Latest research on Glibenclamide

Glyburide is an oral antihyperglycemic agent used for the treatment of non-insulin-dependent diabetes mellitus (NIDDM). It belongs to the sulfonylurea class of insulin secretagogues, which act by stimulating β cells of the pancreas to release insulin. Sulfonylureas increase both basal insulin secretion and meal-stimulated insulin release. Medications in this class differ in their dose, rate of absorption, duration of action, route of elimination and binding site on their target pancreatic β cell receptor. Sulfonylureas also increase peripheral glucose utilization, decrease hepatic gluconeogenesis and may increase the number and sensitivity of insulin receptors. Sulfonylureas are associated with weight gain, though less so than insulin. Due to their mechanism of action, sulfonylureas may cause hypoglycemia and require consistent food intake to decrease this risk. The risk of hypoglycemia is increased in elderly, debilitated and malnourished individuals. Glyburide has been shown to decrease fasting plasma glucose, postprandial blood glucose and glycosolated hemoglobin (HbA1c) levels (reflective of the last 8-10 weeks of glucose control). Glyburide appears to be completely metabolized, likely in the liver. Although its metabolites exert a small hypoglycemic effect, their contribution to glyburide's hypoglycemic effect is thought to be clinically unimportant. Glyburide metabolites are excreted in urine and feces in approximately equal proportions. The half-life of glyburide appears to be unaffected in those with a creatinine clearance of greater than 29 ml/min/1.73m2.

Latest findings

We have previously shown that the infusion of Glibenclamide, a sulfonylurea that acts primarily by inhibiting the K+ATP channel, reduced the magnitude of ST elevation and the incidence of VF in our model. [source, 2016]
We recalled KATP-PNDM patients to switch from insulin injection to oral Glyburide, usually within 18 months of diagnosis. [source, 2016]
Glyburide was started at a dose of 0.1 mg per kilogram twice daily and was increased daily by 0.2 mg per kilogram. [source, 2016]
The dose of Glyburide was increased until insulin independence was achieved or the dose was at least 0.8 mg per kilogram per day. [source, 2016]
The change to sulfonylureas was considered to be successful if a patient was able to stop insulin treatment completely at any dose of Glyburide and was deemed to be unsuccessful if insulin was still required with a dose of Glyburide at least 0.8 mg per kilogram per day. [source, 2016]
The HbA1c of the PNDM group was tested at least 6 months after Glyburide treatment. [source, 2016]
Three cases were placed on Glyburide therapy and 15 cases were on insulin therapy, with good glycemic control in most cases. [source, 2016]
Glucose stimulation reduces insulin secretion, whereas sulfonylureas stimulate the secretion, explaining the rationale of Glyburide therapy. [source, 2016]
Of the two cases, one was responsive to Glyburide and the other presented with severe gastrointestinal reactions and parental worries about side effects and therefore discontinued despite recommendations to the contrary. [source, 2016]
One case with iDEND in the present study responded favorably to oral Glyburide therapy. [source, 2016]