Adult: In patients inadequately controlled on diet alone, or on diet and oral hypoglycaemic agents: As adjunct to diet and exercise to improve glycaemic control: Usual dose: Initially, 25 mg or 50 mg tid. May also initiate with 25 mg or 50 mg daily to minimise gastrointestinal effects, then gradually increase to 25 mg or 50 mg tid. After 4-8 weeks, may further increase dose if necessary, up to 100-200 mg tid. Doses must be individualised according to patient response and tolerance. Dosage regimen recommendations may vary among individual products or between countries (refer to specific product guideline).
Renal Impairment
CrCl (mL/min)
Dosage
<25
Not recommended.
Hepatic Impairment
Contraindicated.
Administration
Should be taken with food. Take w/ 1st bite of each main meal.
Contraindications
Inflammatory bowel disease, colonic ulceration, partial intestinal obstruction or predisposition to intestinal obstruction; chronic intestinal disease associated with marked disorders of digestion or absorption; conditions that may deteriorate due to elevated gas formation in the intestine (e.g. hernia), diabetic ketoacidosis, cirrhosis. Hepatic impairment.
Special Precautions
Patient exposed to stress-related states (e.g. trauma, fever, surgery, infection); may consider temporary insulin administration and treatment discontinuation in these patients if necessary. Not recommended in patients with severe renal impairment (CrCl <25 mL/min). Pregnancy and lactation. Concomitant use with intestinal adsorbents (e.g. charcoal) and digestive enzyme preparations containing carbohydrate-splitting enzymes (e.g. pancreatin, amylase).
Adverse Reactions
Significant: Increased serum transaminase levels. Rarely, hyperbilirubinaemia. Blood and lymphatic system disorders: Thrombocytopenia. General disorders and administration site conditions: Rarely, oedema. Gastrointestinal disorders: Flatulence, diarrhoea, abdominal pain, nausea, vomiting, dyspepsia. Rarely, pneumatosis cystoides intestinalis, ileus or subileus. Hepatobiliary disorders: Rarely, jaundice, hepatitis. Immune system disorders: Hypersensitivity skin reactions (e.g. rash, erythema, exanthema, urticaria). Potentially Fatal: Fulminant hepatitis.
Monitor serum transaminase levels every 3 months during the 1st year and periodically thereafter; postprandial glucose, HbA1c (at least twice yearly in patients with stable glycaemic control or those meeting treatment goals; quarterly in patients with therapy change or those not meeting treatment goals); serum creatinine.
Drug Interactions
May reduce the effect when used with intestinal adsorbents (e.g. charcoal) and digestive enzyme preparations containing carbohydrate splitting enzymes (e.g. pancreatin, amylase). May potentiate the hypoglycaemic effects of insulin and sulfonylureas. May cause enhanced reductions of postprandial blood glucose and increased frequency and severity of gastrointestinal side effects with oral neomycin. Colestyramine may enhance the effects of acarbose. May affect the bioavailability of digoxin. May result in loss of blood glucose control when used with certain agents that produce hyperglycaemia (e.g. thiazides and other diuretics, phenothiazines, corticosteroids, thyroid products, estrogens, oral contraceptives, phenytoin, nicotinic acid, sympathomimetics, Ca channel blockers, isoniazid).
Food Interaction
Increased intake of foods containing sucrose (cane sugar) during therapy may result in gastrointestinal symptoms (e.g. flatulence, bloating, occasional diarrhoea, loose stools).
Action
Description: Acarbose competitively and reversibly inhibits membrane-bound intestinal α-glucosidases and pancreatic α-amylase resulting in the delayed absorption of glucose and degradation of ingested complex carbohydrates and disaccharides in the small intestine. This action leads to a reduced post-prandial rise in blood glucose, therefore decreasing blood glucose fluctuations. Pharmacokinetics: Absorption: <2% (as active drug) and approx 35% (as metabolites) are absorbed from the gastrointestinal tract. Time to peak plasma concentration: Approx 1 hour (active drug). Metabolism: Exclusively metabolised in the gastrointestinal tract mainly by intestinal bacteria and digestive enzymes into at least 13 metabolites, including sulfate, methyl, and glucuronide conjugates as the major metabolites. Excretion: Via urine (approx 34% as inactive metabolites; <2% as unchanged drug and active metabolites); faeces (approx 51% as unabsorbed drug). Elimination half-life: Approx 2 hours.
Chemical Structure
Acarbose Source: National Center for Biotechnology Information. PubChem Database. Acarbose, CID=41774, https://pubchem.ncbi.nlm.nih.gov/compound/Acarbose (accessed on Jan. 20, 2020)
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