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Biomedical subjects

I Elalamy

Publications and source records attributed to I Elalamy.

At least 19 recordsLinked to original sources

[Prevention of thrombosis and vascular inflammation: importance of combined cyclooxygenase and 5-lipoxygenase inhibitors].

Aspirin, a standard non-steroidal anti-inflammatory drug (NSAID) is currently used in antithrombotic treatment. However, its use is limited by largely recognized gastrotoxicity and recommended doses are low. The major side effect of aspirin is related to its ability to suppress prostaglandin (PG) synthesis by constitutive cyclooxygenase-1 (COX-1). Specific inhibitors of COX-2, the inducible isoform of COX which was more recently described, have potent antiinflammatory effects. They are associated with minor risk of gastric tractus toxicity and reduced inflammatory leukocyte components known for their proatherothrombotic properties. Nevertheless, recent findings attributed a significant cardiovascular risk to some of them. 5-lipoxygenase (5-LOX), an enzyme mainly expressed by leukocytes, is responsible for the generation of leukotrienes, the major lipidic proinflammatory mediators. Development of combined inhibitors of 5-LOX and COX isoforms 1 and 2 inaugurate an interesting new therapeutic pathway. Indeed, such inhibitors suppress not only the activation of platelets, leukocytes and endothelial cells but also prevent their metabolic and functional interactions. In addition to their broad spectrum inhibition, they may be associated with the minor gastrotoxic effect. Thus, platelet-leukocyte interactions which dominate the underlying inflammatory process particularly in atherosclerosis, might reinforce the benefits of such inhibitors.

Arachidonate 5-Lipoxygenase↗

D-dimer levels, constitutional thrombophilia, and venous thrombosis prediction: clinical aspects and implications.

The negative predictive value of D-dimers in the diagnosis of a recent venous thromboembolism (VTE) episode is well established. The plasma level of D-dimer is usually increased in hypercoagulable states. The measurement of D-dimer could be of clinical interest in patients with constitutional thrombophilia as there is no close relationship between the clinical expression and the genotype indicating the existence of a hypercoagulable state. Moreover, the predictive value of D-dimer testing in patients with thrombophilia has been questioned. The review of the literature and results of a recent study of our group are presented. Decreased levels of D-dimer are observed in patients receiving an oral anticoagulant treatment versus untreated patients. In contrast, no significant difference was observed between those with and those without thrombophilia among treated or untreated patients. Patients with constitutional thrombophilia are supposed to have an increased risk of postoperative VTE. The review of the existing literature could not confirm this opinion but this could be due to the fact that most patients receive a prophylactic treatment. Thus, there is an indirect evidence of its efficacy in these patients.

Administration, Oral↗

[Intra-individual variability of the platelet anti-aggregation effect of aspirin in coronary patients].

UNLABELLED: Several studies have reported a biochemical resistance to aspirin in 5 to 10% of coronary patients. However, the stability of the platelet anti-aggregation effect with aspirin over time remains poorly understood. OBJECTIVE: To study the intra-individual variability at 6 months of the anti-platelet action of aspirin in coronary patients. METHOD: Prospective study including 40 consecutive patients with acute coronary syndrome and taking regular aspirin (250 mg a day). The biochemical impact of aspirin was determined by measuring the time to occlusion (TO) on a collagen/epinephrine cartridge with PFA-100. The determination of the TO was performed 2 months (TO1) and then 8 months (TO2) after starting aspirin. In our population, a resistance to aspirin was defined as a TO < or =125 sec. RESULTS: The median value for TO was generally stable over the two periods, at 158 sec for TO1 and 179 sec for TO2 (p = 0.29). Among the 9 initially resistant patients (22.5%), 4 became sensitive to aspirin without changing the dosage, while only one of the 31 initially sensitive patients became biochemically resistant. CONCLUSION: the existence of a medium term intra-individual variability in the antiplatelet response to aspirin in coronary patients underlines the importance of biochemical surveillance in these high vascular risk patients.

Acute Disease↗

[Clopidogrel and thrombopenia. A case report].

We report our experience with a case of isolated profound thrombocytopenia after clopidogrel (thienopyridine) administration. No adverse event such as bleeding or thrombotic event had occurred, although clopidogrel has been discontinued two weeks after the coronary artery stenting. Despite the safety of clopidogrel, this case demonstrates that clopidogrel can be associated not only with thrombotic thrombocytopenic purpura but also with isolated thrombocytopenia.

Angioplasty, Balloon, Coronary↗

A novel homozygous splice junction mutation in GPIIb associated with alternative splicing, nonsense-mediated decay of GPIIb-mRNA, and type II Glanzmann's thrombasthenia.

This work reports the study of a patient suffering a bleeding disorder clinically diagnosed as Glanzmann's thrombasthenia (GT). Immunoblotting and flow cytometric analysis showed a low (</= 10% of control) platelet content of GPIIb-IIIa, confirming it was indeed a type II GT. The molecular genetic analysis of the proband revealed the presence of a homozygous G188A transition in GPIIb. This mutation alters the consensus sequence of the splice donor site of intron 1 changing arginine 63 for lysine (R63K). No other mutation than [G188A]GPIIb was found in the proband and her parents after complete analysis of GPIIb and GPIIIa coding sequences, and the promoter, 3'-UTR, and intronic flanking regions of GPIIb. The GT phenotype of the proband is the result of a limited availability of GPIIb-mRNA. The etiopathogenic role of the [G188A]GPIIb mutation is supported by the following observations: (i) both parents, who are heterozygous for the [G188A]GPIIb mutation, show a marked decrease in the platelet content of GPIIb-mRNA; (ii) exontrap analysis demonstrated that the G188A mutation leads to a marked reduction in the steady-state level of GPIIb-mRNA. The reduced availability of platelet GPIIb-mRNA associated with the G188A mutation seems to be caused by either inefficient RNA splicing or a preferred utilization of alternative intronic donor sites that generate an in-frame STOP codon with the result of activation of nonsense-mediated mRNA decay, or both.

Alternative Splicing↗

Potential use of D-dimer measurement in patients treated with oral anticoagulant for a venous thromboembolic episode.

AIM: We compared the level of plasma D-dimer in patients with previous venous thromboembolism (VTE), receiving or not oral anticoagulant treatment (OAT) and investigated its predictive value for the risk of VTE recurrence after OAT withdrawal. METHODS: We have studied 149 patients, 81 receiving oral anticoagulants and 68 after treatment interruption. Patients with known causes of D-dimer increase were excluded. D-dimer measurements were performed by Vidas analyzer (bioMérieux, France). RESULTS: A significantly lower D-dimer plasma level was found in patients under OAT than in untreated patients, 197+/-134 ng/ml versus 399+/-239 ng/ml, respectively (p<0.001). This decrease was similar in the different age populations and whether the patient had thrombophilia (n=84) or not. There was no correlation between INR and D-dimer levels. During a mean follow-up of 30 months, no recurrence occurred in patients under OAT versus 7 untreated patients. Among them, 3 had a D-dimer below 500 ng/ml, and 3 others had a level above 500 ng/ml. The last patient was not tested. CONCLUSION: The physician should be informed of the decrease of D-dimer under OAT, since the usual cut-off of 500 ng/ml used for deep vein thrombosis (DVT) exclusion is probably lower in such treated patients. It has been recently proposed that normal D-dimer level had a high negative predictive value for VTE recurrence when this dosage was performed 3 months after OAT interruption. The small number of recurrences observed in our study with an available result of D-dimer measured more than 3 months after OAT discontinuation does not allow a definite

Administration, Oral↗

Markers of activated coagulation in patients with factor V Leiden and/or G20210A prothrombin gene mutation.

The activated protein C (APC) resistance phenotype associated with an abnormal factor V Leiden (FVL), and the G20210A prothrombin gene mutation are the most common findings in patients with venous thromboembolism (VTE). In a group of 210 patients, we compared the levels of markers of coagulation activation in carriers of FVL (71 heterozygous, 30 homozygous), G20210A prothrombin mutation (88 heterozygous) or both mutations combined (21 heterozygous), in order to assess whether these markers allow identification of a group of patients with a higher risk of thrombosis; they were also compared to normal values. A total of 143 patients had a personal history of VTE and 67 were asymptomatic. None of them had other hereditary causes of thrombophilia or an antiphospholipid syndrome. None were currently treated with either anticoagulant or hormonal treatment. Pregnant women were excluded. No significant difference between the four groups of patients could be found in the levels of F1+2, TAT and DDI. Levels were all significantly higher than the control values (p<0.05). The levels of F1+2 and TAT were similar in patients with or without a history of VTE, regardless of the type of mutation. DDI levels were significantly higher in patients with a history of VTE than in asymptomatic subjects (443+/-248 vs. 333+/-222 ng/ml, p=0.02) but with only 57% sensitivity and specificity. In conclusion, our study confirms the hypercoagulable state found in mutation carriers and points out the inability of F1+2 and TAT assays to identify a group of subjects at higher risk of thrombosis, within carriers of genetic risk factors. Although the sensitivity and specificity of DDI assay are low, high DDI concentrations tend to be associated with the risk of VTE.

Adult↗

[Treatment of deep venous thrombosis by low molecular weight heparins. Comments on the recommendations of the North American Consensus].

LMW heparins have recently come into use in North America for treatment of venous thrombosis. Their first line recommendation is a major innovation of the last north american consensus conference on antithrombotics published in Chest at the beginning of 2001. This recommendation is grade 1A regarding its advantageous benefit-risk ratio. An earlier oral vitamine K antagonist treatment and a more regular nomogram use allow to reduce the relay duration and to obtain more often the targeted INR. The more predictable anticoagulant response with weight-based doses induces a simplified anti-Xa activity survey limited to renal dysfunction and obese or less than 50 Kg body weight persons but a regular platelet count remains mandatory. Several questions need to be discussed: once or twice daily subcutaneous injection use and treatment duration which seem related to the persistence of triggering factors, the variety of thrombophilia and comorbidity conditions. Due to a greater evidence-based medicine, the antithrombotic strategy becomes more related to a closer evaluation of the individual thrombotic risk level.

Adult↗

[What is the place of aspirin in venous thrombosis prophylaxis?].

Since Virchow triade, it is well established that venous thrombosis is a multifactorial process involving various cellular and plasmatic protagonists. Aspirin antihrombotic efficacy seems not only due to its antiplatelet effects and thromboxane A2 synthesis inhibition. Anti-Platelet Trialists Collaboration metaanalysis stressed in 1994 the interest of aspirin treatment leading to 40% reduction of thrombosis relative risk. Regarding studies heterogeneity and outcomes criteria variety, its use in such context remains a matter of debate. Is the recent publication of PEP trial showing a significant decrease of pulmonary embolism mortality (0.6 versus 0.3%, p = 0.03) able to reinforce aspirin use in venous thrombosis prophylaxis? Were numerous and consecutive criticisms justified? Is there still a potential indication for aspirin in this setting? The experts of the last ACCP consensus conference recommended not to recommend aspirin in venous thrombosis prophylaxis with the highest level of evidence (grade A).

Aspirin↗

[Biological markers for acute phase hemostasis in coronary thrombosis].

Associated with rheological conditions, multiple factors regarding haemostasis and fibrinolysis contribute to the instability and rupture of atherosclerotic plaque. Various biological parameters are modified during the occurrence of a coronary thrombotic episode, but do these increasingly identified alterations constitute a cause or a direct consequence of this accident? With the increasing identification of markers more and more sensitive but of limited specificity, the relative abundance of studies in the literature contrasts with the paucity of effective assets for everyday clinical practice. In fact, the potential use of these indicators in the evaluation of the pathogenesis of vascular accident, their eventual prognostic value, their predictive nature in therapeutic strategy, and their relevance for patient classification and follow up remain to be established on a wider scale. There is growing interest in the detection of evidence of cellular cooperation or a vascular compartment lesion thanks to the development of new diagnostic tools such as flux cytometry or immunoenzymology. While advances in biology have allowed undeniable clarifications of the physiopathology of coronary accidents and in the management of thrombotic pathology, it must nevertheless be endeavoured to give a practical response to the numerous questions where doubt remains, and to pursue the search for markers or tests clinically relevant.

Acute-Phase Reaction↗

Perioperative activation of hemostasis in vascular surgery patients.

BACKGROUND: Perioperative activation of hemostasis could play an important role in the occurrence of postoperative cardiac events. The authors conducted a prospective study to assess platelet function, coagulation, and fibrinolysis status during and after infrarenal aortic surgery. METHODS: Seventeen patients were studied. Excluded were patients with preoperative coagulopathies or liver disease, or cardiac or renal insufficiency; patients receiving anticoagulant treatment, antiplatelet agents, nonsteroidal antiinflammatory agents, fresh frozen plasma, or platelet concentrates; and patients undergoing reoperation and septic patients. Blood samples were drawn before induction (T1), 1 h after incision (T2), 1 h after extubation (T3), 24 h postoperatively (T4), 48 h postoperatively (T5), and at day 7 (T6). The following tests were performed: platelet count, platelet aggregation, platelet flow cytometry for CD62 and CD63, usual coagulation tests, thrombin--antithrombin complexes, plasminogen activator inhibitor 1. RESULTS: A significant increase of adenosine diphosphate--induced platelet aggregation was observed postoperatively at T4 and T5. This was not associated with a change of flow cytometry profile. No increase of thrombin--antithrombin complex levels was observed. A higher fibrinogen rate was detected at T5 and T6. Greater amounts of plasminogen activator inhibitor 1 were detected at T3 and T4. Thus, thrombin generation was limited and fibrinolysis was impaired postoperatively. Platelets were not activated in the postoperative period, as shown by flow cytometry, but were prone to be activated, as shown by aggregation studies. CONCLUSION: The association of more easily activated platelets with a higher fibrinogen rate and a temporary shut down of fibrinolysis during the early postoperative period may indicate an increased thrombotic risk in patients undergoing major vascular surgery.

Aged↗

The role of platelet factor 4 in platelet aggregation induced by the antibodies implicated in heparin-induced thrombocytopenia.

Heparin-induced thrombocytopenia (HIT) is a severe side effect of heparin treatment. Recent studies using immunological methods demonstrated that antibodies contained in plasma, or in purified total immunoglobulin (Ig)G from patients suffering HIT, recognize as target antigen the complex heparin/platelet factor (PF4). In the present study, the role of PF4 in in-vitro platelet aggregation induced by purified total IgG or platelet-poor plasma from patients suffering HIT was investigated. In order to demonstrate the functional role of PF4, an anti-PF4 antibody that specifically blocked PF4 was used. In an experimental system composed of washed platelet suspension, incubation of F(ab')2 fragments (0.125 microg/ml) of the polyclonal anti-PF4 antibody resulted in complete inhibition of platelet aggregation triggered by purified total IgG from patients suffering HIT and heparin. In platelet-rich plasma, a significantly higher concentration (4.25 microg/ml) of the anti-PF4 F(ab')2 was required to inhibit platelet aggregation induced by HIT-PPP and heparin. Intermediate concentrations of the anti-PF4 antibody partially inhibited platelet aggregation. In plasma milieu, the concentration of PF4 was about five-fold higher in comparison with that measured in the purified system. The intensity of platelet aggregation depended on the concentration of HIT-IgG. Platelet aggregation was abolished in the presence of high concentrations of heparin (superior or equal to 10 IU/ml). The present study shows that PF4 is essential for platelet aggregation triggered by the antibodies related to HIT in the presence of heparin. The concentration of PF4 that is available to bind with heparin or with the HIT-related antibodies is critical for platelet aggregation induced by HIT antibodies.

Antibodies↗

Platelet release of trimolecular complex components MT1-MMP/TIMP2/MMP2: involvement in MMP2 activation and platelet aggregation.

Matrix metalloproteinase 2 (MMP2) has been reported to be secreted by collagen-stimulated platelets, and active MMP2 has been shown to play a role in platelet aggregation. It has been demonstrated that MMP2 activation is dependent on the complex (membrane type 1 [MT1]-MMP/tissue inhibitor of MMP2 [TIMP2]) receptor and MMP2. We have investigated human platelets as a possible source of MT1-MMP, and we have studied its role in MMP2 activation and in platelet aggregation. Gelatin zymograms showed the existence of MMP2 at proforms (68 kd) and activated-enzyme forms (62-59 kd) in supernatants of resting and activated platelets, respectively. No gelatinolytic activity was associated with the platelet pellet after aggregation, suggesting a total release of MMP2 during cell activation. By Western blot analysis in nonreduced conditions, MT1-MMP was found on resting platelet membranes in 2 forms-the inactive 45-kd form and an apparent 89-kd form, which totally disappeared under reduced conditions. After platelet degranulation, only the 45-kd form was detected. Reverse transcription-polymerase chain reaction experiments showed the expression in platelets of messenger RNA encoding for MMP2, MT1-MMP, and TIMP2. Flow cytometry analysis showed that MT1-MMP, MMP2, and TIMP2 expressions were enhanced at the activated platelet surface. MMP inhibitors, recombinant TIMP2, and synthetic BB94 inhibited collagen-induced platelet aggregation in a concentration-dependent manner, indicating the role of activated MT1-MMP in the modulation of platelet function. In conclusion, our results demonstrate the expression of the trimolecular complex components (MT1-MMP/TIMP2/MMP2) by blood platelets as well as the ability of MMP inhibitors to modulate the aggregating response.

Blood Platelets↗

Inhibition by extracellular cAMP of phorbol 12-myristate 13-acetate-induced prostaglandin H synthase-2 expression in human pulmonary microvascular endothelial cells. Involvement of an ecto-protein kinase A activity.

Exposure of human pulmonary microvascular endothelial cells (HPMECs) to phorbol 12-myristate 13-acetate (PMA) leads to the increase of prostaglandin H synthase (PGHS)-2 protein levels. Under same conditions and according to its constitutive nature, no significant variation of PGHS-1 protein was noted. The elevation of the intracellular cAMP rate is known to enhance PGHS-2 levels through a protein kinase A pathway in various cells. To determine whether the extracellular cAMP also regulates the inducible expression of PGHS, cultured HPMECs were exposed to cAMP alone or in combination with PMA. The PMA-induced PGHS-2 protein was attenuated by the extracellular cAMP. In addition, PGHS-2 activity evaluated through 6-keto-PGF1alpha generation, which was enhanced by PMA was inhibited by extracellular cAMP. Furthermore, in HPMEC medium, PMA-induced PGHS-2 expression was accompanied by the generation of a transferable activity (TA) able to abolish platelet aggregation. This resulting TA was dependent from PGHS-2 pathway, because NS-398, a selective inhibitor of PGHS-2, suppressed its production. The inhibitory TA released by treated HPMECs was also prevented by extracellular cAMP. The specific protein kinase A (PKA) inhibitor blocked the extracellular cAMP effect on both PMA-induced 6-keto-PGF1alpha synthesis and inhibitory TA generation, suggesting the involvement of PKA signaling at the outer surface of HPMECs. Accordingly, we established, in phosphorylation experiments, the presence of an endothelial ecto-protein kinase activity, able to phosphorylate the synthetic substrate kemptide in a cAMP-dependent mode. Reverse transcription-polymerase chain reaction analysis showed that PMA-induced PGHS-2 mRNA was markedly reduced by extracellular cAMP. Together, these findings provide the first experimental evidence that extracellular cAMP is able to reduce HPMEC PGHS-2 expression in terms of mRNA, protein, and enzyme activity through an ecto-PKA pathway. In addition, they outline the potential role of endothelial PGHS-2 in the limitation of platelet activation during inflammatory processes.

Carcinogens↗

[Aspirin and hemostasis].

Aspirin is one hundred years old, though its use has clearly evolved during the last 25 years. Identifying its action mechanism has allowed us to better understand the antithrombotic impact. Prostaglandin H synthetase (PGHS) is a bifunctional enzyme with cyclooxygenase and peroxydase activities. There are two isoforms: constitutive PGHS-1 and inducible PGHS-2. Aspirin irreversive acetylates the platelet cyclooxygenase involved in the formation of thromboxane A2, a powerful proaggregating agent and vasoconstrictor. More than 95% of inhibition of this synthesis takes place in two to three days using very weak doses of aspirin, on the order of 30 to 50 mg per day. Under some circumstances, this inhibition requires higher dosages. Certain clinical and biological circumstances could lead to a resistance to aspirin, making a readjustment of doses and sometimes complementary explorations necessary. The ISIS 2 study showed in an apparently irrefutable way the entry of aspirin into the antithrombotics arsenal, with a significant risk reduction of vascular death and recurrence of infarctus. Numerous studies have confirmed this efficacy. Consensus studies are based on information showing total coherence between the dose necessary to acetylate the enzyme to inhibit thromboxane A2 platelet production and the clinical antithrombotic effect. Aspirin seems to have a secure place, and it begins the third millennium in relative peace with new extra-platelet potentialities outside the framework of hemostasis and thrombosis.

Anti-Inflammatory Agents, Non-Steroidal↗

Heparin-induced thrombocytopenia: laboratory diagnosis and management.

Heparin-induced thrombocytopenia (HIT), a drug-induced immunohaematological adverse reaction, is a rare but potentially very severe condition. The main problem for this complex syndrome is its recognition and management, which should be as early as possible to avoid the development of life-threatening complications. Most studies have reported heterogeneous populations of patients with other diseases that potentially induce thrombocytopenia. There is no gold standard diagnostic criteria, and we have established a score with anamnestic criteria that allows us to evaluate the likelihood of HIT. In clinical practice, the diagnosis is based on the analysis of clinical features and laboratory tests. Platelet aggregation test (PAT) and an ELISA test (heparin platelet-induced antibodies) are generally performed by expert laboratories to confirm the occurrence of HIT. In our experience, both tests are concordant in the majority of patients. PAT seems to correlate better with the clinical features while ELISA appears more specific. Regarding their limits, both are complementary in the determination of HIT diagnosis coupled to the clinical score system. The treatment often requires a multidisciplinary approach. Danaparoid (Orgaran) or lepirudin (Refludan) are the two alternative treatments for HIT patients with marketing approval. To avoid further exposure to heparin, every HIT patient should carry a written document that confirms the immunoallergy.

Animals↗