A 12-year prospective study of the relationship between islet antibodies and beta-cell function at and after the diagnosis in patients with adult-onset diabetes.

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A 12-year prospective study of the relationship between islet antibodies and beta-cell function at and after the diagnosis in patients with adult-onset diabetes. / Borg, Henrik; Gottsäter, Anders; Fernlund, Per; Sundkvist, Göran.

I: Diabetes, Vol. 51, Nr. 6, 2002, s. 1754-1762.

Forskningsoutput: TidskriftsbidragArtikel i vetenskaplig tidskrift

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T1 - A 12-year prospective study of the relationship between islet antibodies and beta-cell function at and after the diagnosis in patients with adult-onset diabetes.

AU - Borg, Henrik

AU - Gottsäter, Anders

AU - Fernlund, Per

AU - Sundkvist, Göran

N1 - The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Endocrinology (013241500), Unit for Clinical Vascular Disease Research (013242410), Clinical Chemistry, Malmö (013016000), Pediatrics/Urology/Gynecology/Endocrinology (013240400)

PY - 2002

Y1 - 2002

N2 - To clarify the relationships between islet antibodies (islet cell antibody [ICA], GAD antibody [GADA], and IA-2 antibody [IA-2A]) versus the progression of beta-cell dysfunction, we have followed a group of diabetic patients from their diagnosis at 21-73 years of age. Patients with ICA had high levels of GADA and/or IA-2A at diagnosis and a more severe beta-cell dysfunction 5 years after diagnosis than those with only GADA in low concentrations. The aim of the current 12-year follow-up study was to examine the further progression of beta-cell dysfunction in relation to islet antibodies at and after diagnosis. Among 107 patients, complete beta-cell failure 12 years after diagnosis was restricted to those with islet antibodies at diagnosis (16 of 21 [77%] with multiple antibodies and 4 of 5 [80%] with only GADA). In contrast, among antibody-negative patients, fasting P-C-peptide levels were unchanged. Most GADA-positive patients (22 of 27 [81%]) remained GADA positive after 12 years. Associated with decreasing fasting P-C-peptide levels (0.85 nmol/l [0.84] at diagnosis vs. 0.51 nmol/l [0.21] 12 years after diagnosis, P < 0.05), ICA developed after diagnosis in 6 of 105 originally antibody negative mostly overweight patients. In conclusion, multiple islet antibodies or GADA alone at diagnosis of diabetes predict future complete beta-cell failure. After diagnosis, GADA persisted in most patients, whereas ICA development in patients who were antibody negative at diagnosis indicated decreasing beta-cell function.

AB - To clarify the relationships between islet antibodies (islet cell antibody [ICA], GAD antibody [GADA], and IA-2 antibody [IA-2A]) versus the progression of beta-cell dysfunction, we have followed a group of diabetic patients from their diagnosis at 21-73 years of age. Patients with ICA had high levels of GADA and/or IA-2A at diagnosis and a more severe beta-cell dysfunction 5 years after diagnosis than those with only GADA in low concentrations. The aim of the current 12-year follow-up study was to examine the further progression of beta-cell dysfunction in relation to islet antibodies at and after diagnosis. Among 107 patients, complete beta-cell failure 12 years after diagnosis was restricted to those with islet antibodies at diagnosis (16 of 21 [77%] with multiple antibodies and 4 of 5 [80%] with only GADA). In contrast, among antibody-negative patients, fasting P-C-peptide levels were unchanged. Most GADA-positive patients (22 of 27 [81%]) remained GADA positive after 12 years. Associated with decreasing fasting P-C-peptide levels (0.85 nmol/l [0.84] at diagnosis vs. 0.51 nmol/l [0.21] 12 years after diagnosis, P < 0.05), ICA developed after diagnosis in 6 of 105 originally antibody negative mostly overweight patients. In conclusion, multiple islet antibodies or GADA alone at diagnosis of diabetes predict future complete beta-cell failure. After diagnosis, GADA persisted in most patients, whereas ICA development in patients who were antibody negative at diagnosis indicated decreasing beta-cell function.

KW - Diabetes Mellitus

KW - Islets of Langerhans : immunology

KW - Human

KW - Islets of Langerhans : physiopathology

KW - Isoenzymes : immunology

KW - Middle Age

KW - Prognosis

KW - Prospective Studies

KW - Support

KW - Non-U.S. Gov't

KW - Glutamate Decarboxylase : immunology

KW - Non-Insulin-Dependent : physiopathology

KW - Fasting

KW - Non-Insulin-Dependent : immunology

KW - Non-Insulin-Dependent : diagnosis

KW - Adult

KW - Aged

KW - Autoantibodies : blood

KW - C-Peptide : blood

U2 - 10.2337/diabetes.51.6.1754

DO - 10.2337/diabetes.51.6.1754

M3 - Article

VL - 51

SP - 1754

EP - 1762

JO - Diabetes

JF - Diabetes

SN - 1939-327X

IS - 6

ER -