title: Normalisation of tissue factor pathway inhibitor activity after glycaemic control optimisation in type 1 diabetic patients.
abstract: Increased plasma concentrations of various markers of endothelial damage have been observed in type I diabetic patients, particularly in those with microangiopathy.
  
  
  OBJECTIVE
  To evaluate the effect of near-normalisation of glycaemic control on different markers of endothelial injury involved in haemostasis in poorly-controlled type 1 diabetic patients.
  
  
  METHODS
  TFPI, thrombomodulin (TM), plasminogen activator inhibitor, tissue-type plasminogen activator and von Willebrand factor were measured in 14 poorly-controlled type 1 diabetic patients free of diabetes-related complications (8 men, 6 women; mean age 29.8 +/- 9.9 years) before (baseline) and after 3 months of intensive therapy and in 14 sex-, age- and BMI-matched control subjects.
  
  
  RESULTS
  After a mean follow-up of 107 +/- 49 days (56-210), HbA1c decreased from 11.2 +/- 2.3 to 6.7 +/- 0.7% (p <0.0001). TFPI activity at baseline was higher than in the control group (126.9 +/- 34 vs 92.0 +/- 13%, p <0.005) and decreased after good glycaemic control was achieved (p <0.005), becoming similar to that in the control group (91.0 +/- 16.5%). The TFPI descent correlated with the variations observed in HbA1c (p <0.05; r = 0.54). TM levels at baseline were significantly higher than in the control group (42.3 +/- 9.1 vs 29.00 +/- 10.9; p <0.005) and did not change. The remaining parameters studied were similar between patients and controls and did not change after glycaemic optimisation.
  
  
  CONCLUSIONS
  Optimisation of glycaemic control normalises the increased activity of TFPI but not the higher TM levels observed in poorly-controlled type I diabetic patients without chronic complications.
authors.affiliation: Department of Endocrinology and Nutrition, Hospital de Sant Pau, Universitat Autònoma de Barcelona, Spain.
authors.forename: M
authors.initials: M
authors.lastname: Rigla
authors.forename: J
authors.initials: J
authors.lastname: Mateo
authors.forename: J
authors.initials: J
authors.lastname: Fontcuberta
authors.forename: J C
authors.initials: JC
authors.lastname: Souto
authors.forename: A
authors.initials: A
authors.lastname: de Leiva
authors.forename: A
authors.initials: A
authors.lastname: Pérez
mesh_terms: D000293:Adolescent; D000328:Adult; D000367:Age Factors; D000368:Aged; D000704:Analysis of Variance; D015415:Biomarkers / Q000097:blood; D001779:Blood Coagulation Factors / Q000378:metabolism; D001786:Blood Glucose / Q000378:metabolism*; D008078:Cholesterol, LDL / Q000097:blood; D003922:Diabetes Mellitus, Type 1 / Q000097:blood* / Q000150:complications / Q000628:therapy; D004730:Endothelium, Vascular / Q000293:injuries / Q000378:metabolism / Q000473:pathology; D005260:Female; D005343:Fibrinolytic Agents / Q000097:blood; D005500:Follow-Up Studies; D006487:Hemostasis; D006801:Humans; D006943:Hyperglycemia / Q000097:blood / Q000150:complications* / Q000628:therapy; D008055:Lipids / Q000097:blood; D008074:Lipoproteins / Q000097:blood* / Q000187:drug effects; D008297:Male; D016555:Matched-Pair Analysis; D008875:Middle Aged; D010446:Peptide Fragments / Q000097:blood; D011516:Prothrombin; D018180:Thrombomodulin / Q000097:blood
chemical_list: D015415:Biomarkers; D001779:Blood Coagulation Factors; D001786:Blood Glucose; D008078:Cholesterol, LDL; D005343:Fibrinolytic Agents; D008055:Lipids; D008074:Lipoproteins; D010446:Peptide Fragments; D018180:Thrombomodulin; C051928:lipoprotein-associated coagulation inhibitor; C045879:prothrombin fragment 1.2; D011516:Prothrombin