Subjects with a shortened activated partial thromboplastin time show increased in‐hospital mortality associated with elevated D‐dimer, C‐reactive protein and glucose levels

REFERENCES

• Ten Boekel E, Bartels PCM. Abnormally short activated partial thromboplastin times are related to elevated plasma levels of TAT, Fl +2, D-dimer and FVIII:C. Pathophys Haemost Thromb 2002; 32: 137–42.
   PubMedGoogle Scholar
• Korte W, Clarke S, Lefkowitz JB. Short activated partial thromboplastin times are related to increased thrombin generation and an increased risk for thromboembolism. Ann J Clin Pathol 2000; 113: 123–7.
   Google Scholar
• Bick RL. Disseminated intravascular coagulation: pathophysiological mechanisms and manifesta-tions. Semin Thromb Hemost 1998; 24: 3–18.
   PubMed Web of Science ®Google Scholar
• McKenna R, Bachmann F, Miro-Quesada M. Thromboembolism in patients with abnormally short activated thromboplastin time. Thromb Haemost 1977; 38: 893–9.
   PubMed Web of Science ®Google Scholar
• Reddy NM, Hall SW, MacKintosh FR. Partial thromboplastin time. Prediction of adverse events and poor prognosis by low abnormal values. Arch Intern Med 1999; 159: 2706— 10.
   Google Scholar
• Guirguis N, Budisavljevic MN, Self S, Rajagopalan PR, Lazarchick J. Acute renal artery and vein thrombosis after renal transplant, associated with a short partial thromboplastin time and factor V Leiden mutation. Ann Clin Lab Sci 2000; 30: 75–8.
   Google Scholar
• Landi G, D'Angelo A, Boccardi E, Candelise L, Mannucci PM, Morabito A, Orazio EN. Venous thromboembolism in acute stroke: prognostic importance of hypercoagulability. Arch Neurol 1992; 49: 279–83.
   PubMed Web of Science ®Google Scholar
• Madi AM, Greci LS, Nawaz H, Katz DL. The activated partial thromboplastin time in early diagnosis of myocardial infarction. Blood Coagul Fibrinolysis 2001; 12: 495–9.
   PubMed Web of Science ®Google Scholar
• Shorr AF, Trotta RF, Alkins SA, Hanzel GS, Diehl LF. D-dimer assay predicts mortality in critically ill patients without dissseminated intra-vascular coagulation or venous thromboembolic disease. Intensive Care Med 1999; 25: 207–10.
   Google Scholar
• Kollef MH, Eisenberg PR, Shannon W. A rapid assay for the detection of circulating D-dimer is associated with clinical outcomes among critically ill patients. Crit Care Med 1998; 26: 1054–69.
   Google Scholar
• Oldgren J, Linder R, Grip L, Siegbahn A, Wallentin L. Coagulation activity and clinical outcome in unstable coronary artery disease. Arterioscler Thromb Vasc Biol 2001; 21: 1059–64.
   Google Scholar
• Shorr AF, Thomas SJ, Alkins SA, Fitzpatrick TM, Ling GS. D-dimer correlates with pro-inflammatory cytokine levels and outcomes in critically ill patients. Chest 2002; 121: 1261–8.
   Google Scholar
• Hogarth M, Gallimore R, Savage P, Palmer A, Starr J, Bulpitt C, Pepys M. Acute phase proteins, C-reactive protein and serum amyloid A protein, as prognostic markers in the elderly inpatient. Age Ageing 1997; 26: 153–8.
   Google Scholar
• Nikfardjam M, Mullner M, Schreiber W, Oschatz E, Exner M, Domanovits H, Laggner A, Huber K. The association between C-reactive protein on admission and mortality in patients with acute myocardial infarction. J Intern Med 2000; 247: 341–5.
   PubMed Web of Science ®Google Scholar
• Toh CH, Ticknor LO, Downey C, Giles AR, Paton RC, Wenstone R. Early identification of sepsis and mortality risks through simple, rapid clot-waveform analysis: implications of lipoprotein-complexed C reactive protein formation. Intensive Care Med 2003; 29: 55–61.
   PubMed Web of Science ®Google Scholar
• Van Den Berghe G, Wouters P, Weekers F, Verwaest C, Bruyninckx F, Schetz M, Vlasselaers D, Ferdinande P, Lauwers P, Bouillon R. Intensive insulin therapy in critically ill patients. N Engl J Med 2001; 345: 1359–67.
   PubMed Web of Science ®Google Scholar
• Dawson SJ, Wiman B, Hamsten A, Green F, Humphries S, Henney AM. The two allele sequences of a common polymorphism in the promoter of the plasminogen activator inhibitor-1 (PAI-1) gene respond differently to interleukin-1 in HepG2 cells. J Biol Chem 1993; 268: 10739–45.
   PubMed Web of Science ®Google Scholar
• Eriksson P, Kallin B, van't Hooft FM, Bavenholm P, Hamsten A. Allele-specific increase in basal transcription of the plasminogen-activator inhibi-tor 1 gene is associated with myocardial infarction. Proc Natl Acad Sci USA 1995; 92: 1851–5.
   Google Scholar
• Ye S, Green FR, Scarabin PY, Nicaud V, Bara L, Dawson SJ, Humphries SE, Evans A, Luc G, Cambou JPea. The 4G/5G genetic polymorphism in the promoter of the plasminogen activator inhibitor-1 (PAI-1) gene is associated with differ-ences in plasma PAI-1 activity but not with risk of myocardial infarction in the ECTIM study. Thromb Haemost 1995; 74: 837–41.
   PubMed Web of Science ®Google Scholar
• Foy CA, Grant PJ. PCR-RFLP detection of PAI-2 gene variants: prevalence in ethnic groups and disease relationship in patients undergoing coronary angiography. Thromb Haemost 1997; 77: 955–8.
   PubMed Web of Science ®Google Scholar
• Ludwig M, Wohn KD, Schleuning WD, Olek K. Allelic dimorphism in the human tissue-type plasminogen activator (TPA) gene as a result of an Alu insertion/deletion event. Hum Genet 1992; 88: 388–92.
   PubMed Web of Science ®Google Scholar
• Jem C, Ladenvall P, Wall U, Jem S. Gene polymorphism of t-PA is associated with forearm vascular release rate of t-PA. Arterioscler Thromb Vasc Biol 1999; 19: 454–9.
   PubMed Web of Science ®Google Scholar
• Kohler HP, Futers TS, Grant PJ. Prevalence of three common polymorphisms in the A-subunit gene of factor XIII in patients with coronary artery disease— association with FXIII activity and antigen levels. Thromb Haemost 1999; 81: 511–5.
   Google Scholar
• Kangsadalampai S, Board PG. The Va134Leu polymorphism in the A subunit of coagulation factor XIII contributes to the large normal range in activity and demonstrates that the activation peptide plays a role in catalytic activity. Blood 1998; 92: 2766–70.
   PubMed Web of Science ®Google Scholar
• Margaglione M, Grandone E, Cappucci G, Colaizzo D, Giuliani N, Vecchione G, d'Addedda M, Di Minno G. An alternative method for PAI-1 promoter polymorphism (4G/ 5G) typing. Thromb Haemost 1997; 77: 605–6.
   Google Scholar
• Toh C, Samis J, Downey C, Walker J, Becker L, Brufatto N, Tejidor L, Jones G, Houdijk W, Giles A, Koschinsky M, Ticknor L, Paton R, Wenstone R, Nesheim M. Biphasic transmittance waveform in the APTT coagulation assay is due to formation of a Ca"-independent complex of C-reactive protein with very-low-density lipoprotein and is a novel marker of impending disseminated intravas-cular coagulation. Blood 2002; 100: 2522–9.
   Google Scholar
• Stegnar M, Uhrin P, Petemel P, Mavri A, Salobir-Pajnic B, Stare J, Binder BR. The 4G/5G sequence polymorphism in the promoter of plasminogen activator inhibitor-1 (PAI-1) gene: relationship to plasma PAI-1 level in venous thromboembolism. Thromb Haemost 1998; 79: 975–9.
   Google Scholar
• Segui R, Estelles A, Mira Y, Espana F, Villa P, Falco C, Vaya A, Grancha S, Ferrando F, Anzar J. PAI-1 promoter 4G/5G genotype as an addi-tional risk factor for venous thrombosis in subjects with genetic thrombophilic defects. Br J Haematol 2000; 111: 122–8.
   PubMed Web of Science ®Google Scholar
• Henry M, Chomiki N, Scarabin PY, Alessi MC, Peiretti F, Arveiller D, Ferrieres J, Evans A, Amouyel P, Poirier 0, Cambien F, Juhan-Vague I. Five frequent polymorphisms of the PAI-1 gene. Lack of association between genotypes, PAI-1 activity, and triglyceride levels in a healthy population. Thromb Vasc Biol ; 1997: 851–8.
   Google Scholar
• Roest M, van der Schouw YT, Banga JD, MJT, de Groot PG, Sixma JJ, Grobbee DE. Plasmino-gen activator inhibitor 4G polymorphism is associated with decreased risk of cerebrovascular mortality in older women. Circulation 2000; 101: 67–70.
   Google Scholar