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Type 1 diabetes

The importance of early detection to prevent serious complications

Type 1 diabetes (T1D), or autoimmune diabetes, results from the immune destruction of pancreatic insulin-producing beta cells. T1D arises through a complex interaction of genetic, environmental, and epigenetic factors.

T1D is commonly diagnosed in pediatric patients at 2 distinct age ranges, with peaks of diagnosis occurring at ages 4–6 and 10–141—yet 25% to 50% of cases are diagnosed during adulthood.2

Clinical presentation of T1D

Common T1D symptoms in the pediatric population include polyuria, polydipsia, and weight loss3—however, up to 30% of youth present with diabetic ketoacidosis (DKA).4 DKA is a medical emergency, often requiring ICU hospitalization and predisposing patients to additional health complications, such as higher lifetime blood sugar levels, or HbA1c, and adverse impacts to a patient’s memory and IQ. Up to 50% of DKA cases occur in children under 3 years of age with poor socioeconomic backgrounds.5

There is a genetic component to T1D. While up to 90% of individuals who develop T1D have no family history of the disease,6 multiple studies show that a positive family history significantly increases an individual’s risk of developing T1D.1, 7–10

Lifetime risk of T1D development based on family history1,7–10

Family History of T1D Lifetime risk
No family history 0.3%
Mother 1%–4%
Father 6%–9%
Non-twin sibling 10%
Dizygotic twin 8%
Monozygotic twin >50%

Early identification and routine monitoring are crucial for better patient care

Children with DKA at the time of a T1D diagnosis have persistently higher HbA1c levels, increasing the risk of long-term complications.10,11 Early identification of T1D and routine monitoring of patients have been associated with a drastic reduction in DKA rates.11–13

Clinical guidelines have been established to help identify T1D at its earliest phases and before progression to DKA, providing presymptomatic and symptomatic staging of T1D. The 3 stages of T1D, based on autoantibodies and blood glucose levels, are shown below.

Stages of type 1 diabetes14

  Autoantibodies Blood sugar Pathophysiology 5-year risk of
clinical diagnosis
of T1DN
Stage 1
Pre-symptomatic		 ≥ 2 autoantibodies Normal glucose tolerance These patients have
developed an autoimmune response against multiple islet autoantibodies and will eventually progress to clinical disease		 44%
Stage 2
Pre-symptomatic		 ≥ 2 autoantibodies Abnormal glucose
tolerance defined as: IGT (2-hour plasma glucose 140–199 mg/dL) and/or IFG (100–125 mg/dL) and/or A1C of 5.7–6.4 or ≥ 10% increase in A1C		 Identifies beta cell
dysfunction and is defined as dysglycemia. Detected using standard provocative testing such as the oral glucose tolerance test (OGTT)		 75%
Stage 3
Symptomatic		 ≥ 2 autoantibodies Clinical diagnosis
established and based on ADA criteria for the diagnosis of diabetes		 Identifies clinical
disease		 –
ADA, American Diabetes Association; IFG, impaired fasting glucose; IGT, impaired glucose tolerance.

How to screen for T1D using antibodies

The American Diabetes Association supports using autoantibody (AAb) screening to diagnose T1D.15 T1D autoantibodies are markers of ongoing damage to insulin-producing beta cells. The four AAbs used in clinical practice to diagnose T1D are: AAbs against insulin (IAA), tyrosine phosphatase IA2 (IA2A), glutamic acid decarboxylase (GAD65), and zinc transporter 8. Numerous clinical trials demonstrate important clinical benefits associated with detecting T1D using an AAb screening approach.16

Benefits associated with T1D detected by autoantibody screening (compared to no screening)16

Study ↓ DKA ↓ HBA1C
Baby Diab and Munich Family Study17 Y Y
DiPis18,19 Y Y
TEDDY20 Y Y
DAISY21 Y Y
DIPP22 Y Y

The recommendation is to use all four AAbs (ie: IA2A, GAD65, IAA, and ZnT8) for T1D screening, diagnosis, and differential diagnosis from other types of diabetes mellitus. This approach is the most powerful for detecting the presence of multiple autoantibodies, a condition eventually associated with the development of T1D in practically 100% of cases.15–23

Comprehensive testing portfolio to identify T1D

With a full suite of AAb tests, we can help you identify more patients with T1D, and identify them earlier, empowering you and your patients to proactively monitor their condition and help reduce the risk of serious complications, including DKA.

Glutamic Acid Decarboxylase-65 Antibody
Insulin Autoantibody

IA-2 Antibody

 

Zinc Transporter 8 (ZnT8) Antibody

GAD65, IA-2, and Insulin Autoantibody
 
References
  1. Felner EI, Klitz W, Ham M, et al. Genetic interaction among three genomic regions creates distinct contributions to early- and late-onset type 1 diabetes mellitus. Pediatr Diabetes. 2005;6(4):213-220. doi:10.1111/j.1399-543X.2005.00132.x
  2. VanBuecken D, Lord S, Greenbaum CJ. Changing the course of disease in type 1 diabetes. In: Feingold KR, Anawalt B, Blackman MR, et al, eds. Endotext. [Internet]. MdText.com, Inc.; 2000. https://www.ncbi.nlm.nih.gov/books/NBK326738/
  3. Roche EF, Menon A, Gill D, et al. Clinical presentation of type 1 diabetes. Pediatr Diabetes. 2005;6(2):75-78. doi:10.1111/j.1399-543x.2005.00110.x
  4. Dabelea D, Rewers A, Stafford JM, et al. Trends in the prevalence of ketoacidosis at diabetes diagnosis: the SEARCH for Diabetes in Youth Study. Pediatrics. 2014;133(4):e938-e945. doi:10.1542/peds.2013-2795
  5. Cherubini V, Grimsmann JM, Åkesson K, et al. Temporal trends in diabetic ketoacidosis at diagnosis of paediatric type 1 diabetes between 2006 and 2016: results from 13 countries in three continents. Diabetologia. 2020;63(8):1530-1541. doi:10.1007/s00125-020-05152-1
  6. Sims EK, Besser REJ, Dayan C, et al. Screening for type 1 diabetes in the general population: a status report and perspective. Diabetes. 2022;71(4):610-623. doi:10.2337/dbi20-0054
  7. Group SfDiYS, Liese AD, D’Agostino RB, Jr, et al. The burden of diabetes mellitus among US youth: prevalence estimates from the SEARCH for Diabetes in Youth Study. Pediatrics. 2006;118(4):1510-1518. doi:10.1542/peds.2006-0690
  8. Lawrence JM, Imperatore G, Dabelea D, et al. Trends in incidence of type 1 diabetes among non-Hispanic white youth in the US, 2002-2009. Diabetes. 2014;63(11):3938-3945. doi:10.2337/db13-1891
  9. Nistico L, Iafusco D, Galderisi A, et al. Emerging effects of early environmental factors over genetic background for type 1 diabetes susceptibility: evidence from a nationwide Italian twin study. J Clin Endocrinol Metab. 2012;97(8):E1483-E1491. doi:10.1210/jc.2011-3457
  10. Patterson CC, Dahlquist GG, Gyurus E, et al. Incidence trends for childhood type 1 diabetes in Europe during 1989-2003 and predicted new cases 2005-20: a multicentre prospective registration study. Lancet. 2009;373(9680):2027-2033. doi:10.1016/S0140-6736(09)60568-7
  11. Alonso GT, Coakley A, Pyle L, et al. Diabetic ketoacidosis at diagnosis of type 1 diabetes in Colorado children, 2010-2017. Diabetes Care. 2020;43(1):117-121. doi:10.2337/dc19-0428
  12. Duca LM, Wang B, Rewers M, et al. Diabetic ketoacidosis at diagnosis of type 1 diabetes predicts poor long-term glycemic control. Diabetes Care. 2017;40(9):1249-1255. doi:10.2337/dc17-0558
  13. Winkler C, Schober E, Ziegler A, et al. Markedly reduced rate of diabetic ketoacidosis at onset of type 1 diabetes in relatives screened for islet autoantibodies. Pediatr Diabetes. 2012;13(4):308-313. doi:10.1111/j.1399-5448.2011.00829.x
  14. Couper JJ, Haller MJ, Greenbaum CJ, et al. ISPAD Clinical Practice Consensus Guidelines 2018: Stages of type 1 diabetes in children and adolescents. Pediatr Diabetes. 2018;19(suppl 27):20-27. doi:10.1111/pedi.12734
  15. American Diabetes Association. 2. Classification and Diagnosis of Diabetes: Standards of Medical Care in Diabetes-2021. Diabetes Care. 2021;44(Suppl 1):S15-S33. doi:10.2337/dc21-S002
  16. Narendran P. Screening for type 1 diabetes: are we nearly there yet? Diabetologia. 2019;62(1):24-27. doi:10.1007/s00125-018-4774-0
  17. Winkler C, Schober E, Ziegler A, et al. Markedly reduced rate of diabetic ketoacidosis at onset of type 1 diabetes in relatives screened for islet autoantibodies. Pediatr Diabetes. 2012;13(4):308-313. doi:10.1111/j.1399-5448.2011.00829.x
  18. Lundgren M, Sahlin Å, Svensson C, et al. Reduced morbidity at diagnosis and improved glycemic control in children previously enrolled in DiPiS follow-up. Pediatr Diabetes. 2014;15(7):494-501. doi:10.1111/pedi.12151
  19. Larsson HE, Vehik K, Bell R, et al. Reduced prevalence of diabetic ketoacidosis at diagnosis of type 1 diabetes in young children participating in longitudinal follow-up. Diabetes Care. 2011;34(11):2347-2352. doi:10.2337/dc11-1026
  20. Steck AK, Larsson HE, Liu X, et al. Residual beta-cell function in diabetes children followed and diagnosed in the TEDDY study compared to community controls. Pediatr Diabetes. 2017;18(8):794-802. doi:10.1111/pedi.12485
  21. Barker JM, Goehrig SH, Barriga K, et al. Clinical characteristics of children diagnosed with type 1 diabetes through intensive screening and follow-up. Diabetes Care. 2004;27(6):1399-1404. doi:10.2337/diacare.27.6.1399
  22. Hekkala AM, Ilonen J, Toppari J, et al. Ketoacidosis at diagnosis of type 1 diabetes: Effect of prospective studies with newborn genetic screening and follow up of risk children. Pediatr Diabetes. 2018;19(2):314-319. doi:10.1111/pedi.12541
  23. Kupila A, Muona P, Simell T, et al. Feasibility of genetic and immunological prediction of type 1 diabetes in a population-based birth cohort. Diabetologia. 2001;44(3):290-297. doi:10.1007/s001250051616

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