We review clinical instances in which A1C should not be used and reflect on the use of other glucose metrics that can be used, in substitution of or in combination with A1C and SMBG, to tailor an individualized approach that will result in better outcomes and patient empowerment.

Intensive insulin therapy is the mainstay of treatment for people with Type 1 diabetes, but hypoglycaemia and weight gain are often limiting factors in achieving glycaemic targets and decreasing the risk of diabetes-related complications. The inclusion of pharmacological agents used traditionally in Type 2 diabetes as adjuncts to insulin therapy in Type 1 diabetes has been explored, with the goal of mitigating such drawbacks. Pramlintide and metformin result in modest HbA 1c and weight reductions, but their use is limited by poor tolerability and, in the case of pramlintide, by frequency of injections and cost. The addition of glucagon-like peptide-1 receptor agonists to insulin results in improved glycaemic control, reduced insulin doses and weight loss, but this is at the expense of higher rates of hypoglycaemia and hyperglycaemia with ketosis. Sodium-glucose co-transporter-2 and dual sodium-glucose co-transporter-2 and -1 inhibitors also improve glucose control, but with reductions in weight and insulin requirements potentiating the risk of acidosis-related events and hypoglycaemia. The high proportion of people with Type 1 diabetes not achieving glycaemic targets, the negative clinical impact of intensive insulin therapy and the rise in obesity and cardiovascular disease and mortality, underline the need for individualized clinical care. The evaluation of new therapies, effective in Type 2 diabetes, as adjuncts to insulin therapy represents a promising strategy, particularly given the beneficial effects on cardiovascular and renal outcomes in people with Type 2 diabetes with or at high risk of complications that are also observed in patients with Type 1 diabetes. As the population with Type 1 diabetes ages, our mission is to evolve and provide better tools and improved therapies to excel, not only in glycaemic control but also in risk reduction and reduction of complications.

Objective: To present 2 cases in which patients previously diagnosed with type 2 diabetes (T2D) rapidly progressed to insulin dependence following cancer treatment with immune checkpoint inhibitors (ICH). Both patients were subsequently found to be positive for glutamic acid decarboxylase 65 antibodies (+GAD), indicative of type 1.5 diabetes (T1.5D). Methods: Patient history, laboratory results, and treatment course, in addition to review of the relevant literature, are presented. Results: The first case involved a 78-year-old man with lung cancer and a 30-year history of T2D (controlled with oral medications [OM]) who developed polydipsia, polyuria, and nocturia 5 weeks post-treatment with nivolumab. Basal bolus insulin was required, and frequent insulin increments were necessary to achieve metabolic control. The patient had no personal or family history of autoimmunity. The second case involved a 55-yearold man with metastatic melanoma and a 4-year history of T2D who required transition from OM to basal bolus insulin following treatment with ipilimumab. Hypophysitis prompted discontinuation of ipilimumab and initiation of pembrolizumab, which was followed by the need for an intensive escalation of insulin dosage for glucose control.