Increases in circulating levels of monocyte‒platelet and neutrophil‒platelet complexes following hip arthroplasty

Abstract

Platelets and leucocytes are important effector cells of the haemostatic and inflammatory responses to tissue injury. To investigate the effects of surgical trauma on platelet activation (assessed by measuring levels of P-selectin and beta-thromboglobulin), leucocyte activation (CD11b expression) and leucocyte-platelet interactions (leucocyte-platelet complexes), 30 patients undergoing primary hip arthroplasty were studied before and at the end of surgery, and on days 1 and 10 post-operatively, using a whole-blood flow cytometry assay. The inflammatory response was followed by measurement of the levels of C-reactive protein and interleukin-6 in plasma, and the activation of coagulation was monitored by determination of prothrombin fragment 1+2 levels. On day 1 post-operatively a significantly increased expression of CD11b on monocytes was noted, but no direct correlation was found between monocyte activation and interleukin-6 production or C-reactive protein at this time point. The percentage of monocyte-platelet and neutrophil-platelet complexes was markedly increased on day 10 post-operatively compared with pre-operative levels, and levels of these complexes were significantly positively correlated with beta-thromboglobulin levels. Activation of coagulation (prothrombin fragment 1+2) on day 10 post-operatively was positively correlated with the extent of surgical trauma (duration of surgery, amount of blood loss) and with the increase in platelet activation (beta-thromboglobulin). In conclusion, hip arthroplasty induces platelet and coagulation activation, and also an inflammatory response that is maintained for more than 10 days post-operatively. This indicates an interaction between the immune and the haemostatic systems in the post-operative phase after hip arthroplasty.

Platelet-derived or soluble CD154 induces vascularized allograft rejection independent of cell-bound CD154

“…Although the controlled circumstance of an elective surgical procedure is not typically viewed as traumatic, CD154 provides a mechanism for immune activation to be stirred proportional to the injury sustained. Indeed, platelet/monocyte complexes have recently been shown to form following elective surgical procedures (27), and there is a known association between worsening ischemic insult and increased rejection rate (28). The accelerated rejection seen when trimers or platelets were added to WT grafts in this study demonstrates that soluble CD154 can be immunostimulatory even in the WT setting and augment immunity in a manner proportionate to its release.…”

Novel uses for anti‐platelet agents as anti‐inflammatory drugs

“…For example, studies with un-separated leukocyte populations reveal a significant increase in platelet-leukocyte complexes in allergic mice and in human asthmatics (Pitchford et al, 2003(Pitchford et al, , 2005. Similar processes occur in patients with COPD (Ferroni et al, 2000), atherosclerosis (Arber et al, 1991;Ott et al, 1996;Neumann et al, 1997;Sarma et al, 2002;Huo et al, 2003) and RA (Joseph et al, 2001;Bunescu et al, 2004). In this regard, experimental models of disease have provided evidence for a requirement of platelets in pulmonary eosinophil and lymphocyte recruitment in rabbits, guineapigs and mice in models of allergic inflammation (LellouchTubiana et al, 1988;Coyle et al, 1990;Pitchford et al, 2003Pitchford et al, , 2005; and neutrophil and monocyte recruitment in atherosclerosis (Arber et al, 1991;Neumann et al, 1997;Hayward et al, 1999) and RA (Schmitt-Sody et al, 2005).…”

“…Interestingly, heterotypic platelet-monocyte and platelet-neutrophil complexes occur in the circulating blood of patients with RA (Endresen and Forre, 1992;Bunescu et al, 2004), and in common with other inflammatory conditions, these interactions may contribute to leukocyte activation and recruitment to the synovium.…”

Controversial Issues Concerning Norepinephrine and Intensive Care Following Severe Traumatic Brain Injury

“…Released thrombin exerts neurotoxic effects, impairs memory functions, and decreases cerebral perfusion under experimental conditions [82] which is inhibited pharmacologically [83]. Following severe injury, elective orthopedic surgery or vascular graft insertion, thrombocytes are in a state of increased activation as judged by expression of surface proteins, release of soluble adhesion molecules [84][85][86][87][88][89], hyperaggregation, and sustained adhesiveness [90][91][92].…”