Endocrine Abstracts

Introduction: Type 1 diabetes (T1DM) is characterised by autoimmune destruction of pancreatic β-cells, which results in insulinopenia. Type 2 diabetes (T2DM) is caused by insulin resistance associated with pancreatic β-cell dysfunction. The combination of these two conditions is classed as double diabetes.

Case report: Female patient aged 16 years with a history of gestational diabetes in her mother. She presented with profound asthenia associated with a cardinal syndrome of 1 month’s duration. Emergency investigations revealed inaugural ketosis (capillary glycaemia of 2.87g/L and positive acetonuria on urine dipstick, alkaline reserves of 17 mEq/l). Clinical examination revealed a BMI of 29 kg/m² and a waist circumference of 90 cm, with acanthosis nigricans on the neck. Paraclinical investigations showed an HbA1c of 14%, a negative infectious workup, a C-peptide of 79 pmol/l (<200 pmol/l) and anti-GAD antibodies >280 IU/ml. Given this clinical and biological picture, the diagnosis of double diabetes was accepted and the patient was started on basal bolus insulin therapy with metformin.

Discussion: Double or hybrid diabetes is a condition characterised by the coexistence of autoimmune T1DM and T2DM, accompanied by the presence of insulin resistance and metabolic syndrome. Initial epidemiological studies have indicated that 4% of patients with T1DM may also develop T2DM. A study led by Mishra in 2018 found a 7% prevalence of double diabetes in young diabetics with an average age of 22. The latest hypotheses suggest that obesity, by promoting insulin resistance, induces glucotoxicity and accelerates β-cell apoptosis. Furthermore, inflammatory phenomena due to excess adipose tissue and the resulting dysregulation of the immune system can trigger T1DM.