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.
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.
authors.affiliation: Department of Medical Sciences, Section of Internal Medicine, Uppsala University Hospital, Sweden. Anna.Scholin@medsci.uu.se
authors.forename: Anna
authors.initials: A
authors.lastname: Schölin
authors.forename: Agneta
authors.initials: A
authors.lastname: Siegbahn
authors.forename: Lars
authors.initials: L
authors.lastname: Lind
authors.forename: Christian
authors.initials: C
authors.lastname: Berne
authors.forename: Göran
authors.initials: G
authors.lastname: Sundkvist
authors.forename: Elisabeth
authors.initials: E
authors.lastname: Björk
authors.forename: F Anders
authors.initials: FA
authors.lastname: Karlsson
mesh_terms: D000293:Adolescent; D000328:Adult; D001323:Autoantibodies / Q000097:blood; D001786:Blood Glucose / Q000032:analysis*; D015992:Body Mass Index; D002096:C-Peptide / Q000097:blood; D002097:C-Reactive Protein / Q000032:analysis*; D003922:Diabetes Mellitus, Type 1 / Q000175:diagnosis / Q000188:drug therapy* / Q000503:physiopathology*; D005260:Female; D006442:Glycated Hemoglobin / Q000032:analysis; D006801:Humans; D007333:Insulin Resistance; D015850:Interleukin-6 / Q000097:blood*; D007444:Inulin / Q000627:therapeutic use; D007515:Islets of Langerhans / Q000276:immunology / Q000503:physiopathology*; D008297:Male; D012044:Regression Analysis
chemical_list: D001323:Autoantibodies; D001786:Blood Glucose; D002096:C-Peptide; D002097:C-Reactive Protein; D006442:Glycated Hemoglobin; D015850:Interleukin-6; D007444:Inulin