Coagulation activation in sickle cell trait: An exploratory study

Chirag Amin, Soheir Adam, Micah J. Mooberry, Abdullah Kutlar, Ferdane Kutlar, Denise Esserman, Julia E. Brittain, Kenneth I. Ataga, Jen Yea Chang, Alisa S. Wolberg, Nigel S. Key

Research output: Contribution to journalArticlepeer-review

23 Scopus citations


Recent epidemiologic data suggest that sickle cell trait (HbAS; AS) is a risk factor for venous thromboembolism. We conducted an exploratory study of healthy subjects with AS under baseline conditions to determine whether a chronic basal hyperactivation of coagulation exists, and if so, what mechanism(s) contribute to this state. Eighteen healthy AS individuals were compared to 22 African-American controls with a normal haemoglobin profile (HbAA; AA) and 17 patients with sickle cell disease (HbSS; SS). Plasma thrombin-antithrombin complexes and D-dimer levels were elevated in AS relative to AA patients (P = 0·0385 and P = 0·017, respectively), and as expected, were much higher in SSversusAA (P < 0·0001 for both). Thrombin generation in platelet poor plasma was indistinguishable between AA and AS subjects, whereas a paradoxical decrease in endogenous thrombin potential was observed in SS (P ≤ 0·0001). Whole blood tissue factor was elevated in SS compared to AA (P = 0·005), but did not differ between AA and AS. Plasma microparticle tissue factor activity was non-significantly elevated in AS (P = 0·051), but was clearly elevated in SS patients (P = 0·004) when compared to AA controls. Further studies in larger cohorts of subjects with sickle cell trait are needed to confirm the results of this preliminary investigation.

Original languageEnglish (US)
Pages (from-to)638-646
Number of pages9
JournalBritish Journal of Haematology
Issue number4
StatePublished - Nov 2015


  • Coagulation
  • Sickle
  • Thrombin
  • Tissue factor
  • Venous thrombosis

ASJC Scopus subject areas

  • Hematology


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