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Biomedical subjects

S Susen

Publications and source records attributed to S Susen.

11 recordsLinked to original sources
PubMed2005

[Prophylaxis of thromboembolic events during urologic surgery].

Few scientific evidences are available in the literature, and the methodologic quality of the studies is often under average. Nevertheless, the conclusions are the following. Nephrectomy, renal transplantation, open surgery of the lower urinary tract and lumbar or pelvic lymph nodes dissection are at high risk for thromboembolic events. Other open or endoscopic urological procedures are at low risk. The laparoscopic approach doesn't change the risk associated with the procedure itself. Thromboprophylaxis is recommended in high-risk procedures. There was no evidence to recommend starting the prophylaxis before more than after the procedure. The use of low molecular weight heparin is recommended for prophylaxis. It can be associated with compressive stockings. It is recommended to treat for around seven days after the procedure. In case of cancer surgery, prophylaxis could be needed for four to six weeks.

Humans↗
PubMed2005

Relevance of tissue factor in cardiovascular disease.

Overexpression and exposition of tissue factor (TF) in atherosclerotic plaques and/or arterial thrombi are critical events in atherothrombosis. TF, the receptor for factor VII (FVII) and activated factor VII (FVIIa), is the principal initiator of blood coagulation and induces thrombin generation leading to fibrin formation and platelet activation. TF also plays a major role in cell migration and angiogenesis. TF activity is downregulated by Tissue Factor Pathway Inhibitor (TFPI), a Kunitz-type inhibitor, which forms a neutralizing complex with TF, FVIIa and activated factor X. In physiological conditions, TF is absent from vascular cells which come into contact with flowing blood and is present as an inactive pool in fibroblasts and smooth muscle cells (SMC). In contrast, TF is widely expressed in atherosclerotic plaques and is found in macrophages, SMCs, and foam-cells and also in extracellular matrix and acellular lipid-rich core. TF expression is up-regulated by inflammatory cytokines and oxidized lipids. Plaque thrombogenicity is directly correlated to their TF content. After fibrous cap disruption, TF is exposed on plaque surface and triggers thrombus formation leading to arterial lumen occlusion and/or downstream embolization. In coronary and carotid plaques, TF content was found to be higher in plaques from symptomatic than asymptomatic patients. Soluble forms of TF and microparticles of monocyte and platelet origin, and bearing TF, constitute "blood-born TF". The contribution of this TF pool to arterial thrombosis is still under discussion. TF pathway is a target for new therapeutic agents that can decrease TF activity, such as active site-inactivated factor VIIa, recombinant TFPI and antibodies against TF or peptides interfering with TF-FVIIa complex activity.

Arteriosclerosis↗
PubMed2004

[Hormone replacement therapy and venous thromboembolism].

Venous thromboemboembolism is a multigenic and a multifactorial disease. Several genetic risk factors have been identified: antithrombin, protein C and protein S deficiencies, and molecular defects in factor V gene (factor V Leiden) or factor II gene (G 20210A transition). Retrospective and prospective studies have demonstrated that hormone replacement therapy (HRT) in women is associated with a 2-3-fold increase of venous thromboembolism events. To minimize this risk, it seems desirable to carefully evaluate the individual clinical risk factors. Prescribing HRT should clearly be avoided in women with previous thromboembolic events. In case of familial thrombophilia, HRT should probably be prescribed with caution. Recent data suggest that transdermal HRT would induce a lower increase in thrombotic risk, but additional studies are needed to determine whether they can be safely used in women at risk. In each case, the net balance of risk and benefit of HRT use must consider the potential beneficial health effects, the most evident being the relief of climacteric symptoms.

Estrogen Replacement Therapy↗
PubMed2003

[Cell therapy to treat heart failure].

INTRODUCTION: Systolic heart failure is mainly due to a decreased left ventricular systolic function after myocardial infarction. Despite significant improvements in medical management of heart failure, the prognostic remains poor, with a 5-years survival only of 30%. PURPOSE: Current treatments are only able to delay progression toward end-stage heart failure. Heart transplantation is accessible only for selected patients. Thus, in the context of post-myocardial infarction, cell therapy appears to be a new original technique, available for the majority of patients and potentially non-invasive. CONCLUSION: After promising results in experimental models, a phase I clinical trial has been conducted in France, showing the feasibility of intracardiac autologous skeletal myoblast implantation. Other studies in Europe and USA are currently testing a variety of cells and delivery systems. A phase II-trial will begin in France.

Animals↗
PubMed2001

[Peripheral arterial revascularization: which antithrombotic agents?].

Thrombotic occlusion after vascular reconstructive surgery is a frequent complication, specially when low-flow arteries and arterial prostheses are involved. Heparin therapy is usually administered in acute arterial insufficiency, and also during the perioperative period, in order to limit thrombus formation or propagation at the surgical or the cross-clamp application sites. The overall benefit of antiplatelet agents, specially aspirin, during the pre, peri and postoperative periods has been clearly demonstrated for arterial prostheses, and is probably useful in venous bypasses. Aspirin therapy also prevents thrombotic complication in other vascular beds, and reduces long-term cardiovascular morbidity and mortality. Oral anticoagulation by vitamin K antagonists, alone or combined with aspirin is perhaps an appropriate choice in selected patients with high risk of graft thrombosis, but cannot be recommended for routine treatments because of an increased risk of hemorrhage.

4-Hydroxycoumarins↗
PubMed2000

Immunomodulatory effect of pentoxifylline during human allograft rejection: involvement of tumor necrosis factor-alpha and adhesion molecules.

BACKGROUND: Pentoxifylline (PTX), a methylxanthine phosphodiesterase inhibitor, is poorly active as an immunosuppressant but prevents the synthesis of proinflammatory cytokines. In a randomized double-blind study comparing PTX versus placebo in 140 patients receiving cadaveric kidney grafts under cyclosporine and prednisone, we have shown that PTX weakened the consequences of rejection on graft survival. To assess the mechanism underlying the beneficial effect recorded during this trial, we analyzed the impact of PTX on tumor necrosis factor (TNF-alpha) production and expression of cell adhesion molecules. METHODS: Plasma levels of TNF-alpha and its soluble receptors (sTNF-RI, sTNF-RII) and of soluble vascular cell adhesion molecule 1 (sVCAM-1) were monitored over the 6 months postgraft period when PTX or placebo were administered. Expression of VCAM-1 and intercellular cell adhesion molecule 1 was scored by immunohistochemical staining of biopsy specimens from patients who underwent rejection crisis. Lymphocyte subset composition was analyzed longitudinally during cytomegalovirus (CMV) infections. RESULTS: Plasma TNF-alpha levels were significantly reduced in the PTX-treated group over the 6 months of administration, and specifically during isolated rejection episodes and during CMV infections. Plasma levels of sTNFR-I, sTNFR-II, and sVCAM-1 did not differ between the two groups of patients, but a decrease in renal tubular VCAM-1 expression was observed in the PTX group. During CMV infections, CD8 lymphocytosis and expansion of CD57+ (CD28-) CD8+ T cells were similar in the two groups. CONCLUSION: The data collected during this double-blind study point to an immunomodulatory role of PTX, the beneficial effect on graft survival resulting from a restraining effect of the drug on the inflammatory conditions involved in acute graft rejection.

Adjuvants, Immunologic↗
PubMed2000

Pentoxifylline prevents upregulation of monocyte tissue factor in renal transplant recipients undergoing post-graft complications.

Pentoxifylline (PTX) has been demonstrated to improve graft survival in renal transplant recipients undergoing post graft complications. As activated monocytes are possible initiators of vascular damage through tissue factor (TF) expression, we evaluated the monocyte TF expression and endothelium activation markers in 140 consecutive patients receiving cadaveric kidney grafts, randomized in a double-blind study comparing PTX versus placebo. Monocyte TF expression and plasma von Willebrand factor, tissue plasminogen activator, thrombomodulin and tumor necrosis factor-alpha (TNF-alpha) levels were determined before transplantation and each month after. Additional samplings were realized in case of acute rejection. TF and TNF-alpha expression were significantly modified after graft. In patients with complications, PTX prevented the increase of TF expression at month one, and after rejection episodes. Endothelium activation markers were significantly modified after graft and in patients with complications but PTX had no significant effect on their plasma levels. These results suggest that the protective effect of PTX on graft survival could be related to the prevention of monocyte TF upregulation associated with complications.

Adult↗
PubMed1999

Monocyte tissue factor response is decreased in patients with hyperlipidemia.

Monocytes are potent regulators of blood coagulation through the expression of tissue factor (TF) on stimulation and of tissue factor pathway inhibitor (TFPI), a selective inhibitor of TF pathway. As hyperlipidemia can modify some monocyte functions, we compared the TF and TFPI expression by circulating monocytes and the plasma TFPI levels between 65 healthy normolipemic controls and 38 nontreated hyperlipemic patients. TF and TFPI relationships with plasma lipoproteins are also examined. TF and TFPI expression were evaluated in peripheral mononuclear cells after isolation from blood by density gradient centrifugation and after short culture with or without lipopolysaccharide (LPS). TF and TFPI activity and antigen were measured in mononuclear cell lysates using amidolytic assay and enzyme-linked immunosorbent assay, respectively. TFPI activity and antigen were measured in plasma using the same methods. Plasma factor VII (FVII) activity and antigen were also determined. LPS-stimulated monocyte TF activity and antigen were lower in hyperlipidemic patients than in controls (0.0001<p<0.03). This decrease of monocyte TF expression in hyperlipidemic patients was not related to an increase of monocyte TFPI. Monocyte TF activity was negatively correlated to atherogenic fractions and positively correlated to protective fractions, specially after ex vivo LPS stimulation. Increased TFPI and FVII plasma levels were found in hyperlipidemic patients compared to controls. These results indicate an impairment of TF production by circulating monocytes from hyperlipidemic subjects, which is linked to the increase of atherogenic lipoprotein fractions. Further studies are required to elucidate the mechanism of this inhibition.

Adult↗
PubMed1995

Detection of monocyte tissue factor after endotoxin stimulation: comparison of one functional and three immunological methods.

Monocyte procoagulant activity is mainly due to tissue factor (TF) expression, but functional assays may not be sufficiently accurate in clinical use, making useful a determination of TF antigen level. The aim of this study was to compare the results of one functional and three immunological TF assays (ELISA, immunocytochemical staining on slides and flow immuno cytometric analysis), in normal monocytes, after standardized stimulation by endotoxin. TF expression was determined in blood mononuclear cells isolated by gradient centrifugation and cultured, with or without various concentrations of endotoxin. On lysed cells, TF activity was determined by amidolytic assay and TF antigen level was determined, after triton extraction, by ELISA (Imubind, American Diagnostica). Mouse monoclonal antibody against TF (4508, American Diagnostica) was used for 1) immunocytochemical (ICC) staining on cytocentrifuge slides (Avidine-Biotine-peroxidase-Complex revelation) and 2) flow cytometric analysis using indirect labeling (Fab'2 Fluoresceine Isothyocyanate revelation). The determination of TF activity and TF antigen by ELISA method were equally sensitive to low concentration of endotoxin (0.005 EU/ml) and well correlated in the presence of higher concentrations of endotoxin. ICC led to a qualitative detection with a similar sensitivity to endotoxin stimulation. Flow cytometric analysis was poorly sensitive to increasing stimulation of monocytes. Of note, the functional, ELISA and immunocytochemical assays for monocyte TF expression were sensitive to endotoxin concentrations as low as 0.005 EU/ml.

Adult↗
PubMed1994

Evidence for time-dependent activation of monocytes in the systemic circulation in unstable angina but not in acute myocardial infarction or in stable angina.

BACKGROUND: Platelet activation plays a pivotal role in the pathogenesis of acute coronary disease. Monocytes are involved in the progression of atherosclerosis and are potent activators of blood coagulation through their ability to synthesize tissue factor (TF). The aim of this study was to compare markers of monocyte and coagulation activation in the systemic blood of patients with unstable angina, acute myocardial infarction, or stable angina. METHODS AND RESULTS: We studied 26 patients with unstable angina (10 +/- 5 hours after the onset of the last episode of pain), 18 patients with acute myocardial infarction (5 +/- 4 hours after the onset of pain), and 34 patients with stable angina. We measured levels of TF expression in peripheral blood mononuclear cells (isolated by gradient centrifugation and incubated for 16 hours, with or without endotoxin stimulation), levels of plasma prothrombin fragment 1 + 2 (F1 + 2), and levels of fibrinogen in peripheral blood. In patients with unstable angina, both stimulated and unstimulated cells exhibited higher levels of TF expression than in patients with stable angina (P = .0001). In patients with acute myocardial infarction, monocyte TF activity did not differ from that in patients with stable angina. Mean levels of F1 + 2 and of fibrinogen did not differ significantly between groups. Only in the unstable angina group, a modest correlation was found between fibrinogen (r = .72, P = .005) and F1 + 2 levels (r = .54, P = .001) levels and the degree of monocyte TF expression. In patients with unstable angina, monocyte TF expression (both stimulated and unstimulated, assessed by biological activity and by antigen techniques) and fibrinogen levels were correlated with the time elapsed from the beginning of the most recent episode of pain (.61 < r < .72, .02 < P < .0001). By contrast, there was no correlation between these variables and the time from onset of pain in patients with acute myocardial infarction. CONCLUSIONS: A time-dependent activation of systemic monocytes and a time-dependent increase in fibrinogen levels occurs in unstable angina but not in myocardial infarction. These findings provide further evidence that a specific inflammatory process occurs in unstable angina. Further studies are required to determine whether monocyte activation is a cause or a consequence of plaque instability in patients with unstable angina and to clarify the interrelations between platelet and monocyte activation in these circumstances.

Adult↗