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Diabetes Mellitus

Acarbose is used as monotherapy as an adjunct to diet and exercise for the management of type 2 (noninsulin-dependent) diabetes mellitus (NIDDM) in patients whose hyperglycemia cannot be controlled by diet and exercise alone. Acarbose also may be used in combination with a sulfonylurea, metformin, or insulin as an adjunct to diet and exercise for the management of type 2 diabetes mellitus in patients whose hyperglycemia cannot be controlled with acarbose, metformin, insulin, or sulfonylurea monotherapy, diet, and exercise.

The American Diabetes Association (ADA) currently classifies diabetes mellitus as type 1 (immune mediated or idiopathic), type 2 (predominantly insulin resistance with relative insulin deficiency to predominantly an insulin secretory defect with insulin resistance), gestational diabetes mellitus, or that associated with certain conditions or syndromes (e.g., drug- or chemical-induced, hormonal, that associated with pancreatic disease, infections, specific genetic defects or syndromes). Type 1 diabetes mellitus was previously described as juvenile-onset (JOD) diabetes mellitus, since it usually occurs during youth. Type 2 diabetes mellitus previously was described as adult-onset (AODM) diabetes mellitus. However, type 1 or type 2 diabetes mellitus can occur at any age, and the current classification is based on pathogenesis (e.g., autoimmune destruction of pancreatic β cells, insulin resistance) and clinical presentation rather than on age of onset. Many patients' diabetes mellitus does not easily fit into a single classification. Epidemiologic data indicate that the incidence of type 2 diabetes mellitus is increasing in children and adolescents such that 8-45% of children with newly diagnosed diabetes have nonimmune-mediated diabetes mellitus; most of these individuals have type 2 diabetes mellitus, although other types, including idiopathic or nonimmune-mediated type 1 diabetes mellitus, also have been reported.

Patients with type 2 diabetes mellitus have insulin resistance and usually have relative (rather than absolute) insulin deficiency. Most patients with type 2 diabetes mellitus (about 80-90%) are overweight or obese; obesity itself also contributes to the insulin resistance and glucose intolerance observed in these patients. Patients with type 2 diabetes mellitus who are not obese may have an increased percentage of abdominal fat, which is an indicator of increased cardiometabolic risk. While children with immune-mediated type 1 diabetes generally are not overweight, the incidence of obesity in children with this form of diabetes is increasing with the increasing incidence of obesity in the US population. Distinguishing between type 1 and type 2 diabetes in children may be difficult since obesity may occur with either type of diabetes mellitus, and autoantigens and ketosis may be present in a substantial number of children with features of type 2 diabetes mellitus (e.g., obesity, acanthosis nigricans).

Oral antidiabetic agents are not effective as sole therapy in patients with type 1 diabetes mellitus; insulin is necessary in these patients.

Patients with type 2 diabetes mellitus are not dependent initially on insulin (although many such patients eventually require insulin for glycemic control) nor are they prone to ketosis; however, insulin may be required for correction of symptomatic or persistent hyperglycemia that is not controlled by dietary regulation or oral antidiabetic agents, and ketosis occasionally may develop during periods of severe stress (e.g., acute infection, trauma, surgery). Type 2 diabetes mellitus is a heterogeneous subclass of the disease; hyperglycemia in these patients often is accompanied by other metabolic abnormalities such as obesity, hypertension, hyperlipidemia, and impaired fibrinolysis. Although endogenous insulin is present in type 2 diabetic patients, plasma insulin concentrations may be decreased, increased, or normal. In type 2 diabetic patients, glucose-stimulated secretion of endogenous insulin is frequently, but not always, reduced and decreased peripheral sensitivity to insulin is almost always associated with glucose intolerance.

Glycemic Control and Microvascular Complications

Current evidence from epidemiologic and clinical studies supports an association between chronic hyperglycemia and the pathogenesis of microvascular complications in patients with diabetes mellitus, and results of randomized, controlled studies in patients with type 1 or 2 diabetes mellitus indicate that intensive management of hyperglycemia with near-normalization of blood glucose and glycosylated hemoglobin (hemoglobin A1c[HbA1c]) concentrations provides substantial benefits in terms of reducing chronic microvascular (e.g., retinopathy, nephropathy, neuropathy) complications associated with the disease. HbA1c concentration reflects the glycosylation of other proteins throughout the body as a result of recent hyperglycemia and is used as a predictor of risk for development of diabetic microvascular complications. Microvascular complications of diabetes are the principal causes of blindness and renal failure in developed countries and are more closely associated with hyperglycemia than are macrovascular complications.

In the Diabetes Control and Complications Trial (DCCT), the reduction in risk of microvascular complications in patients with type 1 diabetes mellitus correlated continuously with the reduction in glycosylated hemoglobin concentration produced by intensive insulin treatment (e.g., a 40% reduction in risk of microvascular disease for each 10% reduction in hemoglobin A1c). These data imply that any decrease in glycosylated hemoglobin levels is beneficial and that complete normalization of blood glucose concentrations may prevent diabetic microvascular complications. Data from the largest United Kingdom Prospective Diabetes Study (UKPDS) and other smaller studies in patients with type 2 diabetes mellitus are generally consistent with the same benefits on microvascular complications as those observed with type 1 diabetes mellitus in the DCCT study.

Data from long-term follow-up (over 10 years) of UKPDS patients with type 2 diabetes mellitus who received initial therapy with conventional (diet and oral antidiabetic agents [e.g., sulfonylureas] or insulin to achieve fasting plasma glucose concentrations below 270 mg/dL without symptoms of hyperglycemia) antidiabetic treatment or intensive (stepwise introduction of a sulfonylurea [i.e., chlorpropamide, glyburide], then insulin, or an oral sulfonylurea and insulin, or insulin alone to achieve fasting plasma glucose concentration of 108 mg/dL) antidiabetic regimens indicate that intensive treatment with monotherapy generally is not capable of maintaining strict glycemic control (i.e., maintenance of blood glucose concentrations of 108 mg/dL or normal values) over time and that combination therapy eventually becomes necessary in most patients to attain target glycemic levels in the long term; in UKPDS, intensive treatment that eventually required combination therapy in most patients resulted in median HbA1c concentrations of 7%. Because of the benefits of strict glycemic control, the goal of therapy for type 2 diabetes mellitus is to lower blood glucose to as close to normal as possible, which generally requires aggressive management efforts (e.g., mixing therapy with various antidiabetic agents including sulfonylureas, metformin, insulin, and/or possibly others) over time. For additional information on clinical studies demonstrating the benefits of strict glycemic control on microvascular complications in patients with type 1 or 2 diabetes mellitus,

Glycemic Control and Macrovascular Complications

Current evidence indicates that appropriate management of dyslipidemia, blood pressure, and vascular thrombosis provides substantial benefits in terms of reducing macrovascular complications associated with diabetes mellitus; intensive glycemic control generally has not been associated with appreciable reductions in macrovascular outcomes in controlled trials. Reduction in blood pressure to a mean of 144/82 mm Hg (''tight blood pressure control'') in patients with diabetes mellitus and uncomplicated mild to moderate hypertension in UKPDS substantially reduced the incidence of virtually all macrovascular (e.g., stroke, heart failure) and microvascular (e.g., retinopathy, vitreous hemorrhage, renal failure) outcomes and diabetes-related mortality; blood pressure and glycemic control were additive in their beneficial effects on these end points. While intensive antidiabetic therapy titrated with the goal of reducing HbA1c to near-normal concentrations (6-6.5% or less) has not been associated with appreciable reductions in cardiovascular events during the randomized portion of controlled trials examining such outcomes, results of long-term follow-up (10-11 years) from DCCT and UKPDS indicate a delayed cardiovascular benefit in patients treated with intensive antidiabetic therapy early in the course of type 1 or type 2 diabetes mellitus. For additional details regarding the effects of intensive antidiabetic therapy on macrovascular outcomes,

Treatment Goals

The ADA currently states that it is reasonable to attempt to achieve in patients with type 2 diabetes mellitus the same blood glucose and HbA1c goals recommended for patients with type 1 diabetes mellitus. Based on target values for blood glucose and HbA1c used in clinical trials (e.g., DCCT) for type 1 diabetic patients, modified somewhat to reduce the risk of severe hypoglycemia, ADA currently recommends target preprandial (fasting) and peak postprandial (1-2 hours after the beginning of a meal) plasma glucose concentrations of 70-130 and less than 180 mg/dL, respectively, and HbA1c concentrations of less than 7% (based on a nondiabetic range of 4-6%) in general in patients with type 1 or type 2 diabetes mellitus who are not pregnant. HbA1c concentrations of 7% or greater should prompt clinicians to initiate or adjust antidiabetic therapy in nonpregnant patients with the goal of achieving HbA1c concentrations of less than 7%. Patients with diabetes mellitus who have elevated HbA1c concentrations despite having adequate preprandial glucose concentrations should monitor glucose concentrations 1-2 hours after the start of a meal. Treatment with agents (e.g., α-glucosidase inhibitors, exenatide, pramlintide) that principally lower postprandial glucose concentrations to within target ranges also should reduce HbA1c.

More stringent treatment goals (i.e., an HbA1c concentration less than 7 or less than 6% in nonpregnant or pregnant patients, respectively) can be considered in selected patients. An individualized HbA1c concentration goal that is closer to normal without risking substantial hypoglycemia is reasonable in patients with a short duration of diabetes mellitus, no appreciable cardiovascular disease, and a long life expectancy. Less stringent treatment goals may be appropriate in patients with long-standing diabetes mellitus in whom the general HbA1c concentration goal of less than 7% is difficult to obtain despite adequate education on self-management of the disease, appropriate glucose monitoring, and effective dosages of multiple antidiabetic agents, including insulin. Achievement of HbA1c concentrations of less than 7% is not appropriate or practical for some patients, and clinical judgment should be used in designing a treatment regimen based on the potential benefits and risks (e.g., hypoglycemia) of more intensified therapy. For additional details on individualizing treatment in patients with diabetes mellitus,

Considerations in Initiating and Maintaining Antidiabetic Therapy

When initiating therapy for patients with type 2 diabetes mellitus who do not have severe symptoms, most clinicians recommend that diet be emphasized as the primary form of treatment; caloric restriction and weight reduction are essential in obese patients. Although appropriate dietary management and weight reduction alone may be effective in controlling blood glucose concentration and symptoms of hyperglycemia, many patients receiving dietary advice fail to achieve adequate glycemic control with dietary modification alone.

Recognizing that lifestyle interventions often fail to achieve or maintain the target glycemic goal within the first year of initiation of such interventions, ADA currently suggests initiation of metformin concurrently with lifestyle interventions at the time of diagnosis of type 2 diabetes mellitus. Other experts suggest concurrent initiation of lifestyle interventions and antidiabetic agents only when HbA1c levels of 9% or greater are present at the time of diagnosis of type 2 diabetes mellitus. ADA and other clinicians state that lifestyle interventions should remain a principal consideration in the management of diabetes even after pharmacologic therapy is initiated. The manufacturer states that patients and clinicians should recognize that dietary management is the principal consideration in the management of diabetes mellitus and that antidiabetic therapy is used only as an adjunct to, and not as a substitute for or a convenient means to avoid, proper dietary management. The importance of regular physical activity should be emphasized, and cardiovascular risk factors should be identified and corrective measures employed when feasible. If lifestyle interventions alone are initiated and these interventions fail to reduce symptoms and/or blood glucose concentrations within 2-3 months of diagnosis, initiation of monotherapy with an oral antidiabetic agent (e.g., metformin, sulfonylurea) or insulin should be considered. For more information on the stepwise approach to the management of type 2 diabetes mellitus,

Acarbose Monotherapy

Acarbose lowers postprandial blood glucose concentrations and thereby reduces fluctuations in the daily blood glucose concentration-time profile in patients with type 2 diabetes mellitus and in lean or obese nondiabetic individuals; fasting blood glucose concentrations either are not affected or are mildly decreased. Reductions in blood glucose produced by recommended dosages of acarbose as monotherapy in patients with type 2 diabetes mellitus generally have been associated with reductions in HbA1c concentration of about 0.4-0.77%. In placebo-controlled trials in type 2 diabetic patients, monotherapy with acarbose (25-300 mg 3 times daily) produced greater lowering of postprandial plasma glucose and HbA1c concentrations than dietary therapy alone. A limited number of comparative clinical studies indicate that acarbose monotherapy is as effective as monotherapy with a sulfonylurea (e.g., tolbutamide, glyburide) for the management of mild to moderate postprandial hyperglycemia in patients with type 2 diabetes mellitus.

While acarbose monotherapy may be effective in patients who have had primary or secondary failure to sulfonylureas, limited data are available concerning such use. Primary failure to acarbose may be the result of individual variations in the sensitivity of intestinal α-glucosidases to the drug, impaired insulin secretion, severe insulin resistance, or poor compliance with a diet low in simple sugars. Data on the incidence of primary failures in patients receiving initial monotherapy with acarbose are limited, and data comparing the probabilities of primary failure with acarbose and other oral antidiabetic agents are not available. In addition, no long-term data are available on the incidence of secondary failure to acarbose, but adequate glycemic control has been maintained for at least 1 year in compliant patients receiving the drug.

Combination Therapy

Acarbose also is useful as an adjunct to other antidiabetic drug therapy (e.g., sulfonylureas, metformin) in patients with type 2 diabetes mellitus, possibly because these drugs have different mechanisms of antidiabetic effect. Reductions in blood glucose produced by acarbose combined with other oral antidiabetic agents (e.g., sulfonylurea given at maximum dose, metformin given at 2-5.5 g daily) in patients with type 2 diabetes mellitus generally have resulted in reductions in HbA1c concentrations of about 0.5-0.65% and decreases in 1-hour postprandial glucose concentrations of about 34 mg/dL.

In a comparative clinical trial in type 2 diabetic patients receiving acarbose or tolbutamide alone or in combination as an adjunct to dietary therapy, combined therapy with acarbose (200 mg 3 times daily) and tolbutamide (250-1000 mg 3 times daily) resulted in better glycemic control (as determined by postprandial plasma glucose and HbA1c concentrations) and less weight gain than therapy with diet alone, acarbose alone, or tolbutamide alone; in addition, the mean daily dosage of tolbutamide when used as adjunctive therapy (1.9 g) was less than that when the drug was given as monotherapy (2.4 g). In patients receiving maximum dosage of a sulfonylurea, addition of acarbose (50-300 mg 3 times daily) to such therapy reduced HbA1c concentrations and allowed a reduction in sulfonylurea dosage compared with that in patients receiving sulfonylurea monotherapy. Addition of acarbose (50-100 mg 3 times daily for 6 months) to patients with type 2 diabetes mellitus receiving insulin (mean daily dosage of 61 units) has reduced HbA1c concentrations by a mean of 0.69% and has decreased 1-hour postprandial glucose concentrations by 36 mg/dL. In a long-term study in patients receiving acarbose alone or combined with a sulfonylurea, metformin, or insulin, the reduction in HbA1c concentration was sustained throughout the year-long study in those receiving acarbose alone or in combination with sulfonylureas or metformin; however, the statistically significant effect on HbA1c noted at 6 months in those receiving insulin and acarbose was no longer evident at 1 year.

Some clinicians consider using combined therapy with acarbose and other oral antidiabetic agents in patients not adequately controlled with monotherapy; such regimens may delay initiation or avoid institution of insulin. However, some experts currently recommend initiating therapy with metformin and adding another antidiabetic agent, such as a sulfonylurea, insulin, or a thiazolidinedione, if patients fail to achieve or maintain target HbA1c goals. The choice of additional second-line therapy depends on the degree of glycemic control achieved during metformin monotherapy, which is the preferred agent for initiation of oral antidiabetic therapy. In patients with HbA1c values exceeding 8.5% or symptomatic hyperglycemia despite metformin monotherapy, consideration should be given to adding insulin. Concomitant therapy with insulin (e.g., given as intermediate- or long-acting insulin at bedtime or rapid-acting insulin at meal times) and one or more oral antidiabetic agents appears to improve glycemic control with lower dosages of insulin than would be required with insulin alone and may decrease the potential for body weight gain associated with insulin therapy. Oral antidiabetic therapy combined with insulin therapy may delay progression to either intensive insulin monotherapy or to a second daytime injection of insulin combined with oral antidiabetic therapy. However, such combined therapy may increase the risk of hypoglycemic reactions.

When glycemic control is closer to the target HbA1c goal with metformin monotherapy (e.g., HbA1c less than 7.5%), an agent with less hypoglycemic activity than insulin and/or slower onset of action may be considered (e.g., sulfonylurea, thiazolidinedione) as additional therapy to metformin. While some experts state that α-glucosidase inhibitors are not recommended as second-line therapy after failure of metformin monotherapy because of lesser efficacy, frequent adverse GI effects, and relatively greater cost compared with other antidiabetic agents, α-glucosidase inhibitors may be appropriate for treatment of type 2 diabetes mellitus in selected patients.

Acarbose should not be used as sole antidiabetic therapy in patients whose diabetes is complicated by ketoacidosis with or without coma; instead, such patients should receive insulin.

Precautions and Other Considerations

Patients should be advised fully and completely about the nature of diabetes mellitus, what they must do to prevent and detect complications, and how to control their condition. Patients should be instructed that dietary regulation is the principal consideration in the management of diabetes and that acarbose therapy is used only as an adjunct to, and not a substitute for, proper dietary regulation. Patients also should be advised that they should not neglect dietary restrictions, develop a careless attitude about their condition, or disregard instructions about body-weight control, exercise, hygiene, and avoidance of infection.

Because of its mechanism of action, acarbose should not cause hypoglycemia when administered alone in the fasted or postprandial state. However, hypoglycemia, including hypoglycemic shock, may occur when the drug is used concomitantly with a sulfonylurea antidiabetic agent and/or insulin. If hypoglycemia occurs, appropriate adjustments in the dosage of these agents should be made. Oral glucose (dextrose), the absorption of which is not inhibited by acarbose, should be used instead of sucrose (table sugar) for the treatment of mild to moderate hypoglycemia in patients receiving acarbose. Severe hypoglycemia may require the use of either IV glucose or parenteral glucagon.

Therapy with acarbose, particularly in dosages exceeding 150 mg daily (50 mg 3 times daily), may be associated with elevations in serum aminotransferase (i.e., ALT [SGPT], AST [SGOT]) concentrations and, in rare instances, hyperbilirubinemia. The manufacturer recommends that serum aminotransferase determinations be performed every 3 months during the first year of acarbose therapy and periodically thereafter. If elevations in serum aminotransferase concentrations occur, the dosage of acarbose should be reduced; withdrawal of the drug may be necessary, particularly if the elevated serum aminotransferase concentrations persist.

Dosage and Administration


Acarbose is administered orally. The drug should be administered at the beginning (with the first bite) of each main meal. If a patient misses a dose of acarbose, a double dose should not be taken to make up for the missed dose; instead, the next dose should be taken at the next meal. To minimize GI adverse effects, rich foods, sauces, and certain beverages, including beer and carbonated soft drinks, should be avoided. Gas-producing foods such as beans, nuts, bran cereals, broccoli, and cabbage should be limited. Meals and snacks should be low in fat, and patients should drink plenty of water, especially in the early morning, midmorning, and afternoons. Food portions should be small to moderate, and overeating should be avoided. Food should be eaten slowly and chewed thoroughly. A food diary should be kept to target problem foods. If the prescribed diet designed to minimize GI adverse effects is not observed, adverse GI effects may be intensified.


Safety and efficacy of acarbose in children younger than 18 years of age have not been established.

Dosage of acarbose must be individualized carefully based on patient response and tolerance. The goal of therapy should be to reduce both postprandial blood (or plasma) glucose and glycosylated hemoglobin (hemoglobin A1c [HbA1c]) values to normal or near normal using the lowest effective dosage of acarbose, either when used as monotherapy or in combination with a sulfonylurea antidiabetic agent, metformin, or insulin.(Glucose concentrations in plasma generally are 10-15% higher than those in whole blood; glucose concentrations also may vary according to the method and laboratory used for these determinations.) During initiation of therapy and titration of dosage, 1-hour postprandial glucose determinations should be performed to determine therapeutic response and the minimum effective dosage of acarbose; thereafter, HbA1c values should be monitored at intervals of approximately 3 months (the life-span of erythrocytes) to evaluate long-term glycemic control.

For the management of type 2 (noninsulin-dependent) diabetes mellitus (NIDDM), the usual initial adult dosage of acarbose is 25 mg given at the beginning (with the first bite) of each main meal. However, some patients may benefit from a more gradual dosage titration to reduce adverse GI effects. Therapy with the drug in these patients should be initiated at a low dosage (25 mg once daily) and increased gradually as necessary to the usual initial dosage of 25 mg 3 times daily. Subsequent dosage should be adjusted according to the patient's therapeutic response and tolerance, using the lowest possible effective dosage. Once an acarbose dosage of 25 mg 3 times daily has been reached, the dosage of acarbose may be increased at intervals of 4-8 weeks until the desired 1-hour postprandial glucose concentration (e.g., less than 180 mg/dL) is achieved or a maximum dosage of 50 mg 3 times daily (for patients weighing 60 kg or less) or 100 mg 3 times daily (for patients weighing more than 60 kg) is reached. Common adverse GI effects (e.g., flatulence, diarrhea, abdominal discomfort) usually develop during the first few weeks of therapy and generally diminish in frequency and intensity with time (4-8 weeks), although flatulence usually is only abated rather than returned to pretreatment levels. If adverse GI effects occur despite adherence to the prescribed diet, a clinician should be consulted, and the dosage of acarbose temporarily or permanently reduced.(See Dosage and Administration: Administration.) The usual maintenance dosage of acarbose ranges from 50-100 mg 3 times daily; use of the 50-mg dosage 3 times daily may be associated with fewer adverse effects and has efficacy similar to the 100-mg dosage 3 times daily. Since patients with low body weight may be at increased risk for elevated serum aminotransferase concentrations, only patients with body weight exceeding 60 kg should be considered for dosages exceeding 50 mg 3 times daily. If no further reduction in postprandial glucose or HbA1c concentrations occurs at the maximum recommended dosage of acarbose (100 mg 3 times daily), consideration should be given to lowering the dosage. Dosages of acarbose higher than those recommended by the manufacturer (e.g., 200-300 mg 3 times daily) have been evaluated, but clinically important differences in postprandial plasma glucose and HbA1c concentrations have not been shown consistently; the manufacturer states that acarbose dosages exceeding 100 mg 3 times daily are not recommended since such dosages have been associated with an increased risk of elevated serum aminotransferase concentrations. Once an effective and tolerated dosage of acarbose is established, that dosage should be maintained. Although satisfactory control of blood glucose concentrations may be achieved within a few days after dosage adjustment, the full effect of the drug may be delayed for up to 2 weeks.

Dosage in Renal and Hepatic Impairment

Acarbose is not recommended for use in diabetic patients with renal impairment (i.e., serum creatinine exceeding 2 mg/dL) since no information is available concerning the use of the drug in such patients; however, in a study in nondiabetic individuals with renal impairment, plasma concentrations of acarbose increased in proportion to the degree of renal dysfunction. Acarbose is contraindicated in patients with cirrhosis; however, the manufacturer makes no specific recommendations regarding use of the drug in other conditions associated with hepatic impairment, since studies have not been performed.

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