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Nicolas De Prost - One of the best experts on this subject based on the ideXlab platform.
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pneumococcal Purpura fulminans in asplenic or hyposplenic patients a french multicenter exposed unexposed retrospective cohort study
Critical Care, 2020Co-Authors: Damien Contou, Remi Coudroy, Gwenhael Colin, Jeanmarc Tadie, Martin Cour, Romain Sonneville, Armand Mekontso Dessap, Nicolas De ProstAbstract:Pneumococcal infections remain the main cause of overwhelming post-splenectomy infections, and Purpura fulminans may develop in almost 20% of patients with overwhelming post-splenectomy infection. We aimed at describing the impact of asplenia/hyposplenia on the clinical features and the outcomes of adult patients admitted to the intensive care unit (ICU) for pneumococcal Purpura fulminans. A 17-year national multicenter retrospective cohort study included adult patients admitted to 55 French ICUs for an infectious Purpura fulminans from 2000 to 2016. Patients with pneumococcal Purpura fulminans were analyzed according to the absence or presence of asplenia/hyposplenia. Among the 306 patients admitted to the ICU for Purpura fulminans, 67 (22%) had a pneumococcal Purpura fulminans, of whom 34 (51%) had asplenia (n = 29/34, 85%) or hyposplenia (n = 5/34, 15%) and 33 (49%) had eusplenia. The prevalence of pneumococcal Purpura fulminans was seven times higher in asplenic/hyposplenic patients compared to eusplenic patients with Purpura fulminans (n = 34/39, 87% vs. n = 33/267, 12%; p < 0.001). The median time interval between the occurrence of asplenia/hyposplenia and ICU admission was 20 [9–32] years. Pneumococcal vaccine coverage was 35% in asplenic/hyposplenic patients. Purpura was more frequently reported before ICU admission in asplenic/hyposplenic patients (n = 25/34, 73% vs. n = 13/33, 39%; p = 0.01). The rate of bacteremia did not differ between asplenic/hyposplenic and eusplenic patients (n = 31/34, 91% vs n = 27/33, 82%; p = 0.261). SAPS II (60 ± 14 vs. 60 ± 18; p = 0.244) and SOFA (13 [1–5] vs. 14 [1–4, 6]; p = 0.48) scores did not differ between asplenic/hyposplenic and eusplenic patients. There were no significant differences between asplenic/hyposplenic and eusplenic patients regarding the rate of limb amputation (n = 9/34, 26% vs. 15/33, 45%; p = 0.11) and hospital mortality (n = 20/34, 59% vs. n = 15/33, 45%; p = 0.27). Half of pneumococcal Purpura fulminans episodes occurred in asplenic or hyposplenic patients. Pneumococcal vaccine coverage was reported in one third of asplenic/hyposplenic patients. Half of pneumococcal Purpura fulminans episodes occurred more than 20 years after splenectomy. Outcomes of pneumococcal Purpura fulminans did not show significant differences between patients with or without asplenia or hyposplenia, although the small number of patients included limited our power to detect potential differences between groups.
Remi Coudroy - One of the best experts on this subject based on the ideXlab platform.
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pneumococcal Purpura fulminans in asplenic or hyposplenic patients a french multicenter exposed unexposed retrospective cohort study
Critical Care, 2020Co-Authors: Damien Contou, Remi Coudroy, Gwenhael Colin, Jeanmarc Tadie, Martin Cour, Romain Sonneville, Armand Mekontso Dessap, Nicolas De ProstAbstract:Pneumococcal infections remain the main cause of overwhelming post-splenectomy infections, and Purpura fulminans may develop in almost 20% of patients with overwhelming post-splenectomy infection. We aimed at describing the impact of asplenia/hyposplenia on the clinical features and the outcomes of adult patients admitted to the intensive care unit (ICU) for pneumococcal Purpura fulminans. A 17-year national multicenter retrospective cohort study included adult patients admitted to 55 French ICUs for an infectious Purpura fulminans from 2000 to 2016. Patients with pneumococcal Purpura fulminans were analyzed according to the absence or presence of asplenia/hyposplenia. Among the 306 patients admitted to the ICU for Purpura fulminans, 67 (22%) had a pneumococcal Purpura fulminans, of whom 34 (51%) had asplenia (n = 29/34, 85%) or hyposplenia (n = 5/34, 15%) and 33 (49%) had eusplenia. The prevalence of pneumococcal Purpura fulminans was seven times higher in asplenic/hyposplenic patients compared to eusplenic patients with Purpura fulminans (n = 34/39, 87% vs. n = 33/267, 12%; p < 0.001). The median time interval between the occurrence of asplenia/hyposplenia and ICU admission was 20 [9–32] years. Pneumococcal vaccine coverage was 35% in asplenic/hyposplenic patients. Purpura was more frequently reported before ICU admission in asplenic/hyposplenic patients (n = 25/34, 73% vs. n = 13/33, 39%; p = 0.01). The rate of bacteremia did not differ between asplenic/hyposplenic and eusplenic patients (n = 31/34, 91% vs n = 27/33, 82%; p = 0.261). SAPS II (60 ± 14 vs. 60 ± 18; p = 0.244) and SOFA (13 [1–5] vs. 14 [1–4, 6]; p = 0.48) scores did not differ between asplenic/hyposplenic and eusplenic patients. There were no significant differences between asplenic/hyposplenic and eusplenic patients regarding the rate of limb amputation (n = 9/34, 26% vs. 15/33, 45%; p = 0.11) and hospital mortality (n = 20/34, 59% vs. n = 15/33, 45%; p = 0.27). Half of pneumococcal Purpura fulminans episodes occurred in asplenic or hyposplenic patients. Pneumococcal vaccine coverage was reported in one third of asplenic/hyposplenic patients. Half of pneumococcal Purpura fulminans episodes occurred more than 20 years after splenectomy. Outcomes of pneumococcal Purpura fulminans did not show significant differences between patients with or without asplenia or hyposplenia, although the small number of patients included limited our power to detect potential differences between groups.
Mathieu Coureuil - One of the best experts on this subject based on the ideXlab platform.
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An ADAM-10 dependent EPCR shedding links meningococcal interaction with endothelial cells to Purpura fulminans
PLoS Pathogens, 2018Co-Authors: Herve Lecuyer, Delphine Borgel, Xavier Nassif, Zoé Virion, Jean-philippe Barnier, Soraya Matczak, Sandrine Bourdoulous, Elsa Bianchini, François Saller, Mathieu CoureuilAbstract:Purpura fulminans is a deadly complication of Neisseria meningitidis infections due to extensive thrombosis of microvessels. Although a Disseminated Intra-vascular Coagulation syndrome (DIC) is frequently observed during Gram negative sepsis, it is rarely associated with extensive thrombosis like those observed during meningococcemia, suggesting that the meningococcus induces a specific dysregulation of coagulation. Another specific feature of N. meningitidis pathogenesis is its ability to colonize microvessels endothelial cells via type IV pili. Importantly, endothelial cells are key in controlling the coagulation cascade through the activation of the potent anticoagulant Protein C (PC) thanks to two endothelial cell receptors among which the Endothelial Protein C Receptor (EPCR). Considering that congenital or acquired deficiencies of PC are associated with Purpura fulminans, we hypothesized that a defect in the activation of PC following meningococcal adhesion to microvessels is responsible for the thrombotic events observed during meningococcemia. Here we showed that the adhesion of N. meningitidis on endothelial cells results in a rapid and intense decrease of EPCR expression by inducing its cleavage in a process know as shedding. Using siRNA experiments and CRISPR/Cas9 genome edition we identified ADAM10 (A Disintegrin And Metalloproteinase-10) as the protease responsible for this shedding. Surprisingly, ADAM17, the only EPCR sheddase described so far, was not involved in this process. Finally, we showed that this ADAM10-mediated shedding of EPCR induced by the meningococcal interaction with endothelial cells was responsible for an impaired activation of Protein C. This work unveils for the first time a direct link between meningococcal adhesion to endothelial cells and a severe dysregulation of coagulation, and potentially identifies new therapeutic targets for meningococcal Purpura fulminans.
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pathogenesis of meningococcal Purpura fulminans
Pathogens and Disease, 2017Co-Authors: Herve Lecuyer, Delphine Borgel, Xavier Nassif, Mathieu CoureuilAbstract:Purpura fulminans (PF) is a dreadful and frequent complication of Neisseria meningitidis invasive infection, and is associated with a high mortality rate. This syndrome begins with dermal microvessels thrombosis that rapidly lead to hemorrhagic skin necrosis. In this review, we discuss the prothrombotic events occurring during meningococcal infection. Moreover, recent data from an experimental mouse model have highlighted the critical role of the meningococcus adhesion to the endothelium in the development of PF lesions, thus opening new therapeutic perspectives.
Howard Hast - One of the best experts on this subject based on the ideXlab platform.
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mowat wilson syndrome presenting as Purpura fulminans in a healthy infant
Pediatrics, 2019Co-Authors: Alexander P Sun, Claudia Nevarez, Howard HastAbstract:Introduction: Purpura fulminans is a rapidly progressive syndrome of intravascular thrombosis and hemorrhagic infarction of the skin associated with vascular collapse. It is most commonly a complication of Neisseria meningitidis sepsis, and less frequently attributable to Streptococcus pneumoniae. The most common predisposing factor for invasive pneumococcal infection is splenic dysfunction. Case Report: A 10-month old girl with history of gross motor developmental delay presented to an outside hospital with one day of rhinorrhea, tactile fever, drowsiness and poor feeding. She was hypotensive and tachycardic, and had a generalized tonic-clonic seizure and petechial rash that quickly progressed to purpuric. CSF …
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mowat wilson syndrome presenting with Purpura fulminans
Pediatrics, 2019Co-Authors: Claudia Nevarez G Flores, Alexander P Sun, Howard HastAbstract:Purpura fulminans is a rapidly progressive syndrome of intravascular thrombosis and hemorrhagic infarction of the skin. The most common infectious etiology is Neisseria meningitidis sepsis, and less commonly it has been documented as a complication of invasive Streptococcus pneumoniae. In children who are otherwise healthy, splenic dysfunction is a significant predisposing factor for invasive pneumococcal infection. We present the case of a 10-month-old girl with a history of developmental delay, who developed an overwhelming infection complicated by Purpura fulminans and was found to have previously undiagnosed Mowat-Wilson syndrome with anatomic asplenia. We propose screening patients with clinical features suggestive of Mowat-Wilson syndrome for asplenia to evaluate the need for additional preventive care.
Damien Contou - One of the best experts on this subject based on the ideXlab platform.
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pneumococcal Purpura fulminans in asplenic or hyposplenic patients a french multicenter exposed unexposed retrospective cohort study
Critical Care, 2020Co-Authors: Damien Contou, Remi Coudroy, Gwenhael Colin, Jeanmarc Tadie, Martin Cour, Romain Sonneville, Armand Mekontso Dessap, Nicolas De ProstAbstract:Pneumococcal infections remain the main cause of overwhelming post-splenectomy infections, and Purpura fulminans may develop in almost 20% of patients with overwhelming post-splenectomy infection. We aimed at describing the impact of asplenia/hyposplenia on the clinical features and the outcomes of adult patients admitted to the intensive care unit (ICU) for pneumococcal Purpura fulminans. A 17-year national multicenter retrospective cohort study included adult patients admitted to 55 French ICUs for an infectious Purpura fulminans from 2000 to 2016. Patients with pneumococcal Purpura fulminans were analyzed according to the absence or presence of asplenia/hyposplenia. Among the 306 patients admitted to the ICU for Purpura fulminans, 67 (22%) had a pneumococcal Purpura fulminans, of whom 34 (51%) had asplenia (n = 29/34, 85%) or hyposplenia (n = 5/34, 15%) and 33 (49%) had eusplenia. The prevalence of pneumococcal Purpura fulminans was seven times higher in asplenic/hyposplenic patients compared to eusplenic patients with Purpura fulminans (n = 34/39, 87% vs. n = 33/267, 12%; p < 0.001). The median time interval between the occurrence of asplenia/hyposplenia and ICU admission was 20 [9–32] years. Pneumococcal vaccine coverage was 35% in asplenic/hyposplenic patients. Purpura was more frequently reported before ICU admission in asplenic/hyposplenic patients (n = 25/34, 73% vs. n = 13/33, 39%; p = 0.01). The rate of bacteremia did not differ between asplenic/hyposplenic and eusplenic patients (n = 31/34, 91% vs n = 27/33, 82%; p = 0.261). SAPS II (60 ± 14 vs. 60 ± 18; p = 0.244) and SOFA (13 [1–5] vs. 14 [1–4, 6]; p = 0.48) scores did not differ between asplenic/hyposplenic and eusplenic patients. There were no significant differences between asplenic/hyposplenic and eusplenic patients regarding the rate of limb amputation (n = 9/34, 26% vs. 15/33, 45%; p = 0.11) and hospital mortality (n = 20/34, 59% vs. n = 15/33, 45%; p = 0.27). Half of pneumococcal Purpura fulminans episodes occurred in asplenic or hyposplenic patients. Pneumococcal vaccine coverage was reported in one third of asplenic/hyposplenic patients. Half of pneumococcal Purpura fulminans episodes occurred more than 20 years after splenectomy. Outcomes of pneumococcal Purpura fulminans did not show significant differences between patients with or without asplenia or hyposplenia, although the small number of patients included limited our power to detect potential differences between groups.
