Older age of childhood type 1 diabetes onset is associated with islet autoantibody positivity >30 years later: the Pittsburgh Epidemiology of Diabetes Complications Study

To examine the association between islet autoantibody positivity and clinical characteristics, residual β‐cell function (C‐peptide) and prevalence of complications in a childhood‐onset (age <17 years), long‐duration (≥32 years) type 1 diabetes cohort.

[1]  Felicia A. Hanzu,et al.  Autoimmune Diabetes Mellitus , 2020, Encyclopedia of Behavioral Medicine.

[2]  R. Oram,et al.  Beta cells in type 1 diabetes: mass and function; sleeping or dead? , 2019, Diabetologia.

[3]  Teresa L. Mastracci,et al.  Proinsulin Secretion Is a Persistent Feature of Type 1 Diabetes , 2018, Diabetes Care.

[4]  P. Bingley,et al.  Beta cell function and ongoing autoimmunity in long-standing, childhood onset type 1 diabetes , 2016, Diabetologia.

[5]  C. Kanaka-Gantenbein,et al.  The prevalence of early subclinical somatic neuropathy in children and adolescents with Type 1 diabetes mellitus and its association with the persistence of autoantibodies to glutamic acid decarboxylase (GAD) and islet antigen-2 (IA-2). , 2016, Diabetes research and clinical practice.

[6]  N. Morgan,et al.  Differential Insulitic Profiles Determine the Extent of β-Cell Destruction and the Age at Onset of Type 1 Diabetes , 2016, Diabetes.

[7]  B. Shields,et al.  The majority of patients with long-duration type 1 diabetes are insulin microsecretors and have functioning beta cells , 2013, Diabetologia.

[8]  C. C. Richardson,et al.  High frequency of autoantibodies in patients with long duration type 1 diabetes , 2013, Diabetologia.

[9]  Zhiguang Zhou,et al.  Zinc transporter 8 autoantibody (ZnT8A) could help differentiate latent autoimmune diabetes in adults (LADA) from phenotypic type 2 diabetes mellitus , 2013, Diabetes/metabolism research and reviews.

[10]  D. Faustman,et al.  Persistence of Prolonged C-peptide Production in Type 1 Diabetes as Measured With an Ultrasensitive C-peptide Assay , 2012, Diabetes Care.

[11]  A. Ziegler,et al.  Kinetics of the post-onset decline in zinc transporter 8 autoantibodies in type 1 diabetic human subjects. , 2010, The Journal of clinical endocrinology and metabolism.

[12]  Jennifer K. Sun,et al.  Residual Insulin Production and Pancreatic β-Cell Turnover After 50 Years of Diabetes: Joslin Medalist Study , 2010, Diabetes.

[13]  P. Bingley,et al.  Harmonization of glutamic acid decarboxylase and islet antigen-2 autoantibody assays for national institute of diabetes and digestive and kidney diseases consortia. , 2010, The Journal of clinical endocrinology and metabolism.

[14]  C. Schmid,et al.  A new equation to estimate glomerular filtration rate. , 2009, Annals of internal medicine.

[15]  G. Bruno,et al.  Fasting Plasma C-Peptide and Micro- and Macrovascular Complications in a Large Clinic-Based Cohort of Type 1 Diabetic Patients , 2009, Diabetes Care.

[16]  Marian Rewers,et al.  The cation efflux transporter ZnT8 (Slc30A8) is a major autoantigen in human type 1 diabetes , 2007, Proceedings of the National Academy of Sciences.

[17]  R. G. Miller,et al.  Changes in glycaemic control and risk of coronary artery disease in type 1 diabetes mellitus: findings from the Pittsburgh Epidemiology of Diabetes Complications Study (EDC) , 2007, Diabetologia.

[18]  Å. Lernmark,et al.  Antibodies to GAD65 and peripheral nerve function in the DCCT , 2007, Journal of Neuroimmunology.

[19]  R. Rizza,et al.  Sustained beta cell apoptosis in patients with long-standing type 1 diabetes: indirect evidence for islet regeneration? , 2005, Diabetologia.

[20]  A. Gown,et al.  Heterogeneity of islet pathology in two infants with recent onset diabetes mellitus , 2004, Virchows Archiv.

[21]  Å. Lernmark,et al.  Antibodies to glutamic acid decarboxylase and peripheral nerve function in type 1 diabetes. , 2000, The Journal of clinical endocrinology and metabolism.

[22]  R. Bretzel,et al.  Persistent GAD 65 antibodies in longstanding IDDM are not associated with residual beta-cell function, neuropathy or HLA-DR status. , 1997, Hormone and metabolic research = Hormon- und Stoffwechselforschung = Hormones et metabolisme.

[23]  A. Ziegler,et al.  No Association of Antibodies to Glutamic Acid Decarboxylase and Diabetic Complications in Patients With IDDM , 1995, Diabetes Care.

[24]  M B Brown,et al.  A Practical Two-Step Quantitative Clinical and Electrophysiological Assessment for the Diagnosis and Staging of Diabetic Neuropathy , 1994, Diabetes Care.

[25]  C. Mathias,et al.  High Prevalence of Autoantibodies to Glutamic Acid Decarboxylase in Long-Standing IDDM Is Not a Marker of Symptomatic Autonomic Neuropathy , 1994, Diabetes.

[26]  D. Pipeleers,et al.  Pancreatic beta cells in insulin-dependent diabetes. , 1992, Diabetes/metabolism reviews.

[27]  Å. Lernmark,et al.  CHAPTER 10 – Autoimmune Diabetes Mellitus , 1992 .

[28]  Grading diabetic retinopathy from stereoscopic color fundus photographs--an extension of the modified Airlie House classification. ETDRS report number 10. Early Treatment Diabetic Retinopathy Study Research Group. , 1991, Ophthalmology.

[29]  L. Kuller,et al.  Prevalence of Complications in IDDM by Sex and Duration: Pittsburgh Epidemiology of Diabetes Complications Study II , 1990, Diabetes.

[30]  L. Kuller,et al.  Factors Associated With Avoidance of Severe Complications After 25 Yr of IDDM: Pittsburgh Epidemiology of Diabetes Complications Study I , 1990, Diabetes Care.

[31]  H. Langford The hypertension detection and follow-up program. , 1984, New York state journal of medicine.

[32]  The hypertension detection and follow-up program: Hypertension detection and follow-up program cooperative group. , 1976, Preventive medicine.