P-509: Prevalence of type 2 diabetes in children and adolescents at a referral center of diabetes
B Tschiedel, M Dalla Lana, S Lavigne, A Fornari, G Vissoky, M PuñalesAbstract
Introduction
The global prevalence of type 2 diabetes mellitus (T2DM) in children and adolescents has increased markedly, largely driven by the obesity epidemic and influenced by genetic susceptibility, ethnicity, and socioeconomic factors. In Brazil, the ERICA study reported a prevalence of 3.3% among school-aged adolescents.
Objectives
To determine the prevalence of youth-onset T2D in a tertiary referral diabetes center and to characterize clinical features, glycemic control (HbA1c), and associated comorbidities in individuals diagnosed before 20 years of age.
Methods
This cross-sectional study identified 203 cases of youth-onset T2D among 5,302 individuals diagnosed with diabetes before 20 years of age attended at a public referral center. Clinical, laboratory, and comorbidity data were obtained from medical records of 46 patients under active follow-up.
Results
The prevalence of T2D in this cohort was 3.8% (203/5,302). Among the 46 patients under follow-up, mean age at diagnosis was 13.7 ± 3.5 years, with a predominance of females (71.7%). Diabetic ketoacidosis at diagnosis occurred in 6.5%, all with negative pancreatic autoantibodies. A positive family history of T2DM was reported in 80.4%. Excess of weight (overweight and obesity) was present in 84.8%, and acanthosis nigricans in 63.0%. Most adolescents were Caucasian (71.7%). Mean HbA1c at diagnosis was 9.5 ± 2.7%. Dyslipidemia was identified in 65.2%, while hypertension was present in 34.8%. Metformin was prescribed in 80.4% of cases, either as monotherapy or in combination with insulin.
Conclusions
Youth-onset T2D accounted for 3.8% of diabetes cases in this referral center. The condition was strongly associated with familial predisposition, female predominance, obesity, and cardiometabolic comorbidities, underscoring the interplay between genetic and environmental factors in disease pathogenesis.