Preventive effects of octreotide (SMS 201‐995) on diabetic ketogenesis during insulin withdrawal.

Abstract

835 ,umol 1-1 h, AUC, P = NS) were not significant, but the peak increments of acetoacetate (1413 ± 354 ,umol F-1 vs 612 ± 176 ,mol F-1, P < 0.05), ,3-hydroxybutyrate (2180 ± 475 ,umol 1-1 vs 922 ± 246 ,umol 1-1, P < 0.01) and the decrements in plasma bicarbonate (-8 ± 1 ,umol F-1 vs -4 ± 1 ,umol F-1, P < 0.05) and pH (-0.07 + 0.01 vs -0.03 ± 0.01, P < 0.05) were significantly less with octreotide. 4 At the same time peak increments of glucagon were lower with octreotide treatment (329 ± 206 pg ml-' vs 39 ± 30 pg ml-', P < 0.05). 5 We conclude that, despite accelerated lipolysis and provision of substrate for ketogenesis during insulin withdrawal, this somatostatin analogue significantly reduces ketogenesis resulting from insulin deprivation, probably secondary to decreasing glucagon secretion. This drug may be useful in short term prophylactic treatment of diabetic patients during periods of increased risk for ketoacidosis.

Association of diabetic ketoacidosis, severe hypoglycemia and glycemic control among children and young adults with type 1 diabetes mellitus treated with premixed versus basal-bolus insulin therapy

“…In addition, approximately 28%–65% of instances of DKA occurred in young T1DM patients due to omitted insulin injections; therefore, omitting insulin injection is the major cause of DKA in children and young adults with T1DM [13] , [21] , [22] , [23] , [24] , [25] . In patients with T1DM, after 4–6 h of withdrawal from insulin administration ketone bodies will increase, which eventually increases the risk of DKA [26] , [27] .After premixed insulin injection, serum insulin concentration may reach its maximum level 60–100 min after injection and down to relatively low level after around 15–18 h [28] , [29] , [30] , [31] . If patients miss one dose of premixed insulin injection, it means not only losing one-third to one-half of the total daily insulin dose, but also means exposing the patient in a relative or absolute insulin deficiency period, which would increase the risk of DKA.…”

Diabetic Ketoacidosis

“…Diem et al were assessed preventive effects of octreotide on diabetic ketogenesis during insulin withdrawal. Octreotide led to a marked suppression of beta-hydroxybutyrate, acetoacetate and glucagon levels and an associated diminution of bicarbonate consumption and the fall in pH [190]. Anthony et al reported a case of DKA with glucagonoma who was unresponsive to conventional therapy and treated with octreotide [191].…”

HHS in type 1 diabetes associated with medication overdose: can counter‐regulatory hormone suppression prevent diabetic ketoacidosis?

“…Circulating levels of CRHs including glucagon, growth hormone, cortisol and catecholamines are higher in patients with DKA compared to HHS, and administration of cortisol, glucagon and catecholamines to patients with type 1 diabetes results in ketosis. The causative role of CRH excess in DKA is convincingly demonstrated by studies utilising somatostatin and its analogue octreotide to mediate glucagon suppression, with administration to insulin‐deprived patients with type 1 diabetes resulting in profound suppression of ketogenesis and a less significant effect on hyperglycaemia . Finally, CRH suppression with beta‐blockers and somatostatin has shown relevance in the prevention and treatment of DKA.…”