Older age of childhood type 1 diabetes onset is associated with islet autoantibody positivity >30 years later: the Pittsburgh Epidemiology of Diabetes Complications Study
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R. G. Miller | T. Orchard | D. Becker | T. Costacou | L. Yu
[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.