# Early Detection of Pediatric Type 1 Diabetes: The Expanding Role of Screening

**Authors:** Marco Calderone, Sara Aramnejad, Elèna Giliberto, Bruno Bombaci, Mariarosaria La Rocca, Arianna Torre, Fortunato Lombardo, Giuseppina Salzano, Stefano Passanisi

PMC · DOI: 10.3390/children13020235 · Children · 2026-02-07

## TL;DR

This paper reviews how screening for type 1 diabetes in children can help detect the disease early and prevent complications like diabetic ketoacidosis.

## Contribution

The paper provides a comprehensive review of current screening strategies and technologies for early detection of pediatric type 1 diabetes.

## Key findings

- Screening can reduce diabetic ketoacidosis at diagnosis and improve metabolic outcomes.
- New autoantibody detection methods enhance the feasibility of large-scale screening.
- Population-based screening is supported as a strategy to shift diagnosis to a predictable trajectory.

## Abstract

Type 1 diabetes (T1D) is a common chronic autoimmune disease in childhood, often presenting abruptly and frequently complicated by diabetic ketoacidosis at diagnosis. T1D develops through well-defined presymptomatic stages characterized by islet autoimmunity and progressive dysglycemia, offering a window for early identification. This narrative review summarizes current evidence on screening for T1D in children and adolescents, focusing on target populations, screening strategies, and methodological approaches for autoantibody detection. Data from major international programs involving familial, high-risk, and general population screening are discussed, highlighting their impact on reducing diabetic ketoacidosis at onset, improving metabolic outcomes, and facilitating structured follow-up and family education. Advances in assay technologies, including electrochemiluminescence, multiplex platforms, and novel ultrasensitive methods, have enhanced the feasibility and accuracy of large-scale screening. The review also examines the public health implications, cost-effectiveness, and ethical considerations of implementing population-based screening, particularly in light of emerging disease-modifying therapies such as teplizumab. Overall, available evidence supports screening as a meaningful strategy to shift T1D diagnosis from an acute emergency to a predictable clinical trajectory, with potential benefits extending from individual patient outcomes to healthcare system sustainability.

## Linked entities

- **Diseases:** Type 1 diabetes (MONDO:0005147), diabetic ketoacidosis (MONDO:0012819)

## Full-text entities

- **Genes:** TNF (tumor necrosis factor) [NCBI Gene 7124] {aka DIF, IMD127, TNF-alpha, TNFA, TNFSF2, TNLG1F}, KRT20 (keratin 20) [NCBI Gene 54474] {aka CD20, CK-20, CK20, K20, KRT21}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}, SLC30A8 (solute carrier family 30 member 8) [NCBI Gene 169026] {aka ZNT8, ZnT-8}, IL1B (interleukin 1 beta) [NCBI Gene 3553] {aka IL-1, IL1-BETA, IL1F2, IL1beta}, HLA-DRB4 (major histocompatibility complex, class II, DR beta 4) [NCBI Gene 3126] {aka DR4, DRB4, HLA-DR4B, HLA-DRB, HLA-DRB4*}, GAD2 (glutamate decarboxylase 2) [NCBI Gene 2572] {aka GAD65}, CTLA4 (cytotoxic T-lymphocyte associated protein 4) [NCBI Gene 1493] {aka ALPS5, CD, CD152, CELIAC3, CTLA-4, GRD4}, GAD1 (glutamate decarboxylase 1) [NCBI Gene 2571] {aka CPSQ1, DEE89, GAD, GAD-67, SCP}, TNFRSF25 (TNF receptor superfamily member 25) [NCBI Gene 8718] {aka APO-3, DDR3, DR3, LARD, TNFRSF12, TR3}, PTPRN (protein tyrosine phosphatase receptor type N) [NCBI Gene 5798] {aka IA-2, IA-2/PTP, IA2, ICA512, R-PTP-N}, IGHG3 (immunoglobulin heavy constant gamma 3 (G3m marker)) [NCBI Gene 3502] {aka IgG3}, TGM2 (transglutaminase 2) [NCBI Gene 7052] {aka G(h), TG(C), TGC, hTG2, tTG}, HLA-A (major histocompatibility complex, class I, A) [NCBI Gene 3105] {aka HLAA}
- **Diseases:** hyperglycemia (MESH:D006943), injury (MESH:D014947), inflammatory (MESH:D007249), IA-2A. (MESH:C536042), flu-like syndrome (MESH:D007251), lymphopenia (MESH:D008231), Diabetes (MESH:D003920), anxiety (MESH:D001007), polyuria (MESH:D011141), vitiligo (MESH:D014820), pancreatic autoimmunity (MESH:D000081012), alopecia (MESH:D000505), autoimmune disease (MESH:D001327), skin rash (MESH:D005076), retinopathy (MESH:D058437), hypoglycemic (MESH:C000721848), autoimmune and metabolic dysfunction (MESH:D008659), CD (MESH:D002446), IA (MESH:D050031), cytopenia (MESH:D006402), COVID-19 (MESH:D000086382), infections (MESH:D007239), rheumatologic diseases (MESH:D012216), insulin deficiency (MESH:D007333), polydipsia (MESH:D059606), dermatological disorders (MESH:D000168), weight loss (MESH:D015431), depressive symptoms (MESH:D003866), AITD (MESH:D013967), DKA (MESH:D016883), Autoimmune Diabetes (MESH:D003922), islet autoimmunity (MESH:D007516), beta-cell dysfunction (MESH:D007340), ketonuria (MESH:D007662), Islet (MESH:C531777), impaired glucose tolerance (MESH:D018149)
- **Chemicals:** canakinumab (MESH:C541220), ADAP (-), rituximab (MESH:D000069283), DPT (MESH:C059372), Teplizumab (MESH:C502540), lanthanide (MESH:D028581), glucose (MESH:D005947)
- **Species:** Severe acute respiratory syndrome coronavirus 2 (no rank) [taxon 2697049], Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

2 figures with captions in the complete paper: https://tomesphere.com/paper/PMC12939036/full.md

## References

81 references — full list in the complete paper: https://tomesphere.com/paper/PMC12939036/full.md

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Source: https://tomesphere.com/paper/PMC12939036