[Post-hyperglycaemic hypoglycaemia: effects of somatostatin (author's transl)]

Precise recordings of reactive (post-hyperglycaemic) hypoglycaemia were ensured by continuous blood glucose monitoring during oral glucose tolerance tests. The definition of hypoglycaemia was limited to the following criteria: absence of chemical diabetes; fall in blood sugar to less than 30% of the fasting level or to less than 2.50 mmol/l (0.45 g/l); development of clinical signs of hypoglycaemia. An infusion of somatostatin over 4 hours slowed down the initial rise in blood sugar during the first 90 minutes and the rise was prolonged throughout the infusion whatever its duration. The maximum glycaemia reached was 13.3 mmol/l (2.40 g/l) at the 250th minute. Interruption of the infusion led to a rapid fall in blood sugar to a level identical (2.1 and 2.5 mmol/l) with and without somatostatin respectively. Somatostatin infusions, while frankly diabetogenic in certain circumstances, do not prevent reactive hypoglycaemia but rather delay its onset.