title: Thrombin-activatable fibrinolysis inhibitor is activated in an instant blood-mediated inflammatory reaction after intraportal islet transplant.
abstract: OBJECTIVE
  Activated thrombin-activatable fibrinolysis inhibitor is a coagulation factor in some thrombotic diseases. However, available data on whether thrombin-activatable fibrinolysis inhibitor is activated in islet transplant are limited. In this study, changes of plasma-activated thrombin-activatable fibrinolysis inhibitor levels in instant blood-mediated inflammatory reaction after islet transplant were assessed.
  
  
  METHODS
  Plasma concentrations of thrombin-antithrombin complex, D-dimer, C-peptide, and activated thrombin-activatable fibrinolysis inhibitor were assessed at 0 minutes, 30 minutes, 1 hour, 6 hours, 12 hours, and 24 hours after an intraportal islet transplant using rats via an enzyme-linked immunosorbent assay, or solid-phase, 2-site chemiluminescent immunometric assay. We recovered the liver at 1 hour after the transplant for histologic examination.
  
  
  RESULTS
  Thrombin-antithrombin complex, C-peptide, and activated thrombin-activatable fibrinolysis inhibitor levels increased immediately after we stopped islet infusion, and their peak levels occurred at 1 hour after islet infusion. D-dimer levels increased continually after islet infusion was stopped, and peaked 24 hours after infusion. Histologic examination of the liver 1 hour after islet infusion revealed frequent portal venous thrombi, with entrapped islets. The entrapped islets showed a disrupted morphology.
  
  
  CONCLUSIONS
  Activated thrombin-activatable fibrinolysis inhibitor was generated and peaked 1 hour after islet transplant according with activating coagulation, indicating that thrombin-activatable fibrinolysis inhibitor is activated and accumulated at levels in instant blood-mediated inflammatory reaction was sufficient to affect fibrinolysis.
authors.affiliation: Department of General Surgery, Shanghai East Hospital, Tongji University, Shanghai, PR China.
authors.forename: Shenggang
authors.initials: S
authors.lastname: Wang
authors.forename: Zhongxin
authors.initials: Z
authors.lastname: Zhao
authors.forename: Zhuangzhi
authors.initials: Z
authors.lastname: Cong
authors.forename: Guangjun
authors.initials: G
authors.lastname: Suo
mesh_terms: D000818:Animals; D000990:Antithrombin III; D015415:Biomarkers / Q000097:blood; D001777:Blood Coagulation; D002096:C-Peptide / Q000097:blood; D025901:Carboxypeptidase B2 / Q000097:blood*; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism; D007249:Inflammation / Q000097:blood / Q000209:etiology* / Q000473:pathology; D016381:Islets of Langerhans Transplantation / Q000009:adverse effects* / Q000379:methods; D008099:Liver / Q000378:metabolism / Q000473:pathology / Q000601:surgery*; D008297:Male; D010447:Peptide Hydrolases / Q000097:blood; D017207:Rats, Sprague-Dawley; D013997:Time Factors
chemical_list: D015415:Biomarkers; D002096:C-Peptide; D005338:Fibrin Fibrinogen Degradation Products; C046193:antithrombin III-protease complex; C036309:fibrin fragment D; D000990:Antithrombin III; D010447:Peptide Hydrolases; D025901:Carboxypeptidase B2; C585366:Cpb2 protein, rat