RETRACTED ARTICLE: Does continuous heparinization  influence platelet function in the  intensive care patient?

Boldt, Joachim; Müller, Matthias J.; Rothe, Alf; Lenzen, P; Hempelmann, G.

doi:10.1007/s001340050374

Cited by 3 publications

(3 citation statements)

References 25 publications

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“…In agreement with some previous reports [18,19], we observed decreased agonist‐induced platelet aggregation in the septic patients. Moreover, flow cytometry confirmed this aggregation defect, demonstrating concomitant alteration in the GPIIbIIIa integrin conformational changes with decreased avidity for the PAC‐1 antibody and fibrinogen binding in the platelets of the septic patients.…”

Section: Discussionsupporting

confidence: 93%

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Platelet function in sepsis

Yaguchi

Lobo

Vincent

et al. 2004

Journal of Thrombosis and Haemostasis

157

102

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Summary. Background: Coagulation abnormalities and thrombocytopenia are common in severe sepsis, but sepsis-related alterations in platelet function are ill-defined. Objectives: The purpose of this study was to elucidate the effect of sepsis on platelet aggregation, adhesiveness, and growth factor release. Patients and methods: Agonist-induced platelet aggregation was measured in platelet-rich plasma separated from blood samples collected from 47 critically ill patients with sepsis of recent onset. Expression of platelet adhesion molecules was measured by flow cytometry and the release of vascular endothelial growth factor (VEGF) and platelet-derived growth factor (PDGF) was measured by ELISA in the supernatant of platelet aggregation. Results: Septic patients had consistently decreased platelet aggregation compared with controls, regardless of the platelet count, thrombin generation, or overt disseminated intravascular coagulation (DIC) status. The severity of sepsis correlated to the platelet aggregation defect. Adhesion molecules, receptor expression (CD42a, CD42b, CD36, CD29, PAR-1), and a-granule secretion detected by P-selectin expression remained unchanged but the release of growth factors was differentially regulated with increased VEGF and unchanged PDGF after agonist activation even in uncomplicated sepsis. Conclusions: Sepsis decreases circulating platelets' hemostatic function, maintains adhesion molecule expression and secretion capability, and modulates growth factor production. These results suggest that sepsis alters the hemostatic function of the platelets and increases VEGF release in a thrombinindependent manner.

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Section: Discussionsupporting

confidence: 93%

“…However, sepsis‐generated cytokines do not seem to activate human platelets either directly or via thrombin [17]. In clinical studies, several investigators have reported decreased platelet aggregability during sepsis [18,19], whereas Gawaz et al . [20] noted increased platelet aggregability.…”

Section: Introductionmentioning

confidence: 99%

Platelet function in sepsis

Yaguchi

Lobo

Vincent

et al. 2004

Journal of Thrombosis and Haemostasis

157

102

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“…Determining the response to heparin prior to its use may be available for predicting the development of heparin-induced aggregates in circulation and avoiding unexpected platelet sequestration and consumption especially in patients with thromboembolic disease. Thus, evaluating the response to heparin may improve the safety of heparin treatment in intensive-care patients [13,21].…”

Section: Discussionmentioning

confidence: 99%

Characteristics of Heparin-Induced Platelet Aggregates in Chronic Hemodialysis with Long-Term Heparin Use

Matsuo

Kario

et al. 2000

Pathophysiol Haemos Thromb

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This study investigated the usefulness of a new platelet aggregometer with a laser-scattering method for detection of heparin-induced small platelet aggregates in chronic hemodialysis patients. Using this device, small platelet aggregates (particle size 9–25 µm) were detectable, but these aggregates could not be detected using a conventional light transmittance aggregometer. The laser-scattering intensity of the small aggregates was increased with an increasing dosage of heparin as agonist. These aggregates were disaggregated by heparin neutralization with protamine sulfate. Induction of small platelet aggregates by heparin was inhibited by preincubation with nafamostat mesilate, a synthetic protease inhibitor, and cilostazol, a platelet phosphodiesterase inhibitor, but not by the therapeutic doses of aspirin or argatroban, a selective thrombin inhibitor. The dialysis patients with long-term heparin use could be divided into two groups: responders to heparin, who formed small aggregates with a scattering intensity over 0.51 × 10⁵ V after addition of 0.5 IU/ml of heparin obtained from normal platelet-rich plasma without inductor, and nonresponders, who showed an intensity under 0.51 × 10⁵ V. The rate of heparin responders among dialysis patients was significantly higher than the rate among normal subjects. Heparin-induced small aggregates were detected in 13 (36.1%) of 36 normal subjects with no history of heparin infusion and in 37 (62.7%) of 59 dialysis patients who received heparin anticoagulation during each dialysis session. Dialysis patients with coronary heart disease did not have a significantly higher rate of heparin responders than patients without complications. There was no significant difference in the positivity rate between cases complicated by diabetes and those without diabetes. In patients who had more than 2 episodes of thrombotic occlusions of an arteriovenous fistula, the rate of responders and the enhancement of scattering intensity of small aggregates by heparin were significantly increased compared with these in patients without occlusions during the preceding 2 years. Moreover, dialysis patients with a positive heparin response showed a marked increase in scattering intensity of small aggregates after heparin infusion in each dialysis session. Determination of the response to heparin prior to heparin use in dialysis patients with repeated thromboembolic complication may be useful in choosing anticoagulant regimens.

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The Role of P2Y<sub>12</sub> Receptor and Activated Platelets During Inflammation

Liverani¹,

Kilpatrick²,

Tsygankov³

et al. 2014

CDT

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Platelets play an important role not only during thrombosis, but also in modulating immune responses through their interaction with immune cells and by releasing inflammatory mediators upon activation. The P2Y12 receptor is a Gi-coupled receptor that not only regulates ADP-induced aggregation but that can also dramatically potentiate secretion, when platelets are activated by other stimuli. Considering the importance of P2Y12 receptor in platelet function, a class of anti-platelet drugs, thienopyridines, have been designed and successfully used to prevent thrombosis. This review will focus on the role of activated platelets in inflammation and the effects that P2Y12 antagonism exerts on the inflammatory process. A change in platelet functions was noted in patients treated with thienopyridines during inflammatory conditions, suggesting that platelets may modulate the inflammatory response. Further experiments in a variety of animal models of diseases, such as sepsis, rheumatoid arthritis, myocardial infarction, pancreatitis and pulmonary inflammation have also demonstrated that activated platelets influence the inflammatory state. Platelets can secrete inflammatory modulators in a P2Y12–dependent manner, and, as a result, directly alter the inflammatory response. P2Y12 receptor may also be expressed in other cells of the immune system, indicating that thienopyridines could directly influence the immune system rather than only through platelets. Overall the results obtained to date strongly support the notion that activated platelets significantly contribute to the inflammatory process and that antagonizing P2Y12 receptor can influence the immune response.

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RETRACTED ARTICLE: Does continuous heparinization influence platelet function in the intensive care patient?

Cited by 3 publications

References 25 publications

Platelet function in sepsis

Platelet function in sepsis

Characteristics of Heparin-Induced Platelet Aggregates in Chronic Hemodialysis with Long-Term Heparin Use

The Role of P2Y<sub>12</sub> Receptor and Activated Platelets During Inflammation

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