Critical Care

, 7:P018 | Cite as

Relationship between platelet counts, C-reactive protein and plasma fibrinolytic capacity in critically ill patients

  • K Zouaoui Boudjeltia
  • M Piagnerelli
  • E Carlier
  • S Jamart
  • Ph Cauchie
  • M Vanhaeverbeek
Meeting abstract
  • 2.4k Downloads

Keywords

Platelet Count Fibrinogen Endothelium Dysfunction Inflammatory Marker Biological Data 

Background

Multiple Organ Failure (MOF) complicating the sepsis remains the first cause of death in the ICU. A recent study showed that vascular endothelial damage was the primary cause of MOF in patients with thrombopenia and that humoral mediators played a major role in the development of this process [1]. Other parameters like C-protein reactive were also probably important via a direct effect on endothelial cells and increasing the secretion of IL-6. In this study, we aimed to evaluate the relation between the platelet counts (PC), the C-reactive protein and plasma fibrinolytic capacity (as a marker of endothelium dysfunction) in ICU patients.

Methods

We studied blood samples of ICU patients with (n = 11) and without (n = 21) sepsis at the first day of admission. Fibrinolytic capacity was evaluated by the Euglobulin Clot Lysis Time (ECLT) determined by a new method [2]. We also collected biological data and the SAPS II score for each patients. The correlations were depicted by Spearman's test.

Results

The ECLT was significantly correlated with CRP (R = 0.64; P < 0.001) and PC (R = -0.4; P = 0.02). The two-way ANOVA showed that the sepsis status increased significantly the ECLT (P = 0.023) and that platelets under 208,500 cells/μl (median of the histogram of PC was used as the cut-off) also increased the ECLT (P = 0.023). However, there was no interaction (P = 0.184).

Conclusion

Platelets can protect the endothelium against several forms of oxidative injuries [3]. With this study we showed that the decrease of the platelets count could favor the endothelium dysfunction and impaired fibrinolytic capacity, and this independently of sepsis. In addition, C-reactive protein is not only an inflammatory marker, but it might be involved in the endothelium damage.
 

Sepsis (n = 11)

Nonsepsis (n = 21)

P value

CRP (mg%)

25 (17–30)

6.9 (2.1–11.6)

< 0.001

WBC (× 103 cells/μl)

10.5 (7.7–12.9)

9.8 (8–12)

0.69

Fibrinogen (mg%)

662 (597–686)

455 (333–542)

< 0.001

SAPS

48 (39–56)

23 (15–35)

0.003

Platelets (× 103 cells/μl)

186 (123–227)

229 (179–296)

0.17

ECLT (min)

987 (845–1375)

599 (477–950)

0.01

Data presented as median (25–75%).

References

  1. 1.
    Hirokazu U, et al.: Crit Care Med 2002, 30: 2242-2248.CrossRefGoogle Scholar
  2. 2.
    Zouaoui Boudjeltia K, et al.: BMC Biotechnology 2002, 2: 8. 10.1186/1472-6750-2-8CrossRefPubMedGoogle Scholar
  3. 3.
    Vincent JL, et al.: Crit Care Med 2002, 30: S313-S317. 10.1097/00003246-200205001-00022CrossRefPubMedGoogle Scholar

Copyright information

© BioMed Central Ltd 2003

Authors and Affiliations

  • K Zouaoui Boudjeltia
    • 1
  • M Piagnerelli
    • 1
  • E Carlier
    • 2
  • S Jamart
    • 2
  • Ph Cauchie
    • 1
  • M Vanhaeverbeek
    • 1
  1. 1.Experimental Medicine Laboratory, ULB 222 UnitA. Vésale HospitalMontigny-le-TilleulBelgium
  2. 2.Department of Intensive CareA. Vésale HospitalMontigny-le-TilleulBelgium

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