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DOI: 10.1160/TH08-04-0243
Peculiar whole blood rotation thromboelastometry (Rotem) profile in 40 sideropenic anaemia patients
Publication History
Received:
18 April 2008
Accepted after major revision:
03 September 2008
Publication Date:
23 November 2017 (online)
![](https://www.thieme-connect.de/media/10.1055-s-00035024/200806/lookinside/thumbnails/10-1160-th08-04-0243-1.jpg)
Summary
The ROtation ThromboElastoMetry analyser (ROTEM®, Pentapharm, Munich, Germany) is useful for studying whole blood (WB) clot formation and lysis.Reduction of haematocrit (HCT) has been reported to influence traditional thromboelastography parameters without compromising “in vitro” blood coagulation. We performed this case-control study to evaluate ROTEM profiles in sideropenic anaemia patients with different degrees of reduction of HCT levels. Forty consecutively referred patients with sideropenic anaemia were enrolled. A group of 40 healthy age and gender matched subjects acted as a control. The influence of HCT on ROTEM was assessed in the study population and in a model of artificially reconstituted blood with modified HCT values. Cases presented significantly increased levels of maximum clot firmness (MCF) as compared to controls (p<0.001) mimicking a sort of “hypercoagulable profile”. How-ever, thrombin generation tests failed to detect an increase in thrombin generation in cases as compared to controls. A statistically significant inverse linear correlation between HCT and MCF (p<0.0001) was found.In addition,ROTEM profiles following “in vitro” manipulation of HCT confirmed the inverse linear correlation between HCT and MCF found in the study population. In conclusion, the increased clot firmness found by ROTEM in anaemic patients is likely to be related to the method in itself rather than representing a marker of hypercoagulability “in vivo”.Since ROTEM is widely used by anaesthesiologists when deciding the optimisation of products supplementation during surgery,attention should be paid in the case of anaemic patients taking depending on the peculiar thrombo-elastography profile found.
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References
- 1 Luddington RJ. Thrombelastography/thromboel-astometry. Clin Lab Haematol 2005; 27: 81-90.
- 2 Hvitfeldt Poulsen L, Christiansen K, Sørensen B. et al. Whole blood thrombelastographic profiles using minimal tissue factor activation can display hyper-coagulation in thrombosis-prone patients. Scand J Clin Lab Invest 2006; 66: 329-336.
- 3 Sørensen B, Ingerslev J. Whole blood clot formation phenotypes in hemophilia A and rare coagulation disorders Patterns of response to recombinant factor VIIa. J Thromb Haemost 2004; 02: 102-110.
- 4 Johansen RF, Sørensen B, Ingerslev J. Acquired haemophilia: dynamic whole blood coagulation utilized to guide haemostatic therapy. Haemophilia 2006; 12: 190-197.
- 5 Sørensen B, Ingerslev J. A direct thrombin inhibitor studied by dynamic whole blood clot formation Haemostatic response to ex-vivo addition of recombinant factor VIIa or activated prothrombin complex concentrate. Thromb Haemost 2006; 96: 446-453.
- 6 Gerotziafas GT, Chakroun T, Samama MM. et al. In vitro comparison of the effect of fondaparinux and enoxaparin on whole blood tissue factor-triggered thromboelastography profile. Thromb Haemost 2004; 92: 1296-1302.
- 7 Pusateri AE, Ryan KL, Delgado A V. et al. Effects of increasing doses of activated recombinant factor VII on haemostatic parameters in swine. Thromb Haemost 2005; 93: 275-283.
- 8 Gerotziafas GT, Chakroun T, Depasse F. et al. The role of platelets and recombinant factor VIIa on thrombin generation, platelet activation and clot formation. Thromb Haemost 2004; 91: 977-985.
- 9 Kawaguchi C, Takahashi Y, Hanesaka Y. et al. The in vitro analysis of the coagulation mechanism of activated factor VII using thrombelastogram. Thromb Haemost 2002; 88: 768-772.
- 10 Coakley M, Reddy K, Mackie I. et al. Transfusion triggers in orthotopic liver transplantation: a comparison of the thromboelastometry analyzer, the thromboelastogram, and conventional coagulation tests. J Cardiothorac Vasc Anesth 2006; 20: 548-553.
- 11 Niemi TT, Suojaranta-Ylinen RT, Kukkonen SI. et al. Gelatin and hydroxyethyl starch, but not albumin, impair hemostasis after cardiac surgery. Anesth Analg 2006; 102: 998-1006.
- 12 Anderson L, Quasim I, Soutar R. et al. An audit of red cell and blood product use after the institution of thromboelastometry in a cardiac intensive care unit. Transfus Med 2006; 16: 31-39.
- 13 Niemi TT, Munsterhjelm E, Poyhia R. et al. The effect of N-acetylcysteine on blood coagulation and platelet function in patients undergoing open repair of abdominal aortic aneurysm. Blood Coagul Fibrinolysis 2006; 17: 29-34.
- 14 Iseline BM, Willimann PFX, Seifert B. et al. Isolated reduction of haematocrit does not compromise in vitro blood coagulation. Br J Anaeth 2001; 87: 246-249.
- 15 Calatzis AN, Fritzsche P, Calatzis AL. et al. A comparison of the technical principle of the ro TEG coagulation analyser and conventional thrombelastographic system [abstract]. Ann Hematol 1996; 72 (Suppl. 01) 87.
- 16 Zuckerman L, Cohen E, Vaughan J. et al. Comparison of thrombelastography with common coagulation tests. Thromb Haemost 1981; 46: 752-756.
- 17 Spiezia L, Marchioro P, Radu C. et al. Whole blood coagulation assessment using rotation thrombelastogram thromboelastometry in patients with acute deep vein thrombosis. Blood Coagul Fibrinolysis 2008; 19: 355-360.
- 18 Mann KG, Brummel-Ziedins K, Orfeo T. et al. Models of blood coagulation. Blood Cells Mol Dis 2006; 36: 108-117.
- 19 Barbui T, Finazzi G. Risk factors and prevention of vascular complications in polycythemia vera. Semin Thromb Hemost 1997; 23: 455-461.
- 20 Tefferi A, Elliot M. Thrombosis in myeloprolifeative disorders: prevalence, prognostic factors, and the role of leukocytes andJAK2V617F. SeminThrombHe-most 2007; 33: 313-320.
- 21 Landolfi R, Di Gennaro L, Barbui T. et al. and the European Collaboration on Low-Dose Aspirin in Polycythemia Vera (ECLAP). Leukocytosis as a major thrombotic risk factor in patients with polycythemia vera. Blood 2007; 109: 2446-2452.
- 22 Bellucci S, Michiels JJ. The role of JAK2 V617F mutation, spontaneous erythropoiesis and mega-karyocytopoiesis, hypersensitive platelets, activated leukocytes, and endothelial cells in the etiology of thrombotic manifestations in polycythemia vera and essential thrombocythemia. Semin Thromb Hemost 2006; 32: 381-398.
- 23 Gisslinger H, Mullner M, Pabinger I. et al. Mutation of the prothrombin gene and thrombotic events in patients with polycythemia vera or essential thrombocythemia: a cohort study. Haematologica 2005; 90: 408-410.
- 24 Kwaan HC, Wang J. Hyperviscosity in polycythemia vera and other red cell abnormalities. Semin Thromb Hemost 2003; 29: 451-458.
- 25 Fries D, Innerhofer P, Klinger A. et al. The effect of the combined administration of colloids and lactated Ringer’s solution on the coagulation system: an in vitro study using thrombelastograph coagulation analysis (ROTEG). Anesth Analg 2002; 94: 1280-1287.
- 26 Fenger-Eriksen C, Anker-Moller E, Heslop J. et al. Thrombelastographic whole blood clot formation after ex vivo addition of plasma substitutes: improvements of the induced coagulopathy with fibrinogen concentrate. Br J Anaesth 2005; 94: 324-329.