title: Increased plasma fibrin gel porosity in patients with Type I diabetes during continuous subcutaneous insulin infusion.
abstract: BACKGROUND
  Patients with Type 1 diabetes have a tighter plasma fibrin gel structure, to which impaired glycemic control might contribute. Improved glycemic control can be achieved with continuous subcutaneous insulin infusion (CSII).
  
  
  OBJECTIVE
  The aim of the present study was to investigate the effect of CSII on plasma fibrin gel properties and circulating markers of inflammatory activity in patients with Type 1 diabetes.
  
  
  METHODS
  Twenty-eight patients were investigated before and after 4-6 months' treatment with CSII. Fibrin gel structure formed in vitro from plasma samples was investigated by liquid permeation of hydrated fibrin gel networks. P-fibrinogen was analyzed by a syneresis method. Comparisons were made between patients with improved (> 0.5%) and unchanged (< 0.5%) glucosylated hemoglobin (HbA1c) during CSII.
  
  
  RESULTS
  Eighteen patients showed improved and 10 patients unchanged HbA1c during CSII. P-fibrinogen, high sensitive C-reactive protein and serum amyloid A-antigen were not significantly changed, while fibrin gel permeability (Ks) and fiber mass-length ratio ( micro ) increased in both groups (P < 0.02). P-insulin and triglycerides decreased (P < 0.05) in both groups, while reductions of total cholesterol and intercellular adhesion molecule-1 were seen only in patients with improved HbA(1c) (P < 0.05). Absolute changes in Ks were inversely correlated to changes in plasma fibrinogen (r = 0.50; P < 0.01) and in LDL-cholesterol (r = 0.46; P < 0.05).
  
  
  CONCLUSIONS
  Treatment with CSII in patients with Type 1 diabetes is associated with increased plasma fibrin gel porosity. Slight attenuation of the inflammatory activity was also observed. The changes in fibrin gel porosity seem to be mainly mediated by changes in plasma fibrinogen and blood lipids, and are probably secondary to improved insulin sensitivity.
authors.affiliation: Departments of Endocrinology and Diabetology, Karolinska Hospital, Karolinska Institutet, Stockholm, Sweden. gun.jorneskog@ks.se
authors.forename: G
authors.initials: G
authors.lastname: Jörneskog
authors.forename: L-O
authors.initials: LO
authors.lastname: Hansson
authors.forename: N H
authors.initials: NH
authors.lastname: Wallen
authors.forename: M
authors.initials: M
authors.lastname: Yngen
authors.forename: M
authors.initials: M
authors.lastname: Blombäck
mesh_terms: D000293:Adolescent; D000328:Adult; D015415:Biomarkers / Q000097:blood; D015815:Cell Adhesion Molecules / Q000097:blood; D018925:Chemokines / Q000097:blood; D016207:Cytokines / Q000097:blood; D003922:Diabetes Mellitus, Type 1 / Q000097:blood* / Q000188:drug therapy*; D005260:Female; D005337:Fibrin / Q000378:metabolism*; D005340:Fibrinogen / Q000378:metabolism; D006442:Glycated Hemoglobin / Q000032:analysis; D006403:Hematologic Tests; D006801:Humans; D007249:Inflammation / Q000097:blood; D007263:Infusions, Parenteral; D007328:Insulin / Q000008:administration & dosage*; D008055:Lipids / Q000097:blood; D008297:Male; D016062:Porosity
chemical_list: D015415:Biomarkers; D015815:Cell Adhesion Molecules; D018925:Chemokines; D016207:Cytokines; D005337:Fibrin; D005340:Fibrinogen; D006442:Glycated Hemoglobin; D007328:Insulin; D008055:Lipids