Cost-effectiveness analysis of screening for type 1 diabetes in children in the Russian Federation

Objective. Cost-effectiveness analysis of screening for type 1 diabetes (T1D) in 6-year-old children by measuring autoantibodies to beta-cell and pancreatic islet antigens followed by longitudinal monitoring of individuals with positive results. Material and methods. The Markov model was used to predict efficacy, direct and indirect costs for three screening scenarios in 6-year-old children after testing for autoantibodies to beta-cell and pancreatic islet antigens: 1) general population; 2) first-degree relatives (FDR); 3) children with autoimmune diseases (AID). For each scenario, two cohorts (screening vs no screening) were simulated over a 50-year time horizon, and incremental cost-effectiveness ratios (ICER) were calculated using quality-adjusted life year (QALY). Results. Across all three scenarios, T1D screening reduced mortality and incidence of long-term complications by preventing diabetic ketoacidosis (DKA) at disease onset and increased QALY. The largest numbers of prevented long-term complications were observed in FDR and AID scenarios: by 18 years for diabetic neuropathy and by 56 years for lower extremity amputation and end-stage chronic kidney disease. In FDR and AID scenarios, ICER fell below 2.3 million rubbles after 7 years. After 16 years, ICER became negative that indicated cost savings alongside higher clinical benefit. In general population, ICER fell below 2.3 million rubbles after 28-year modelling and amounted to 2.287.652.27 RUB per QALY gained. Conclusion. In high-risk groups (FDR and children with AID), T1D screening followed by monitoring of autoantibody-positive individuals is economically justified for Russian healthcare system. In general population, cost-effectiveness emerges only over a long-term horizon (after 28 years). This highlights the need for long-term planning and confirming key clinical effects of screening in routine practice during program scale-up (reduced proportion of DKA at onset and early-disease HbA1c trajectories).