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Decarbay
Method of action:
Treatment option:
Dosage (Posology) and method of administration
Posology
Owing to the great individual variation of glucosidase activity in the intestinal mucosa, there is no fixed dosage regimen, and patients should be treated according to clinical response and tolerance of intestinal side-effects.
Adults
The recommended initial dose is 50 mg three times a day. However, some patients may benefit from more gradual initial dose titration to minimise gastrointestinal side-effects. This may be achieved by initiating treatment at 50 mg once or twice a day, with subsequent titration to a three times a day regimen.
If after six to eight weeks' treatment patients show an inadequate clinical response, the dosage may be increased to 100 mg three times a day. A further increase in dosage to a maximum of 200 mg three times a day may occasionally be necessary.
If distressing complaints develop in spite of strict adherence to the diet, the dose should not be increased further and if necessary should be reduced according to the severity of the side-effects and the clinical judgment of the prescriber.
Decarbay is intended for continuous long-term treatment.
Elderly
No modification of the normal adult dosage regimen is necessary.
Paediatric population
The efficacy and safety of Decarbay in children and adolescents have not been established. Decarbay is not recommended for patients under the age of 18 years.
Method of administration
Decarbay tablets are taken orally and should be chewed with the first mouthful of food, or swallowed whole with a little liquid directly before the meal.
Decarbay Tablets are administered orally and should be chewed with the first mouthful of food, or swallowed whole with a little liquid directly before the meal. Owing to the great individual variation of glucosidase activity in the intestinal mucosa, there is no fixed dosage regimen, and patients should be treated according to clinical response and tolerance of intestinal side-effects.
Adults
The recommended initial dose is 50mg three times a day. However, some patients may benefit from a more gradual initial dose titration to minimise gastrointestinal side-effects. This may be achieved by initiating treatment at 50mg once or twice a day, with subsequent titration to a three times a day regimen.
If after six to eight weeks of treatment patients show an inadequate clinical response, the dosage may be increased to 100mg three times a day. A further increase in dosage to a maximum of 200mg three times a day may occasionally be necessary.
If distressing complaints develop in spite of strict adherence to the diet, the dose should not be increased further and if necessary should be reduced according to the severity of the side-effects and the clinical judgment of the prescriber.
Decarbay is intended for continuous long-term treatment.
Elderly patients
No modification of the normal adult dosage regimen is necessary.
Children and adolescents under 18 years
The efficacy and safety of Decarbay in children and adolescents have not been established. Decarbay is not recommended for patients under the age of 18 years.
Undesirable effects
The frequencies of adverse drug reactions (ADRs) reported with Decarbay, based on placebo-controlled studies (Decarbay 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 knownâ€.
| System Organ Class (MedDRA) | Very common | Common | Uncommon | Rare | Not known |
| Blood and lymphatic system disorders | Thrombocytopenia | ||||
| Immune system disorders | Drug hypersensivity and hypersensivity (rash, erythema, exanthema, urticaria) | ||||
| Vascular disorders | Oedema | ||||
| Gastrointestinal disorders | Flatulence | Diarrhoea Gastrointestinal and abdominal pains | Nausea Vomiting Dyspepsia | Subileus/Ileus Pneumatosis cystoides intestinalis | |
| Hepatobiliary disorders | Increase in transaminases | Jaundice | Hepatitis | ||
| Skin and subcutaneous tissue disorders | 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 Decarbay, clinically relevant abnormal liver function tests (three times above upper limit of normal range) were rarely observed. Abnormal values may be transient under ongoing Decarbay 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.
Reporting of suspected adverse reactions
Reporting suspected adverse reactions after authorisation of the medicinal product is important. It allows continued monitoring of the benefit/risk balance of the medicinal product. Healthcare professionals are asked to report any suspected adverse reactions via the Yellow Card Scheme at: www.mhra.gov.uk/yellowcard.
The frequencies of adverse drug reactions (ADRs) reported with Decarbay based on placebo-controlled studies with Decarbay sorted by CIOMS III categories of frequency (placebo-controlled studies in clinical trial database: Decarbay N = 8,595; placebo N = 7,278; status: 10 Feb 2006) 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 (status: 31 Dec 2005) and for which a frequency could not be estimated, are listed under “Not knownâ€.
System Organ Class (MedDRA) | Very common | Common | Uncommon | Rare | Not known |
Blood and lymphatic system disorders | Thrombocytopenia | ||||
Immune system disorders | Allergic reaction (rash, erythema, exanthema, urticaria) | ||||
Vascular disorders | Oedema | ||||
Gastrointestinal disorders | Flatulence | Diarrhoea Gastrointestinal and abdominal pains | Nausea Vomiting Dyspepsia | Subileus/Ileus Pneumatosis cystoides intestinalis | |
Hepatobiliary disorders | Increase in liver enzymes | Jaundice | Hepatitis |
< The MedDRA preferred term is used to describe a certain reaction and its synonyms and related conditions. ADR term representation is based on MedDRA version 11.1. >
In addition, events reported as liver disorder, hepatic function abnormal and liver injury have been received, particularly from Japan.
Individual cases of fulminant hepatitis with fatal outcome have been reported in Japan. The relationship to Decarbay is unclear.
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.
In patients receiving the recommended daily dose of 150 to 300 mg Decarbay, clinically relevant abnormal liver function tests (three times above upper limit of normal range) were rarely observed. Abnormal values may be transient under ongoing therapy with Decarbay..
Overdose
When Decarbay tablets are taken with drinks and/or meals containing carbohydrates overdose may lead to meteorism, flatulence and diarrhoea. If Decarbay tablets are taken independently of food, excessive intestinal symptoms need not be anticipated.
No specific antidotes to Decarbay are known.
Intake of carbohydrate-containing meals or beverages should be avoided for 4-6 hours.
Diarrhoea should be treated by standard conservative measures.
When Decarbay Tablets are taken with drinks and/or meals containing carbohydrates overdose may lead to meteorism, flatulence and diarrhoea. If Decarbay Tablets are taken independently of food, excessive intestinal symptoms need not be anticipated.
No specific antidotes to Decarbay are known.
Intake of carbohydrate-containing meals or beverages should be avoided for 4-6 hours.
Diarrhoea should be treated by standard conservative measures.
Qualitative and quantitative composition
Therapeutic indications
Indications
Decarbay is recommended for the treatment of non-insulin dependent (NIDDM) diabetes mellitus in patients inadequately controlled on diet alone, or on diet and oral hypoglycaemic agents.
Mode of action
Decarbay is a competitive inhibitor of intestinal alpha-glucosidases with maximum specific inhibitory activity against sucrase. Under the influence of Decarbay, the digestion of starch and sucrose into absorbable monosaccharides in the small intestine is dose-dependently delayed. In diabetic subjects, this results in a lowering of postprandial hyperglycaemia and a smoothing effect on fluctuations in the daily blood glucose profile.
In contrast to sulphonylureas Decarbay has no stimulatory action on the pancreas.
Treatment with Decarbay also results in a reduction of fasting blood glucose and to modest changes in levels of glycated haemoglobin (HbA1, HbA1c). The changes may be a reduction or reduced deterioration in HbA1 or HbA1c levels, depending upon the patient's clinical status and disease progression. These parameters are affected in a dose-dependent manner by Decarbay.
Following oral administration, only 1-2% of the active inhibitor is absorbed.
Indications
Decarbay Tablets are recommended for the treatment of non-insulin dependent (NIDDM) diabetes mellitus in patients inadequately controlled on diet alone, or on diet and oral hypoglycaemic agents.
Mode of action
Decarbay is a competitive inhibitor of intestinal alpha-glucosidases with maximum specific inhibitory activity against sucrase. Decarbay dose-dependently delays the digestion of starch and sucrose into absorbable monosaccharides in the small intestine. In patients with diabetes, this results in a lowering of postprandial hyperglycaemia and a smoothing effect on fluctuations in the daily blood glucose profile.
In contrast to sulphonylurea drugs, Decarbay has no stimulatory action on the pancreas.
Treatment with Decarbay Tablets also results in a reduction of fasting blood glucose and to modest changes in levels of glycated haemoglobin (HbA1, HbA1c). The changes may be a reduction or reduced deterioration in HbA1 or HbA1c levels, depending upon the patient's clinical status and disease progression. These parameters are affected in a dose-dependent manner by Decarbay.
Following oral administration, only 1-2% of the active inhibitor is absorbed.
Contraindications
Decarbay is also contra-indicated in patients with inflammatory bowel disease, colonic ulceration, partial intestinal obstruction or in patients predisposed to intestinal obstruction. In addition, Decarbay should not be used in patients who have chronic intestinal diseases associated with marked disorders of digestion or absorption and in patients who suffer from states which may deteriorate as a result of increased gas formation in the intestine, e.g. larger hernias.
Decarbay is contra-indicated in patients with severe hepatic impairment.
As Decarbay has not been studied in patients with severe renal impairment, it should not be used in patients with a creatinine clearance < 25 ml/min/1.73 m2.
- Hypersensitivity to Decarbay or any of the excipients
- Use during pregnancy and in nursing mothers.
Decarbay Tablets are also contra-indicated in patients with colonic ulceration, inflammatory bowel disease, partial intestinal obstruction or in patients predisposed to intestinal obstruction.
In addition, Decarbay Tablets should not be used in patients who have chronic intestinal diseases associated with marked disorders of digestion or absorption and in patients who suffer from states which may deteriorate as a result of increased gas formation in the intestine, e.g. larger hernias.
Decarbay Tablets are contra-indicated in patients with hepatic impairment.
As Decarbay has not been studied in patients with severe renal impairment, it should not be used in patients with a creatinine clearance of less than 25 ml/min/1.73m².
Special warnings and precautions for use
Hypoglycaemia: Decarbay has an antihyperglycaemic effect, but does not itself induce hypoglycaemia. If Decarbay is prescribed in addition to other blood glucose lowering drugs (e.g sulphonylureas metformin, or insulin) a fall of the blood glucose values into the hypoglycaemic range may require a dose adaption of the respective co-medication. If acute hypoglycemia develops glucose should be used for rapid correction of hypoglycaemia.
Episodes of hypoglycaemia occurring during therapy must, where appropriate, be treated by the administration of glucose, not sucrose. This is because acarbose will delay the digestion and absorption of disaccharides, but not monosaccharides.
Transaminases: Cases of fulminant hepatitis have been reported during Decarbay therapy. The mechanism is unknown, but Decarbay may contribute to a multifactorial pathophysiology of liver injury. It is recommended that liver enzyme monitoring is considered during the first 6 to 12 months of treatment. If elevated liver enzymes are observed, a reduction in dosage or withdrawal of therapy may be warranted, particularly if the elevations persist. In such circumstances, patients should be monitored at weekly intervals until normal values are established.
The administration of antacid preparations containing magnesium and aluminium salts, e.g. hydrotalcite, has been shown not to ameliorate the acute gastrointestinal symptoms of Decarbay in higher dosage and should, therefore, not be recommended to patients for this purpose.
Hypoglycaemia: When administered alone, Decarbay does not cause hypoglycaemia. It may, however, act to potentiate the hypoglycaemic effects of insulin and sulphonylurea drugs, and the dosages of these agents may need to be changed 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).
Episodes of hypoglycaemia occurring during therapy must, where appropriate, be treated by the administration of glucose, not sucrose. This is because Decarbay will delay the digestion and absorption of disaccharides but not of monosaccharides.
Transaminases: Patients treated with Decarbay may, on rare occasions, experience an idiosyncratic response with either symptomatic or asymptomatic hepatic dysfunction. In the majority of cases this dysfunction is reversible on discontinuation of Decarbay therapy. It is recommended that liver enzyme monitoring is considered during the first six to twelve months of treatment. If elevated transaminases are observed, withdrawal of therapy may be warranted, particularly if the elevations persist. In such circumstances, patients should be monitored at weekly intervals until normal values are established.
The administration of antacid preparations containing magnesium and aluminium salts, e.g. hydrotalcite, has been shown not to ameliorate the acute gastrointestinal symptoms of Decarbay in higher dosage and should, therefore, not be recommended to patients for this purpose.
Effects on ability to drive and use machines
None known.
None known.
Pharmacodynamic properties
Pharmacotherapeutic group: drugs used in diabetes, alpha-glusosidase inhibitors, ATC code: A10BF01
In all species tested, acarbose exerts its activity in the intestinal tract. The action of acarbose is based on the competitive inhibition of intestinal enzymes (α-glucosidases) involved in the degradation of disaccharides, oligosaccharides, and polysaccharides. This leads to a dose-dependent delay in the digestion of these carbohydrates. Glucose derived from these carbohydrates is released and taken up into the blood more slowly. In this way, acarbose reduces the postprandial rise in blood glucose, thus reducing blood glucose fluctuations.
Pharmacotherapeutic group: Alpha glucosidase inhibitors, ATC code: A10BF01
In all species tested, Decarbay exerts its activity in the intestinal tract. The action of Decarbay is based on the competitive inhibition of intestinal enzymes (α-glucosidases) involved in the degradation of disaccharides, oligosaccharides, and polysaccharides. This leads to a dose-dependent delay in the digestion of these carbohydrates. Glucose derived from these carbohydrates is released and taken up into the blood more slowly. In this way, Decarbay reduces the postprandial rise in blood glucose, thus reducing blood glucose fluctuations.
Pharmacokinetic properties
Following administration, only 1-2% of the active inhibitor is absorbed.
The pharmacokinetics of Decarbay were investigated after oral administration of the 14C-labelled substance (200 mg) to healthy volunteers. On average, 35% of the total radioactivity (sum of the inhibitory substance and any degradation products) was excreted by the kidneys within 96 h. The proportion of inhibitory substance excreted in the urine was 1.7% of the administered dose. 50% of the activity was eliminated within 96 hours in the faeces. The course of the total radioactivity concentration in plasma was comprised of two peaks. The first peak, with an average acarbose-equivalent concentration of 52.2 ± 15.7μg/l after 1.1 ± 0.3 h, is in agreement with corresponding data for the concentration course of the inhibitor substance (49.5 ± 26.9 μg/l after 2.1 ± 1.6 h). The second peak is on average 586.3 ± 282.7 μg/l and is reached after 20.7 ± 5.2 h. The second, higher peak is due to the absorption of bacterial degradation products from distal parts of the intestine. In contrast to the total radioactivity, the maximum plasma concentrations of the inhibitory substance are lower by a factor of 10-20. The plasma elimination half-lives of the inhibitory substance are 3.7 ± 2.7 h for the distribution phase and 9.6 ± 4.4 h for the elimination phase.
A relative volume of distribution of 0.32 l/kg body-weight has been calculated in healthy volunteers from the concentration course in the plasma.
Following administration, only 1-2% of the active inhibitor is absorbed.
The pharmacokinetics of Decarbay were investigated after oral administration of the 14C-labelled substance (200mg) to healthy volunteers. On average, 35% of the total radioactivity (sum of the inhibitory substance and any degradation products) was excreted by the kidneys within 96 hours. The proportion of inhibitory substance excreted in the urine was 1.7% of the administered dose. 50% of the activity was eliminated within 96 hours in the faeces. The course of the total radioactivity concentration in plasma comprised two peaks. The first peak, with an average Decarbay-equivalent concentration of 52.2 ± 15.7μg/l after 1.1 ± 0.3 h, is in agreement with corresponding data for the concentration course of the inhibitor substance (49.5 ± 26.9μg/l after 2.1 ± 1.6 h). The second peak is on average 586.3 ± 282.7μg/l and is reached after 20.7 ± 5.2 h. The second, higher peak is due to the absorption of bacterial degradation products from distal parts of the intestine. In contrast to the total radioactivity, the maximum plasma concentrations of the inhibitory substance are lower by a factor of 10-20. The plasma elimination half-lives of the inhibitory substance are 3.7 ± 2.7 h for the distribution phase and 9.6 ± 4.4 h for the elimination phase.
A relative volume of distribution of 0.32 l/kg body-weight has been calculated in healthy volunteers from the concentration course in the plasma.
Pharmacotherapeutic group
Incompatibilities
None stated.
Not applicable.
Special precautions for disposal and other handling
None stated.
Not relevant.
Attention! Always consult to a doctor or pharmacist before using pills or medicines.
Medically reviewed by . Last updated on 6/26/2023
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