Comparaison de deux méthodes de dosage de la protéase du facteur von Willebrand ADAMTS13 (par électrophorèse des multimères du facteur von Willebrand et activité cofacteur de la ristocétine du facteur von Willebrand)

BESANCON-BU Médecine pharmacie (250562102) / SudocPARIS-BIUM (751062103) / SudocSudocFranceF

Taux de microparticules circulantes et leur activité procoagulante en fonction du mode de dialyse (comparaison entre l'hémodialyse et la dialyse péritonéale)

BESANCON-BU Médecine pharmacie (250562102) / SudocSudocFranceF

Serum tissue factor levels correlate with inflammation in ankylosing spondylitis.

International audienceBACKGROUND: Tissue factor, the main initiator of blood coagulation, is released into the bloodstream when vessel damage occurs. Vessel damage may occur in ankylosing spondylitis (AS). OBJECTIVE: To measure tissue factor levels in patients with AS and to look for correlations between tissue factor levels and established clinical and laboratory markers for disease activity. METHODS: We compared patients who met modified New York criteria for AS to healthy untreated controls. Serum tissue factor was assayed using an ELISA. The Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), Bath Ankylosing Spondylitis Functional Index (BASFI), and Bath Ankylosing Spondylitis Global Score (BAS-G) were recorded, as well as the erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) level, and IgA level. ANOVA and t-tests were performed. P values0.05). CONCLUSION: In this preliminary study in patients with AS, tissue factor levels were high and correlated with laboratory tests for inflammation. Tissue factor elevation may be a cause or a consequence of AS inflammation that promotes the occurrence of vascular events

Serum levels of MMP-3 and cathepsin K in patients with ankylosing spondylitis: effect of TNFalpha antagonist therapy.

International audienceOBJECTIVE: To measure serum levels of MMP-3 and cathepsin K in patients with ankylosing spondylitis (AS) and in controls and to look for changes in these variables during TNFalpha antagonist therapy. METHODS: We prospectively studied a group of patients who met New York criteria for AS and a group of healthy volunteers. We recorded age, disease duration, main features of the disease, BASDAI, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP). Serum MMP-3 and cathepsin K were assayed in duplicate using ELISA kits (Quantikine MMP-3, R&D Systems; and Cathepsin K, Biomedica). We also assayed IL-17 (Quantikine IL-17, R&D Systems) and BMP-7 (human BMP-7 DuoSet, R&D Systems). In patients treated with TNFalpha antagonists, the assays were repeated 10 weeks after treatment initiation. The Mann-Whitney test was used for between-group comparisons and the Wilcoxon test for evaluations of changes under treatment. Correlation testing was performed. P-values less than 0.05 were considered significant. RESULTS: We studied 23 outpatients with AS and 21 controls, with mean age of 39.9 years and 41.2 years, respectively (NS). Disease duration was 10.1 years (1.3); most patients had axial disease (n=21) and carried HLA-B27 (n=19). At baseline, the mean BASDAI was 44.1 mm (4.1) and the mean CRP level was 22.3 mg/L (4.7). Serum MMP-3 levels were significantly higher in the patients than in the controls (4.71 vs. 2.79 ng/ml, P=0.04); levels were also higher for cathepsin K (6.4 vs. 3.6 pg/ml) and IL-17 (60.4 vs. 32 pg/ml), but the differences were not statistically significant. No difference was noted for BMP-7. The only positive correlation was between the ESR and the CRP level (P=0.0002). Thirteen patients were evaluated 10 weeks into TNFalpha antagonist therapy (adalimumab, n=7; etanercept, n=4; or infliximab, n=2). Serum MMP-3 decreased significantly (P=0.04); significant decreases were also noted for the ESR, CRP, and BASDAI. CONCLUSION: MMP-3 is significantly increased in patients with active AS but fails to correlate significantly with conventional variables used to assess disease activity. TNFalpha antagonist therapy induces a significant decrease in MMP-3 levels, together with decreases in conventional variables (ESR, CRP, and BASDAI). MMP-3 may be a biomarker for disease activity in AS but supplies no additional information to the clinician

Serum and synovial fluid levels of p40 IL12/23 in spondyloarthropathy patients.

International audienceIL-23 is the main inductor in Th17 polarization of naive T cells, inducing IL-17 production. IL-17 has been demonstrated to be elevated in ankylosing spondylitis (AS). The p40 subunit is common to IL-12 and IL-23. We assessed serum and synovial levels of p40 IL12/23 in spondyloarthropathy (SpA) patients and the evolution under anti-TNF. SpA patients fulfilling ESSG criteria were included. Healthy volunteers served as controls. P40 IL12/23 was assessed using Human Quantikine ELISA (R&D Systems), and at the same time, BASDAI, ESR, CRP, IL-17, MMP-3. Patients treated with anti-TNF were evaluated again after 10 weeks of treatment. Statistical analysis used Mann Whitney and correlation tests. Twenty-seven SpA outpatients (20 men), mean age 40.3 years, mean disease duration 10.5 years, HLA B27 positive n = 21, peripheral arthritis n = 8, mean BASDAI 45.7, mean CRP 30.7 mg/l, and 24 controls (12 men), mean age 50.4 years, were included. There is no statistical difference in serum levels of p40IL12/23 between patients (mean 77.8 pg/ml) and controls (103 pg/ml) and between patients with axial and peripheral involvement. Levels were higher in HLA B-27 negative patients (p = 0.02). No statistical correlation was found between p40 IL12/40 serum levels and each of BASDAI, ESR, CRP, serum levels of IL 17, MMP 3. Fourteen AS patients were treated with TNF blockers. Whereas significant reduction in BASDAI, ESR, and CRP were obvious after treatment, there was no significant change in serum level of p40 IL12/23. Mean levels of synovial p40 IL12/23 were higher in SpA patients (n = 6; mean 536 pg/ml) compared to osteoarthritis patients (n = 3; 133 pg/ml) and compared with paired serum SpA levels. These results suggest that serum levels of p40 IL-12/23 may not be considered as a biologic tool of disease activity assessment in SpA patients

Serum IL-17, BMP-7, and bone turnover markers in patients with ankylosing spondylitis.

International audienc

Correlation between platelet-derived microparticle enumeration by flow cytometry and phospholipid-dependent procoagulant activity in microparticles: the centrifugation step matters!

International audienc

Cord blood volume reduction using an automated system (Sepax) vs. a semi-automated system (Optipress II) and a manual method (hydroxyethyl starch sedimentation) for routine cord blood banking: a comparative study.

International audienceBackground With the development of cord blood banking, solutions have to be found to solve the storage space problem, by reducing the volume of cord blood units (CBU). Methods We compared total nucleated cell (TNC) and CD34(+) cell counts before and after processing with three different CBU volume reduction methods used consecutively in our bank: a manual method based on hydroxyethyl starch sedimentation (HES) (n=447), a top-and-bottom (TB) semi-automated method (n=181) using Optipress II, and the Sepax automated method (n=213). Statistical analysis was done using t-tests, linear regression and Spearman correlation coefficients. Adjusted variables included TNC, CD34(+) cell counts, CD34(+) cell percentage and CB volume before processing. Results TNC recovery was higher with Sepax (80.3+/-7.7%) than with HES (76.8+/-9.1%) and TB (60.7+/-13.5%) (P<0.0001, both). It was higher with HES than with TB (P<0.0001). CD34(+) cell recovery was higher with Sepax (86+/-11.6%) than with HES (81.5+/-12.5%) and TB (82.0+/-17.7%) (P<0.008 and <0.0001, respectively) and results with HES and TB were not significantly different (P=0.7). Interestingly, with Sepax, TNC and CD34(+) cell recoveries were not correlated with pre-processing values (P=0.8 and 0.4, respectively). Discussion In conclusion, the Sepax volume reduction method allows higher TNC and CD34(+) cell recoveries

Early changes in local hemostasis activation following percutaneous coronary intervention in stable angina patients: a comparison between drug-eluting and bare metal stents.

International audienceBACKGROUND: Early change in local intracoronary hemostasis following drug-eluting (DES) and bare metal stent (BMS) implantation has never been assessed in stable angina patients. METHODS: Markers of local platelet activation (soluble glycoprotein V [sGPV] and P-Selectin [CD62P]), coagulation activation (tissue factor [TF], prothrombin fragments 1 + 2 [F1 + 2] and activated factor VII [FVIIa]) and fibrinolysis markers (D-dimers [DD], fibrinogen [FIB], tissue plasminogen activator [t-PA], and plasminogen activator inhibitor type-1 complexes [PAI-1]) were determined in 20 patients with stable angina who underwent percutaneous coronary intervention (PCI). All patients were pretreated with clopidogrel, aspirin, and enoxaparin. Systematic balloon predilation was performed before DES (9 patients) and BMS (11 patients) implantation. All blood samples were drawn 10-20 mm distal to the lesion site. RESULTS: No significant changes in levels of platelet activation markers occurred during PCI. There was a transient significant increase in TF (14%; P = 0.004), in F1 + 2 (40%; P = 0.001), and FVIIa (31%; P = 0.007) following angioplasty. Similarly, a significant 43% increase was observed in DD levels following balloon predilation, associated with an increase of 46%, 60%, and 70% in FIB, t-PA and PAI-1 levels, respectively (all P < 0.0001). All these markers returned to baseline values after stent implantation. No difference was observed between DES and BMS. CONCLUSIONS: Early changes in local hemostasis activation following PCI, were related to balloon predilation. Neither DES nor BMS increased markers of platelet activation, coagulation, or fibrinolysis, under dual antiplatelet and anticoagulant pretreatment