Recent Updates on Type 1 Diabetes Mellitus Management for Clinicians

Abstract

Type 1 diabetes mellitus (T1DM) is a chronic autoimmune condition that requires life-long administration of insulin. Optimal management of T1DM entails a good knowledge and understanding of this condition both by the physician and the patient. Recent introduction of novel insulin preparations, technological advances in insulin delivery and glucose monitoring, such as continuous subcutaneous insulin infusion (CSII) and continuous glucose monitoring and improved understanding of the detrimental effects of hypoglycaemia and hyperglycaemia offer new opportunities and perspectives in T1DM management. Evidence from clinical trials suggests an important role of structured patient education. Our efforts should be aimed at improved metabolic control with concomitant reduction of hypoglycaemia. Despite recent advances, these goals are not easy to achieve and can put significant pressure on people with T1DM. The approach of physicians should therefore be maximally supportive. In this review, we provide an overview of the recent advances in T1DM management focusing on novel insulin preparations, ways of insulin administration and glucose monitoring and the role of metformin or sodium-glucose co-transporter 2 inhibitors in T1DM management. We then discuss our current understanding of the effects of hypoglycaemia on human body and strategies aimed at mitigating the risks associated with hypoglycaemia.

Keywords: Artificial pancreas device systems; Blood glucose self-monitoring; Continuous glucose monitoring; Continuous subsubcutaneous insulin infusion; Diabetes mellitus, type 1; Hypoglycemia; Impaired awareness of hypoglycaemia; Severe hypoglycaemia; Structured education.

Fig. 1. Putative mechanisms linking hypoglycaemia to increased cardiovascular (CV) risk. Hypoglycaemia is characterised by sympathoadrenal activation. Abnormal cardiac repolarisation and deranged autonomic function as well as the acute haemodynamic consequences of hypoglycaemia can induce CV events via arrhythmias (1) and cardiac ischemia (2). Enhanced coagulation and impaired fibrinolysis (3) in addition to platelet activation and aggregation (6) promotes atherothrombosis. Acute leucocytosis and production of pro-inflammatory cytokines (4) as well as upregulation of cell adhesion molecules (5) is likely to encourage atherogenesis in an incremental fashion.