SUN-549 Type 1 Diabetes Mellitus and Measles Infection: Is There a Connection?

Abstract Disclosure: M. Mathiopoulou: None. M. Vidovic: None. N. Durisch: None. S. Burkhard: None. A 28-year-old male initially presented to his primary care physician with an itchy maculopapular rash, sore throat, diarrhea, mild headaches, dysuria, fatigue, and an 8 kg weight loss over the past month. Following hospital admission and laboratory evaluation, which revealed hepatopathy, measles infection was confirmed via PCR. The patient was isolated, and the public health office was informed for contact tracing. His vaccination status was unclear, and his parents were allegedly opposed to vaccinations. The family history for diabetes mellitus was negative. During the initial visit to the general practitioner, the patient was found to have elevated spontaneous blood glucose (12.8 mmol/L), leading to the diagnosis of diabetes mellitus (DM). The HbA1c level was 6.2% (prediabetes range), compared to 5.5% from 2.5 years earlier. Upon hospital admission, his BMI was 17.1 kg/m² (height: 171 cm, weight: 50 kg). The C-peptide was reduced at 0.11 nmol/L (simultaneous glucose: 3.9 mmol/L), indicating insulin deficiency. Tests for autoimmune diabetes antibodies (Anti-GAD, Anti-ZnT8, Anti-IA2, and Anti-islet cell antibodies) were strongly positive, confirming the diagnosis of Type 1 diabetes mellitus (T1DM). During hospitalization, his glucose levels remained within the normal range, and insulin therapy was not yet required. The relationship between measles infection and T1DM onset has been investigated in several studies. Population-based case-control and prospective cohort studies suggest that measles and other viral infections may act as potential triggers of islet autoimmunity in genetically predisposed individuals. Molecular mimicry mechanisms involving measles proteins and Hsp60 could lead to autoimmune beta-cell destruction by imitating beta-cell antigens (Beyerlein et al., 2017; Hyöty et al., 1994). However, large meta-analyses and cohort studies (e.g., in Sweden, Finland, and Italy) demonstrate no consistent evidence linking measles infections or MMR vaccinations to increased T1DM incidence (DeStefano et al., 2001; Glanz et al., 2021). Case reports, on the other hand, have documented rare instances where measles-induced immune dysregulation led to accelerated beta-cell destruction, especially in autoantibody-positive individuals (Onal et al., 2012). The prevailing consensus is that measles infections and vaccinations do not directly cause T1DM but may contribute to its development in specific cases with pre-existing autoimmunity (Ramondetti et al., 2011; Classen et al., 2003). Presentation: Sunday, July 13, 2025