ICD-10 Specific code E10.4: Insulin-dependent diabetes mellitus: With neurological complications

The blood glucose lowering effect of insulin is due to the facilitated uptake of glucose following binding of insulin to receptors on muscle and fat cells and to the simultaneous inhibition of glucose output from the liver.

The blood glucose lowering effect of insulin aspart is due to the facilitated uptake of glucose following binding of insulin to receptors on muscle and fat cells and to the simultaneous inhibition of glucose output from the liver. Insulin aspart produces a more rapid onset of action compared to soluble human insulin, together with a lower glucose concentration, as assessed within the first four hours after a meal. Insulin aspart has a shorter duration of action compared to soluble human insulin after subcutaneous injection.

Insulin degludec binds specifically to the human insulin receptor and results in the same pharmacological effects as human insulin. The blood glucose-lowering effect of insulin is due to the facilitated uptake of glucose following the binding of insulin to receptors on muscle and fat cells and to the simultaneous inhibition of glucose output from the liver.

Insulin detemir is a soluble, long-acting insulin analogue with a prolonged duration of effect used as a basal insulin.

Insulin glargine is a human insulin analogue designed to have a low solubility at neutral pH. After injection, the acidic solution is neutralised leading to formation of a precipitate from which small amounts of insulin glargine are continuously released.

Insulin glulisine is a recombinant human insulin analogue that is equipotent to regular human insulin. Insulin glulisine has a more rapid onset of action and a shorter duration of action than regular human insulin.

The primary activity of insulin lispro is the regulation of glucose metabolism.

Teplizumab binds to CD3 (a cell surface antigen present on T lymphocytes) and delays disease progression in patients with stage 2 T1D. The mechanism may involve partial agonistic signalling leading to deactivation of autoreactive CD8+ T lymphocytes and reduced immune-mediated beta-cell destruction. Teplizumab leads to an increase in the proportion of CD8+ T cells with signs of exhaustion in peripheral blood.