dyspepsia
Not known: Subileus/Ileus, Pneumatosis cystoides intestinalis
Uncommon: Increase in transaminases
Rare: Jaundice
Not known: Hepatitis
Not known: Acute generalised exanthematous pustulosis
In postmarketing, cases of liver disorder, hepatic function abnormal, and liver injury have been reported. Individual cases of fulminant hepatitis with fatal outcome have also been reported, particularly from Japan.
In patients receiving the recommended daily dose of 150 to 300 mg acarbose, clinically relevant abnormal liver function tests (three times above upper limit of normal range) were rarely observed. Abnormal values may be transient under ongoing acarbose therapy.
If the prescribed diabetic diet is not observed the intestinal side effects may be intensified. If strongly distressing symptoms develop in spite of adherence to the diabetic diet prescribed, the doctor must be consulted and the dose temporarily or permanently reduced.
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