A trial of glucagon in the treatment of painful biliary tract disease

Abstract

Seventy-one patients with a clinical diagnosis of painful biliary tract disease have been entered into a double-blind trial of glucagon. Twenty-eight were excluded as gallstones were not proved: of the remainder, 21 patients received glucagon and 22 placebo. Glucagon-treated patients were pain free 14.26 h (+/- 2.77 s.e.m.) after commencing treatment compared to 29.14 h (+/- 6.01 s.e.m.) for the placebo group (P less than 0.05). Tenderness in the right hypochondrium showed a significant improvement when assessed at 12 h (P less than 0.02) and 24 h (P less than 0.1) for those given glucagon. A significant difference in blood glucose levels was seen between the two groups (P less than 0.05). No serious side effects were observed. Glucagon relieves the pain and tenderness associated with painful biliary tract disease more effectively than conventional therapy.

The metabolic response to glucagon and glucagon‐(1‐21)‐peptide in normal subjects and non insulin dependent diabetics.

“…However, its spasmolytic action has been accompanied by metabolic consequences, leading to an inappropriate state of hyperglycaemia (Stower et al, 1982). The metabolic activity of glucagon is dependent on the intact molecule, when it binds to liver plasma membranes and activates adenyl cyclase and lipolysis (Frandsen et al, 1981;Jorgensen et al, 1983).…”

“…However, the smooth muscle relaxant properties of glucagon have only relatively recently been utilised in clinical medicine. Therapeutic studies have centred mainly on the treatment of biliary tract disease when intravenous glucagon was found to be effective in relieving pain and cystic duct obstruction (Paul, 1979;Stower et al, 1982 Figure 1 Glucagon:glucagon-(1-21)-peptide structure. Boxed area represents the 8 amino acids cleaved from glucagon to obtain glucagon-(1-21)-peptide.…”

“…However, all these studies have reported marked hyperglycaemia of up to 25-30% (Stower et al, 1982). Animal studies have demonstrated that the entire glucagon molecule is required to exert the metabolic effects (Frandsen etal., 1981;J0rgensen et al, 1983).…”

Glucagon

“…After excluding 21 patients (no radiological evidence of gallstones) it was concluded that glucagon reduced the amount of pethidine administered for analgesia and the mean time in hours for the patient to become pain free was significantly reduced (14.26 vs 29.14 h). The dose was a 1 mg bolus followed by a 1 mg infusion over 4 h 34 …”