Thromb Haemost 2005; 93(03): 549-553
DOI: 10.1160/TH04-10-0670
Platelets and Blood Cells
Schattauer GmbH

Variability in clinical laboratory practice in testing for disorders of platelet function

Results of two surveys of the North American Specialized Coagulation Laboratory Association
Karen A. Moffat
1   Hamilton Regional Laboratory Medicine Program, Haematology, Hamilton, Ontario, Canada
2   North American Specialized Coagulation Laboratory Association, USA
,
Marlies R. Ledford-Kraemer
2   North American Specialized Coagulation Laboratory Association, USA
3   CLOT-ED Inc, Islamorada, Florida, USA
4   University of Miami School of Medicine, Miami, Florida, USA
,
William L. Nichols
2   North American Specialized Coagulation Laboratory Association, USA
5   Mayo Clinic, Rochester, Minnesota, USA
,
Catherine P. M. Hayward
1   Hamilton Regional Laboratory Medicine Program, Haematology, Hamilton, Ontario, Canada
2   North American Specialized Coagulation Laboratory Association, USA
6   McMaster University, Pathology and Molecular Medicine and Medicine, Hamilton, Ontario, Canada
› Author Affiliations
Financial support: Catherine P. M. Hayward is funded by a Career Investigator Award from the Heart and Stroke Foundation of Ontario and a Canada Research Chair in Molecular Haemostasis from the Government of Canada
Further Information

Publication History

Received 17 October 2004

Accepted after revision 13 February 2004

Publication Date:
14 December 2017 (online)

Summary

Disorders of platelet function are important causes of abnormal bleeding that require laboratory tests for diagnosis. Currently there are limited guidelines on how to perform clinical testing for these disorders. The goal of our study was to obtain information on how disorders of platelet function are currently evaluated in clinical laboratories. Two patterns-of-practice surveys were distributed to laboratories of the North American Specialized Coagulation Laboratory Association (NASCOLA). The information collected was analyzed to determine practices and common problems. Forty-seven NASCOLA laboratories participated and 54% completed both surveys. The majority of the laboratories that responded performed more than 50 aggregation tests per year, mainly using platelet rich plasma based methodologies. A minority performed testing for platelet secretion and dense granule abnormalities. While platelet aggregation results were reviewed in various ways, laboratories most commonly issued a combined report containing quantitative values (% aggregation and/or slope) and a qualitative interpretation. Although laboratories used similar agonists for aggregation testing, the final agonist concentrations varied widely. Several approaches were also used to obtain reference intervals. Comments offered by the participants indicated that performing, and interpreting platelet function tests were challenging for many clinical laboratories. Although common practices have evolved, there is considerable variability in the diagnostic test procedures used by clinical laboratories to evaluate disorders of platelet function. These patterns-of-practice surveys illustrate a need for guidelines and recommendations for clinical laboratories performing tests of platelet function.

 
  • References

  • 1 Hayward CPM. Inherited platelet disorders. Curr Opin Hematol 2003; 10: 362-8.
  • 2 Cattaneo M. Congenital disorders of platelet secretion. In: Gresele P, Page C, Fuster V, Vermylen J, eds. Platelets in thrombotic and non-thrombotic disorders. Pathophysiology, pharmacology and therapeutics. Cambridge UK: The Press Syndicate of the University of Cambridge; 2002; 655-73.
  • 3 Nurden AT, Nurden P. Inherited Disorders of Platelet Function. In: Michelson AD (editor). Platelets. San Diego, CA; Academic Press: 2002: 681-700.
  • 4 Nurden AT, George JN. Inherited abnormalities of the platelet membrane: Glanzmann thrombasthenia, Bernard-Soulier syndrome, and other disorders. In: Colman WR, Hirsh J, Marder VJ, Clowes AW, George JN (editors). Hemostasis and Thrombosis: Basic Principles and Clinical Practise. 4 th Ed. Philadelphia PA: Lippincott Williams and Wilkins; 2001; 921-43.
  • 5 The British Society for Haematology, BCSH Haemostasis and Thrombosis Task Force Guidelines on platelet function testing. J Clin Pathol 1988; 41: 1322-30.
  • 6 Fontana P, Dupont A, Gandrille S. et al. Adenosine diphosphate-induced platelet aggregation is associated with P2Y12 gene sequence variations in healthy subjects. Circulation 2003; 108: 989-95.
  • 7 Kambayashi J, Shinoki N, Nakamura T. et al. Prevalence of impaired responsiveness to epinephrine in platelets among Japanese. Thromb Res 1996; 81: 85-90.
  • 8 Cattaneo M, Lecchi A, Lombardi R. et al. Platelets from a patient heterozygous for the defect of P2cyc receptors for ADP have a secretion defect despite normal thromboxane A2 production and normal granule stores: further evidence that some cases of platelet ‘primary secretion defect’ are heterozygous for a defect of P2cyc receptors. Arterioscler Thromb Vasc Biol 2000; 20: e101-6.
  • 9 Nurden P, Savi P, Heilmann E. et al. An inherited bleeding disorder linked to a defective interaction between ADP and its receptor on platelets. J Clin Invest 1995; 95: 1612-22.
  • 10 Lages B, Weiss HJ. Heterogeneous defects of platelet secretion and responses to weak agonists in patients with bleeding disorders. Br J Haematol 1988; 68: 53-62.
  • 11 Theodoropoulos I, Christopoulos C, Metcalfe P. et al. The effect of human platelet alloantigen polymorphisms on the in vitro responsiveness to adrenaline and collagen. Br J Haematol 2001; 114: 387-93.
  • 12 Yardumian DA, Mackie IJ, Machin SJ. Laboratory investigation of platelet function: a review of methodology. J Clin Pathol 1986; 39: 701-12.
  • 13 Peerschke EIB. The laboratory evaluation of platelet dysfunction. Clin Lab Med 2002; 22: 405-20.
  • 14 Fuse I, Hattori A, Mito M. et al. Pathogenic analysis of five cases with a platelet disorder characterized by the absence of thromboxane A2 (TXA2)-induced platelet aggregation in spite of normal TXA2 binding activity. Thromb Haemost 1996; 76: 1080-5.
  • 15 Nyman D, Eriksson AW, Lehmann W. et al. Inherited defective platelet aggregation with arachidonate as the main expression of a defective metabolism of arachidonic acid. Thromb Res 1979; 14: 739-46.
  • 16 Rao GHR, White JG. Epinephrine potentiation of arachidonate-induced aggregation of cyclooxygenasedeficient platelets. Am J Hematol 1981; 11: 355-66.
  • 17 Rao AK, Willis J, Kowalska MA. et al. Differential requirements for platelet aggregation and inhibition of adenylate cyclase by epinephrine. Studies of a familial platelet alpha2-adrenergic receptor defect. Blood 1988; 71: 494-501.
  • 18 Hayward CPM, Rivard GE, Kane WH. et al. An autosomal dominant, qualitative platelet disorder associated with multimerin deficiency, abnormalities in platelet factor V, thrombospondin, von Willebrand factor, and fibrinogen and an epinephrine aggregation defect. Blood 1996; 87: 4967-78.
  • 19 Weiss HJ, Chervenick PA, Zalusky R. et al. A familial defect in platelet function associated with impaired release of adenosine diphosphate. N Engl J Med 1969; 281: 1264-70.
  • 20 Weiss HJ, Witte LD, Kaplan KL. et al. Heterogeneity in storage pool deficiency: studies on granulebound substances in 18 patients including variants deficient in α -granules, platelet factor 4, β -thromboglobulin, and platelet-derived growth factor. Blood 1979; 54: 1296-319.
  • 21 Weiss HJ, Lages B, Vicic W. et al. Heterogeneous abnormalities of platelet dense granule ultrastructure in 20 patients with congenital storage pool deficiency. Br J Haematol 1993; 83: 282-95.
  • 22 Sadler JE. A revised classification of von Willebrand Disease. Thromb Haemost 1994; 71: 520-5.
  • 23 Laffan M, Brown SA, Collins PW. et al. The diagnosis of von Willebrand disease: a guideline from the UK haemophilia centre doctors’ organization. Haemophilia 2004; 10: 199-217.
  • 24 Cattaneo M. Inherited platelet-based bleeding disorders. J Thromb Haemost 2003; 1: 1628-36.