[Metabolic risks of salbutamol in diabetic patients. A study using somatostatin (author's transl)]

Salbutamol-induced diabetic ketoacidosis having recently been reported, the authors have studied the metabolic changes produced by the drug in 6 nondiabetic patients. All patients received a 3-hour infusion of salbutamol (S) 20 z g/minm. On the following day, three of these were given somatostatin (SRIF) 100 mg/hour mixed with S infused at the same rate, whilst the remaining 3 patients received SRIF alone. On the 3rd day, patients of the first sub-group received the same infection of S and SRIF as before plus exogenous glucagon 90 ng/kg/hour. Somatostatin is know to inhibit insulin and glucagon secretion. Exogenous glucagon was given in order to reproduce the metabolic conditions of insulin-deficient diabetes mellitus. Salbutamol alone induced a small rise in blood glucose and insulin, free fatty acids, glycerol and ketonic bodies, but no changes in endogenous glucagon. SRIF alone produced no significant metabolic variations. In the presence of SRIF, all salbutamol-induced metabolic changes were increased. Adding glucagon mainly resulted in high levels of ketonic bodies. All variations correlated with each other. Thus, whilst the hyperglycaemic, lipolytic and ketogenic effects of S in non-diabetic patients are partly masked by insulin hypersecretion, they are enhanced in the absence of insulin and, to an even greater extent, by an excess of glucagon. Diabetic patients treated with salbutamol should therefore be under close surveillance and have their insulin dosage increased.