Combine islet autoantibodies, contextualized C-peptide, and clinical clues. The result is an explainable phenotype assessment—not a diagnosis or a mathematically validated probability.
Use “not tested” rather than treating missing data as negative.
Select the laboratory interpretation using that assay’s reference range.
Updates when you select “Interpret evidence.”
Autoantibodies: GAD65 is the preferred first test in adults; if negative, IA-2 and/or ZnT8 add sensitivity. Multiple confirmed islet autoantibodies strongly support autoimmune diabetes. A negative panel does not exclude type 1 diabetes.
C-peptide: This tool converts results to nmol/L. A nonfasting value below 0.20 nmol/L supports severe insulin deficiency, 0.20–0.60 nmol/L is an overlap zone, and above 0.60 nmol/L indicates substantial endogenous secretion. Interpretation depends on glucose, timing, diabetes duration, kidney function, and recent metabolic decompensation.
A1C and treatment: A1C describes recent glycemic exposure but does not distinguish diabetes type. Current treatment— including insulin—may reflect severity, clinician choice, or disease duration. The interval from diagnosis to insulin requirement is more discriminating than insulin use alone.
Insulin autoantibodies: IAA is most interpretable before exogenous insulin exposure. Antibodies measured after insulin treatment may reflect therapy rather than spontaneous beta-cell autoimmunity.
Sources: ADA Standards of Care 2026: Diagnosis and Classification; ADA/EASD adult type 1 diabetes consensus report.