Comparison of acute and prolonged effects of glibenclamide and chlorpropamide in patients with non-insulin-dependent diabetes.
Pauli Ylitalo, Heikki Oksala, T Pitkäjärvi
Abstract
Pauli Ylitalo, Heikki Oksala, T Pitkäjärvi
Abstract
The effects of single oral dose of glibenclamide (Gilemid 5 mg) and chlorpropamide (250 mg) on serum insulin and glucose levels and electrolyte (sodium, potassium) balance were studied, in a cross-over double-blind manner, in 11 patients with non-insulin-dependent diabetes. Both drugs increased serum insulin for more than 8 h but less than 24 h. The effect of glibenclamide was slightly stronger than that of chlorpropamide. Serum glucose concentration was significantly decreased by glibenclamide only. Glucose excretion in urine was declined for a longer time by glibenclamide than by chlorpropamide. Neither of the drugs essentially effected on sodium and potassium excretion. After the acute study, all the above patients and 5 additional ones were treated in open care with glibenclamide (2.5-10 mg daily) and chlorpropamide (125-500 mg daily) for 8 weeks in a cross-over manner. Both drugs showed practically similar efficacy; 5 mg of glibenclamide corresponded to 250 mg of chlorpropamide. One patient under chlorpropamide treatment exhibited hyponatraemia. Eight weeks after the commencement of therapy, serum potassium concentration was lower under chlorpropamide than under glibenclamide treatment. The results suggest that, in non-insulin-dependent diabetes, a single oral dose of glibenclamide acts as long as that of chlorpropamide, and that in long-term therapy 5 mg of glibenclamide is equipotent with 250 mg of chlorpropamide.
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The effects of single oral dose of glibenclamide (Gilemid 5 mg) and chlorpropamide (250 mg) on serum insulin and glucose levels and electrolyte (sodium, potassium) balance were studied, in a cross-over double-blind manner, in 11 patients with non-insulin-dependent diabetes. Both drugs increased serum insulin for more than 8 h but less than 24 h. The effect of glibenclamide was slightly stronger than that of chlorpropamide. Serum glucose concentration was significantly decreased by glibenclamide only. Glucose excretion in urine was declined for a longer time by glibenclamide than by chlorpropamide. Neither of the drugs essentially effected on sodium and potassium excretion. After the acute study, all the above patients and 5 additional ones were treated in open care with glibenclamide (2.5-10 mg daily) and chlorpropamide (125-500 mg daily) for 8 weeks in a cross-over manner. Both drugs showed practically similar efficacy; 5 mg of glibenclamide corresponded to 250 mg of chlorpropamide. One patient under chlorpropamide treatment exhibited hyponatraemia. Eight weeks after the commencement of therapy, serum potassium concentration was lower under chlorpropamide than under glibenclamide treatment. The results suggest that, in non-insulin-dependent diabetes, a single oral dose of glibenclamide acts as long as that of chlorpropamide, and that in long-term therapy 5 mg of glibenclamide is equipotent with 250 mg of chlorpropamide.
Key concepts: Chlorpropamide, Glibenclamide, Internal medicine, Endocrinology, Diabetes mellitus, Insulin, Medicine, Chemistry