CRP and IL-6 concentrations are associated with poor glycemic control despite preserved beta-cell function during the first year after diagnosis of type 1 diabetes
(2004) In Diabetes/Metabolism Research & Reviews 20(3). p.205-210- Abstract
- Background The role of non-specific inflammation in beta-cell loss in type 1 diabetes is unclear. in the present study, inflammatory markers were determined in patients with newly diagnosed disease and related to beta-cell function, glycemic control and autoimmunity. Methods Ninety-seven adult patients with type 1 diabetes mellitus (80% islet antibody positives, ab(+)) were examined at diagnosis and 3, 6, 9 and 12 months after the start of insulin treatment. Plasma C-reactive protein (CRP), interleukin-6 (IL-6), C-peptide, islet autoantibodies, insulin requirement and HbA(1c) were assessed. Results The concentrations of CRP were high-normal at diagnosis and did not change during the study period. A positive correlation between CRP at... (More)
- Background The role of non-specific inflammation in beta-cell loss in type 1 diabetes is unclear. in the present study, inflammatory markers were determined in patients with newly diagnosed disease and related to beta-cell function, glycemic control and autoimmunity. Methods Ninety-seven adult patients with type 1 diabetes mellitus (80% islet antibody positives, ab(+)) were examined at diagnosis and 3, 6, 9 and 12 months after the start of insulin treatment. Plasma C-reactive protein (CRP), interleukin-6 (IL-6), C-peptide, islet autoantibodies, insulin requirement and HbA(1c) were assessed. Results The concentrations of CRP were high-normal at diagnosis and did not change during the study period. A positive correlation between CRP at diagnosis and BMI was observed in ab(+) as well as in ab(+) cases. Detectable concentrations of IL-6 were found in 32% (157/485) of the samples and did not change during the study. Ab(-) patients had higher values of CRP at diagnosis and throughout the study compared to the ab(+). Among the ab(+) patients, CRP concentrations during the study were positively correlated to C-peptide at 12 months and an increase in HbA(1c), levels between 6 and 12 months. No associations between the presence or levels of islet autoantibodies and CRP were noted. Conclusions In type 1 diabetes, the islet destructive process and the development of beta-cell remission are not associated with changes in CRP or IL-6. instead, elevated CRP concentrations are prevalent and seem to reflect insulin resistance, as positive associations to BMI, C-peptide and deterioration of glycemic control were observed. Copyright (C) 2004 John Wiley Sons, Ltd. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/898983
- author
- Scholin, A ; Siegbahn, A ; Lind, L ; Berne, C ; Sundkvist, Göran LU ; Bjork, E and Karlsson, FA
- organization
- publishing date
- 2004
- type
- Contribution to journal
- publication status
- published
- subject
- keywords
- plasma C-peptide, autoantibodies, islet, interleukin-6, C-reactive protein, type 1 diabetes, inflammation
- in
- Diabetes/Metabolism Research & Reviews
- volume
- 20
- issue
- 3
- pages
- 205 - 210
- publisher
- John Wiley & Sons Inc.
- external identifiers
-
- wos:000221566300005
- scopus:2642552200
- pmid:15133751
- ISSN
- 1520-7552
- DOI
- 10.1002/dmrr.427
- language
- English
- LU publication?
- yes
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Diabetes Epidemiology and Neuropathy (013241560)
- id
- 15dac135-bec8-471d-9ff5-435dbe75d802 (old id 898983)
- date added to LUP
- 2016-04-01 12:32:18
- date last changed
- 2022-04-29 07:19:32
@article{15dac135-bec8-471d-9ff5-435dbe75d802,
abstract = {{Background The role of non-specific inflammation in beta-cell loss in type 1 diabetes is unclear. in the present study, inflammatory markers were determined in patients with newly diagnosed disease and related to beta-cell function, glycemic control and autoimmunity. Methods Ninety-seven adult patients with type 1 diabetes mellitus (80% islet antibody positives, ab(+)) were examined at diagnosis and 3, 6, 9 and 12 months after the start of insulin treatment. Plasma C-reactive protein (CRP), interleukin-6 (IL-6), C-peptide, islet autoantibodies, insulin requirement and HbA(1c) were assessed. Results The concentrations of CRP were high-normal at diagnosis and did not change during the study period. A positive correlation between CRP at diagnosis and BMI was observed in ab(+) as well as in ab(+) cases. Detectable concentrations of IL-6 were found in 32% (157/485) of the samples and did not change during the study. Ab(-) patients had higher values of CRP at diagnosis and throughout the study compared to the ab(+). Among the ab(+) patients, CRP concentrations during the study were positively correlated to C-peptide at 12 months and an increase in HbA(1c), levels between 6 and 12 months. No associations between the presence or levels of islet autoantibodies and CRP were noted. Conclusions In type 1 diabetes, the islet destructive process and the development of beta-cell remission are not associated with changes in CRP or IL-6. instead, elevated CRP concentrations are prevalent and seem to reflect insulin resistance, as positive associations to BMI, C-peptide and deterioration of glycemic control were observed. Copyright (C) 2004 John Wiley Sons, Ltd.}},
author = {{Scholin, A and Siegbahn, A and Lind, L and Berne, C and Sundkvist, Göran and Bjork, E and Karlsson, FA}},
issn = {{1520-7552}},
keywords = {{plasma C-peptide; autoantibodies; islet; interleukin-6; C-reactive protein; type 1 diabetes; inflammation}},
language = {{eng}},
number = {{3}},
pages = {{205--210}},
publisher = {{John Wiley & Sons Inc.}},
series = {{Diabetes/Metabolism Research & Reviews}},
title = {{CRP and IL-6 concentrations are associated with poor glycemic control despite preserved beta-cell function during the first year after diagnosis of type 1 diabetes}},
url = {{http://dx.doi.org/10.1002/dmrr.427}},
doi = {{10.1002/dmrr.427}},
volume = {{20}},
year = {{2004}},
}