P-037 CLINICAL CASE: HYPERAMYLINAEMIA IN A PATIENT WITH TYPE 2 DIABETES MELLITUS

Abstract Introduction Amylin (islet amyloid polypeptide, IAPP) is a peptide hormone secreted by pancreatic β-cells synchronously with insulin. Normally, it contributes to carbohydrate metabolism regulation by slowing gastric emptying, suppressing glucagon secretion, and modulating appetite. However, in type 2 diabetes mellitus (T2DM), excessive amylin secretion may lead to disturbances in carbohydrate and lipid metabolism and contribute to amyloid degeneration of the islets of Langerhans. Clinical Case Patient: B. S., 72 years old. Diagnosis: Type 2 diabetes mellitus (disease duration >10 years). The patient has been treated with metformin for several years without insulin therapy.Table 1:Anthropometric and Laboratory Data The patient exhibits a combination of hyperamylinaemia, hyperinsulinemia, and pronounced hyperglycemia, reflecting decompensated diabetes in the context of obesity and severe insulin resistance. Elevated amylin levels in T2DM patients may have a dual impact: Carbohydrate Metabolism: Suppression of glucagon secretion and delayed gastric emptying may cause delayed but more pronounced postprandial glucose spikes. This explains the high glycemia and unsatisfactory HbA1c levels in the patient. Lipid Metabolism: Amylin may stimulate hepatic lipogenesis and triglyceride secretion, as reflected by elevated triglycerides and LDL-C and reduced HDL-C. The presence of small, dense LDL particles associated with hyperamylinaemia increases atherogenic risk. Conclusion In a patient with long-standing T2DM, hyperamylinaemia was identified, accompanied by hyperglycemia, hyperinsulinemia, and dyslipidemia. This case highlights the significant role of amylin in the pathogenesis of both carbohydrate and lipid metabolism disturbances in T2DM. Elevated amylin levels are associated with progressive insulin resistance, worsening diabetes compensation, and an increased risk of atherosclerotic complications.