Investigation of Inflammatory and Hemostatic Parameters in Female Patients Undergoing Total Knee Arthroplasty Surgery

Abstract

Tendency to hypercoagulation is a common phenomenon in primary osteoarthritis patients (POA) undergoing total knee arthroplasty (TKA) surgery, but the clinical implications of this condition are not clear. Therefore we aimed to evaluate the inflammatory and coagulation parameters in the patient group and find a possible explanation for the tendency to hypercoagulation occurring in plasma and synovia of inflamed joints. Of the evaluated factors involved in inflammation and coagulation, galectin-3, C reactive protein (CRP), erythrocyte sedimentation rate (ESR), fibrinogen, FVIIa:C, FXII:C, and platelet count increased, whereas tissue factor (TF) activity in synovia, PT, APTT and FVII:C in plasma and synovia were decreased. In conclusion, activation of inflammation and tendency to hypercoagulation is observed in preoperative plasma and synovia of patients undergoing TKA surgery.

Galectin-3 and Plasma Cytokines in Patients With Acute Myocardial Infarction

“…The increase might be due to upregulation of Gal-3, especially at inflammatory sites, as a result of disruption of arteries and macrophage production and secretion. Consistent with this finding, certain studies in the literature 5,11,17,20 have reported the presence of an increased level of Gal-3 in physiological and pathological processes, including immune and inflammatory responses, wound repair, and atherosclerosis. However, knowledge about the contribution of Gal-3 in patients with AMI is still scarce; further studies are necessary to elucidate this mechanism.…”

“…They found intense immunostaining for Gal-3 in foam cells that were present in the atheromatous plaques in the artery walls. Galectins produced by circulating blood cells or endothelial cells have been reported [18][19][20][21] to induce leukocyte attachment to the endothelium by cross-linking carbohydrates on the respective cell surfaces. The expression of Gal-3 is highly upregulated when monocytes differentiate into macrophages, a step in atherogenesis that follows monocyte recruitment from the peripheral blood to the artery wall and also occurs when in vivo or in vitro macrophages or aortic smooth muscle cells are loaded with lipids and transformed into foam cells.…”

Changes in concentrations of haemostatic and inflammatory biomarkers in synovial fluid after intra-articular injection of lipopolysaccharide in horses

“…In contrast, arthritis research in humans has for several years emphasized the importance of haemostasis in joint pathologies [10–13]. Haemostatic proteins such as TAT and fibrinogen have been detected in human SF, where they have been reported to induce or modulate inflammatory responses [14, 17]. Due to the low number of horses, no such assessment of interaction or of causal relationships between inflammatory and haemostatic biomarkers was made in this study.…”

“…24 h at 2–8 °C, then in aliquots at −80 °CWithin 7 monthsNot previously reported in equine synovial fluid, but in synovial fluid of human patients by a colorimetric method using an automatic analyser (Aeroset, USA) [70]FibrinogenBloodCitrate2–8 °CMax. 24 hClauss method, automated coagulometric analyser (ACL 9000, Instrumentation Laboratory, Barcelona, Spain).[22]Synovial fluidCitrate1500 g for 15 min at 20 °CInitially 15–30 min at room temperature then in aliquots at −80 °CWithin 17 monthsQuickVet® Equine Fibrinogen™ Test (Scandinavian Micro Biodevices, Farum, Denmark)Measured in synovial fluid in human osteoarthritis with automatic coagulometer (BFT II Dade Behring, Marburg, Germany) [17]Thrombin-antithrombinBloodCitrate1500 g for 15 min at 20 °CInitially 15–30 min at room temperature then in aliquotsat −80 °CWithin 20 monthsELISA measured in duplicates (Enzygnost TAT micro test kit, Siemens Healthcare Diagnostics, Denmark)[45, 81]Synovial fluidCitrateWithin 20 monthsNot previously reported in equine synovial fluid, but with same assay in synovial fluid of human rheumatoid arthritis and osteoarthritis [14]D-dimerBloodCitrate1500 g for 15 min at 20 °CInitially 15–30 min at room temperature then in aliquots at −80 °CWithin 21 monthsImmunoturbidimetry in duplicates (STA-Liatest D-DI, Diagnostica Stago, Triolab, Denmark)[82, 83]Synovial fluidCitrateWithin 18 months[25, 26], both used a quantitative immune-turbidimetric latex agglutination assay (Miniquant, Biopool, Trinity Biotech, Wicklow, Ireland) EDTA Ethylenediaminetetraacetic acid ELISA Enzyme-linked immunosorbent assay …”

“…Also fibrinogen may play a role in the pathogenesis of IA inflammation [15, 16]. In non-inflamed SF from humans fibrinogen was absent or found in very low levels [13, 17], and in inflammatory joint conditions, such as RA, osteoarthritis (OA) and antigen-induced arthritis, increased SF fibrinogen concentration has been demonstrated [17–19]. Fibrinogen is a key protein in haemostasis, interacting with platelets to form a fibrin-platelet clot to control haemorrhage or exudation from the circulation.…”