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CRP and IL-6 concentrations are associated with poor glycaemic control despite preserved β-cell function during the first year after diagnosis of type 1 diabetes.
Uppsala University, Medicinska vetenskapsområdet, Faculty of Medicine, Department of Medical Sciences.
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Manuscript (Other academic)
URN: urn:nbn:se:uu:diva-90544OAI: oai:DiVA.org:uu-90544DiVA: diva2:162930
Available from: 2003-05-22 Created: 2003-05-22 Last updated: 2010-01-13Bibliographically approved
In thesis
1. Diabetes in Young Adults: Remission, β-cell function and markers of inflammation
Open this publication in new window or tab >>Diabetes in Young Adults: Remission, β-cell function and markers of inflammation
2003 (English)Doctoral thesis, comprehensive summary (Other academic)
Abstract [en]

Type 1 diabetes is caused by immuno-mediated β-cell destruction leading to insulin deficiency and hyperglycaemia. The decline in β-cell function and the clinical course after diagnosis vary. Whether the process of destruction of the β-cells is associated with markers of a non-specific inflammatory response is unknown. The aims of these studies were to identify factors of importance for clinical remission (low insulin need and normoglycaemia) and long-term β-cell function and estimate the degree of non-inflammatory response in type 1 diabetes in young adults. Clinical remission and β-cell function eight years after diagnosis were assessed and related to clinical, biochemical and immunological variables at diagnosis, including islet autoantibodies [ICA, GADA, IA-2A]. Markers of low-grade inflammation in plasma [CRP and IL-6] were estimated and the concentrations were related β-cell function [plasma C-peptide], glycaemic control and autoimmunity at diagnosis and the first year thereafter. The results showed that clinical remission occurred in about half of the patients with newly diagnosed type 1 diabetes. Preserved β-cell function eight years after diagnosis was observed in 16% of the patients classified at diagnosis as having autoimmune type 1 diabetes. Duration of remission was dependent on BMI, degree of metabolic derangement and presence of GADA at diagnosis. BMI at diagnosis was also of importance for preserved β-cell function after eight years of the disease, as were the amount of islet antibodies and presence of ICA. Elevated CRP levels were noted in the majority of cases at diagnosis and both CRP and IL-6 concentrations were stable the first year after clinical diagnosis. High concentrations of CRP and IL-6 did not relate to β-cell destruction or the degree of autoimmunity. CRP concentrations were higher in islet antibody negative than in positive patients. CRP also correlated positively to BMI, C-peptide at 12 months and to increasing HbA1c between six and 12 months. In general, females had shorter remissions, lower concentrations of serum bicarbonate and higher levels and prevalence of GADA at diagnosis, compared to males. Females also had higher HbA1c and CRP values the first year after diagnosis. In summary, BMI at diagnosis is a strong predictor of duration of remission and preservation of β-cell function. Elevated CRP concentrations are correlated to factors linked rather to insulin resistance than to β-cell destruction. Females appear to have a more acute onset and a more severe course of the disease than males.

Place, publisher, year, edition, pages
Uppsala: Acta Universitatis Upsaliensis, 2003. 62 p.
Comprehensive Summaries of Uppsala Dissertations from the Faculty of Medicine, ISSN 0282-7476 ; 1273
Internal medicine, type 1 diabetes, young adults, remission, β-cell function, islet antibodies, gender, CRP, Invärtesmedicin
National Category
Clinical Medicine
Research subject
Internal Medicine
urn:nbn:se:uu:diva-3464 (URN)91-554-5666-9 (ISBN)
Public defence
2003-09-13, Stora aulan, Ingång 50, nb, Akademiska sjukhuset, Uppsala, 13:15
Available from: 2003-05-22 Created: 2003-05-22Bibliographically approved

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