Endocrine Abstracts

MODY as a result of a genetic variant in the HNF1-α gene is traditionally treated with sulphonylureas, often with eventual progression to insulin use due to the loss of beta cell function. We present the case of a 58-year-old female who attended the diabetes service for many years for a genetically confirmed diagnosis of HNF1-α MODY. She was originally diagnosed with pre-diabetes at the age of 16 and eventually commenced on oral hypoglycaemic agents (OHAs) at the age of 23, with transition to insulin at 29. At routine diabetes review at the age of 57, Semaglutide was offered as an adjuvant to basal-bolus insulin in light of suboptimal glycaemic control with HbA1c ranging between 57 – 74 mmol/mol. There were no microvascular complications of diabetes. After 12 months of Semaglutide therapy, her HbA1c had improved to 46 mmol/mol. Dexcom G7 data revealed an improvement in time in range (TIR) from 70% preceding Semaglutide use to 78% after Semaglutide use for 12 months. Total daily dose (TDD) of basal insulin reduced by 42% (25 to 14 units) with a reduction in regular prandial insulin with all meals to PRN Novorapid with high-glycaemic-index foods. There are few case reports surrounding the use of GLP-1 receptor agonists in HNF1-α MODY. One report has shown glycaemic benefit with the addition of Liraglutide when compared with pioglitazone and insulin detemir alone, with another case showing a reduction in HbA1c from 63 to 49 mmol/mol with a switch from Glimepiride to Dulaglutide. We report the safe and efficacious use of Semaglutide in a case of HNF1-α MODY resulting in improved TIR and reduced insulin TDD. The use of GLP1-receptor agonists in HNF1-α MODY have been shown in few case reports to produce beneficial glycaemic outcomes with further evidence required to determine their safety and efficacy.