Yes

Antidiabetic Agent (Sulfonylurea)

Adjunct to diet for the management of mild to moderately severe, stable, noninsulin-dependent (type 2) diabetes mellitus

D

Diabetes complicated by ketoacidosis, therapy of type 1 diabetes, hypersensitivity to sulfonylureas

Patients should be properly instructed in the early detection and treatment of hypoglycemia.

Use caution in renal impairment.

The administration of oral hypoglycemic drugs has been reported to be associated with increased cardiovascular mortality as compared to treatment with diet alone or diet plus insulin.

At higher dosages, sulfonylureas may block the ATP-sensitive potassium channels, which may correspond to an increased risk of cardiovascular events. In May, 2000, the National Diabetes Center issued a warning to avoid the use of sulfonylureas at higher dosages.

>10%:

Central nervous system: Headache, dizziness

Gastrointestinal: Constipation, diarrhea, heartburn, anorexia, epigastric fullness

1% to 10%: Dermatologic: Rash, urticaria, photosensitivity

Monitor patient closely; large number of drugs interact with sulfonylureas

Increased effect: Increases hypoglycemia when coadministered with salicylates or beta-adrenergic blockers; MAO inhibitors; oral anticoagulants, NSAIDs, sulfonamides, phenylbutazone, insulin, clofibrate, fluconazole, gemfibrozil, H₂-antagonists, methyldopa, tricyclic antidepressants

Believed to cause hypoglycemia by stimulating insulin release from the pancreatic beta cells; reduces glucose output from the liver (decreases gluconeogenesis); insulin sensitivity is increased at peripheral target sites (alters receptor sensitivity/receptor density); potentiates effects of ADH; may produce mild diuresis and significant uricosuric activity

Onset of effect: 1 hour

Peak hypoglycemic effects: 8-10 hours

Duration: 12-24 hours, prolonged with renal impairment

Serum half-life:

Parent compound: 0.8-2.4 hours

Metabolite: 5-6 hours

Adults: Oral (elderly patients may be more sensitive and should be started at a lower dosage initially):

At higher dosages, sulfonylureas may block the ATP-sensitive potassium channels, which may correspond to an increased risk of cardiovascular events. In May, 2000, the National Diabetes Center issued a warning to avoid the use of sulfonylureas at higher dosages; see Warnings/Precautions.

Dosing adjustment in renal impairment: Cl_cr <50 mL/minute: Acetohexamide is not recommended in patients with renal insufficiency due to the increased potential for developing hypoglycemia

Dosing adjustment in hepatic impairment: Initiate therapy at lower than recommended doses; further dosage adjustment may be necessary because acetohexamide is extensively metabolized but no specific guidelines are available

May be administered with food

Dizziness is common

Can rarely cause bone marrow suppression use cautiously with clozapine and carbamazepine; MAOIs and TCAs may potentiate hypoglycemic effects

No information available to require special precautions

Use salicylates with caution in patients taking acetohexamide because of potential increased hypoglycemia. NSAIDs such as ibuprofen, naproxen and others may be safely used. Acetohexamide-dependent diabetics (noninsulin-dependent, type 1) should be appointed for dental treatment in mornings to minimize chance of stress-induced hypoglycemia.

If nausea or stomach upset occurs, may be taken with food; take at the same time each day; avoid alcohol

Patients who are anorexic or NPO may need to have their dose held to avoid hypoglycemia

Blood (preferred) and urine glucose concentrations should be monitored when therapy is started; normally takes 7 days to determine therapeutic response

Tablet: 250 mg, 500 mg

Alexander RW, "Prolonged Hypoglycemia Following Acetohexamide Administration," Diabetes, 1966, 15(5):362-4.

Cowen DL, Burtis B, and Youmans J, "Prolonged Coma After Acetohexamide Ingestion," JAMA, 1967, 201(2):141-2.

"Standards of Medical Care for Patients With Diabetes Mellitus. American Diabetes Association," Diabetes Care, 1994, 17(6):616-23.