Leger J.-M.,University Hospital Pitie Salpetriere |
Viala K.,University Hospital Pitie Salpetriere |
Nicolas G.,University of Angers |
Creange A.,University Hospital Henri Mondor |
And 7 more authors.
Neurology | Year: 2013
Objective: To determine whether rituximab 375 mg/m2 was efficacious in patients with immunoglobulin M (IgM) anti-myelin-associated glycoprotein antibody demyelinating neuropathy (IgM anti-MAG demyelinating neuropathy). Methods: Fifty-four patients with IgM anti-MAG demyelinating neuropathy were enrolled in this randomized, double-blind, placebo-controlled trial. The inclusion criteria were inflammatory neuropathy cause and treatment (INCAT) sensory score (ISS) $4 and visual analog pain scale >4 or ataxia score $2. The primary outcome was mean change in ISS at 12 months. Results: Twenty-six patients were randomized to a group receiving 4 weekly infusions of 375 mg/m2 rituximab, and 28 patients to placebo. Intention-to-treat analysis, with imputation of missing ISS values by the last observation carried forward method, showed a lack of mean change in ISS at 12 months, 1.0 ± 2.7 in the rituximab group, and 1.0 ± 2.8 in the placebo group. However, changes were observed, in per protocol analysis at 12 months, for the number of patients with an improvement of at least 2 points in the INCAT disability scale (p = 0.027), the self-evaluation scale (p 5 0.016), and 2 subscores of the Short Form-36 questionnaire. Conclusions: Although primary outcome measures provide no evidence to support the use of rituximab in IgM anti-MAG demyelinating neuropathy, there were improvements in several secondary outcomes in per protocol analysis. Level of evidence: This study provides Class I evidence that rituximab is ineffective in improving ISS in patients with IgM anti-MAG demyelinating neuropathy. © 2013 American Academy of Neurology.
Prevalence of mupirocin resistance among invasive coagulase-negative staphylococci and methicillin-resistan Staphylococcus aureus (MRSA) in France: Emergence of a mupirocin-resistant MRSA clone harbouring mupA
Desroches M.,University Paris - Sud |
Potier J.,University Paris - Sud |
Laurent F.,University of Lyon |
Bourrel A.-S.,University Paris - Sud |
And 3 more authors.
Journal of Antimicrobial Chemotherapy | Year: 2013
Objectives: Mupirocin is the cornerstone of decolonization regimens, a successful strategy to prevent healthcare-associated staphylococcal infections. Several recent studies have reported alarming results: (i) an extending reservoir of mupA, the ancestral mobile resistance gene, among coagulase-negative staphylococci (CoNS); (ii) the emergence of a new resistance gene (mupB); and (iii) a growing number of mupirocin-resistant methi-cillin-resistant Staphylococcus aureus (MRSA), including highly pathogenic clones. We performed a nationwide prospective study in France to detect such trends among invasive staphylococci. Methods: Between October 2011 and February 2012, 367 MRSA and 708 CoNS invasive isolates were collected from 37 hospitals and analysed centrally. Mupirocin MICs were determined using the broth microdilution method. mupA/B PCR was performed for resistant isolates (MIC>1 mg/L). Genetic relatedness between mupir-ocin-resistant MRSA isolates was determined by PFGE analysis and related isolates were tested by microarray. Results: Among MRSA isolates 2.2% (n1/48) were classified as mupirocin resistant; 1.4% (n1/45) showing low-level resistance (MIC ≤256 mg/L) and 0.8% (n1/43) high-level resistance (MIC>256 mg/L). Only the latter isolates carried mupA. A clonal relationship was identified between two mupA-negative MRSA from the same hospital and three mupA-positive MRSA from three distant towns; these three isolates belonged to the Lyon clone. Mupirocin resistance was identified in 10.3% of CoNS, mainly highly resistant mupA-positive isolates (5.6%). The mupB gene was not detected in mupirocin-resistant MRSA or CoNS.Conclusions: This first large national study indicates the need for thorough epidemiological monitoring and a stewardship programme to prevent and detect mupirocin resistance in staphylococci. © The Author 2013. Published by Oxford University Press on behalf of the British Society for Antimicrobial Chemotherapy. All rights reserved.
Bessede T.,University Paris - Sud |
Girodon E.,University Hospital Henri Mondor |
Allory Y.,University Hospital Henri Mondor |
Le Floch A.,University Hospital Henri Mondor |
And 2 more authors.
World Journal of Urology | Year: 2014
Purpose: The aim was to eliminate, by DNA comparison, any identity mismatch between operative and biopsy specimens and to analyse the determinants of all pT0 prostate cancers occurred in a single institution. Methods: All prostate pT0 cases in a single institution over 20 years were investigated. None of the patients had been diagnosed after a transurethral resection of the prostate nor had they received neoadjuvant hormonal treatment. The biopsies performed in other centres had been referred for a centralized pathologic re-analysis. DNA analysis was performed in samples from operative and biopsy specimens, and pairs of tissues were blindly constituted. Correct matching was verified in each pair and compared to the original database in order to comment on the occurrence of identity mismatches in the series. Results: Nineteen patients (0.77 %) had been diagnosed as having pT0 prostate cancer among the 2,462 RP procedures performed over 19 years. The biopsy re-analysis invalidated the initial diagnosis of prostate cancer in one biopsy set performed elsewhere. Among 12 entirely processed cases, the biochemistry procedure evaluated as "very unlikely" the occurrence of an error in tissue identification in the biopsy setting, during the surgical procedure or the pathological analysis. No identification error of tissue samples was established in this first verified pT0 series. Conclusions: Although it must be suspected, specimen identification error was not a cause for pT0 prostate cancer. Only after a full pathological and DNA verification, the pT0 stage remains a sole entity, unexplained in most cases. © 2014 Springer-Verlag Berlin Heidelberg.
Aujesky D.,University of Bern |
Roy P.-M.,University of Angers |
Verschuren F.,Catholic University of Leuven |
Righini M.,University of Geneva |
And 15 more authors.
The Lancet | Year: 2011
Although practice guidelines recommend outpatient care for selected, haemodynamically stable patients with pulmonary embolism, most treatment is presently inpatient based. We aimed to assess non-inferiority of outpatient care compared with inpatient care. We undertook an open-label, randomised non-inferiority trial at 19 emergency departments in Switzerland, France, Belgium, and the USA. We randomly assigned patients with acute, symptomatic pulmonary embolism and a low risk of death (pulmonary embolism severity index risk classes I or II) with a computer-generated randomisation sequence (blocks of 2-4) in a 1:1 ratio to initial outpatient (ie, discharged from hospital ≤24 h after randomisation) or inpatient treatment with subcutaneous enoxaparin (≥5 days) followed by oral anticoagulation (≥90 days). The primary outcome was symptomatic, recurrent venous thromboembolism within 90 days; safety outcomes included major bleeding within 14 or 90 days and mortality within 90 days. We used a non-inferiority margin of 4 for a difference between inpatient and outpatient groups. We included all enrolled patients in the primary analysis, excluding those lost to follow-up. This trial is registered with ClinicalTrials.gov, number NCT00425542. Between February, 2007, and June, 2010, we enrolled 344 eligible patients. In the primary analysis, one (0·6) of 171 outpatients developed recurrent venous thromboembolism within 90 days compared with none of 168 inpatients (95 upper confidence limit [UCL] 2·7; p=0·011). Only one (0·6) patient in each treatment group died within 90 days (95 UCL 2·1; p=0·005), and two (1·2) of 171 outpatients and no inpatients had major bleeding within 14 days (95 UCL 3·6; p=0·031). By 90 days, three (1·8) outpatients but no inpatients had developed major bleeding (95 UCL 4·5; p=0·086). Mean length of stay was 0·5 days (SD 1·0) for outpatients and 3·9 days (SD 3·1) for inpatients. In selected low-risk patients with pulmonary embolism, outpatient care can safely and effectively be used in place of inpatient care. Swiss National Science Foundation, Programme Hospitalier de Recherche Clinique, and the US National Heart, Lung, and Blood Institute. Sanofi-Aventis provided free drug supply in the participating European centres. © 2011 Elsevier Ltd.
Puymirat E.,University of Paris Descartes |
Simon T.,Hopital Saint Antoine |
Simon T.,University Pierre and Marie Curie |
Steg P.G.,University Paris Diderot |
And 11 more authors.
JAMA - Journal of the American Medical Association | Year: 2012
Context: The contemporary decline in mortality reported in patients with ST-segment elevation myocardial infarction (STEMI) has been attributed mainly to improved use of reperfusion therapy. Objective: To determine potential factors-beyond reperfusion therapy - associated with improved survival in patients with STEMI over a 15-year period. Design, Setting, and Patients: Four 1-month French nationwide registries, conducted 5 years apart (between 1995, 2000, 2005, 2010), including a total of 6707 STEMI patients admitted to intensive care or coronary care units. Main Outcome Measures: Changes over time in crude 30-day mortality, and mortality standardized to the 2010 population characteristics. Results: Mean(SD) age decreased from 66.2 (14.0) to 63.3 (14.5) years, with a concomitant decline in history of cardiovascular events and comorbidities. The proportion of younger patients increased, particularly in women younger than 60 years (from 11.8% to 25.5%), in whom prevalence of current smoking (37.3% to 73.1%) and obesity (17.6% to 27.1%) increased. Time from symptom onset to hospital admission decreased, with a shorter time from onset to first call, and broader use of mobile intensive care units. Reperfusion therapy increased from 49.4% to 74.7%, driven by primary percutaneous coronary intervention (11.9% to 60.8%). Early use of recommended medications increased, particularly low-molecular-weight heparins and statins. Crude30-day mortality decreased from 13.7% (95% CI, 12.0-15.4) to 4.4% (95% CI, 3.5-5.4), whereas standardized mortality decreased from 11.3% (95% CI, 9.5-13.2) to 4.4% (95% CI, 3.5-5.4). Multivariable analysis showed a consistent reduction in mortality from 1995 to 2010 after controlling for clinical characteristics in addition to the initial population risk score and use of reperfusion therapy, with odds mortality ratios of 0.39 (95%, 0.29-0.53, P<.001) in 2010 compared with 1995. Conclusion: In France, the overall rate of cardiovascular mortality among patients with STEMI decreased from 1995 to 2010, accompanied by an increase in the proportion of women younger than 60 years with STEMI, changes in other population characteristics, and greater use of reperfusion therapy and recommended medications. ©2012 American Medical Association. All rights reserved.
Calvet D.,University of Paris Descartes |
Mas J.-L.,University of Paris Descartes |
Algra A.,University Utrecht |
Becquemin J.-P.,University Hospital Henri Mondor |
And 9 more authors.
Stroke | Year: 2014
Background and Purpose - Randomized clinical trials show higher 30-day risk of stroke or death after carotid artery stenting compared with surgery. We examined whether operator experience is associated with 30-day risk of stroke or death in the Carotid Stenting Trialists' Collaboration database. Methods - The Carotid Stenting Trialists' Collaboration is a pooled individual patient database including all patients recruited in 3 randomized trials of stenting versus endarterectomy for symptomatic carotid stenosis (Endarterectomy Versus Angioplasty in patients with Symptomatic Severe Carotid Stenosis trial, Stent-Protected Angioplasty versus Carotid Endarterectomy trial, and International Carotid Stenting Study). Lifetime carotid artery stenting experience, lifetime experience in stenting procedures excluding the carotid, and annual number of procedures performed within the trial (in-trial volume), divided into tertiles, were used to measure operator experience. The outcome event was the occurrence of any stroke or death within 30 days of the procedure. The analysis was done per protocol. Results - Among 1546 patients who underwent carotid artery stenting, 120 (7.8%) had a stroke or death within 30 days of the procedure. The 30-day risk of stroke or death did not differ according to operator lifetime carotid artery stenting experience (P=0.8) or operator lifetime stenting experience excluding the carotid (P=0.7). In contrast, the 30-day risk of stroke or death was significantly higher in patients treated by operators with low (mean ≤3.2 procedures/y; risk 10.1%; adjusted risk ratio=2.30 [1.36-3.87]) and intermediate annual in-trial volumes (3.2-5.6 procedures/y; 8.4%; adjusted risk ratio=1.93 [1.14-3.27]) compared with patients treated by high annual in-trial volume operators (>5.6 procedures/y; 5.1%). Conclusions - Carotid stenting should only be performed by operators with annual procedure volume ≥6 cases per year. © 2013 American Heart Association, Inc.
Decousser J.W.,University Hospital Henri Mondor |
Decousser J.W.,University Paris Est Creteil |
Jansen C.,University Paris Est Creteil |
Jansen C.,University Hospital Henri Mondor |
And 9 more authors.
Eurosurveillance | Year: 2013
We report the first outbreak of carbapenem-resistant NDM-1-producing Acinetobacter baumannii in Europe, in a French intensive-care unit in January to May 2013. The index patient was transferred from Algeria and led to the infection/colonisation of five additional patients. Concurrently, another imported case from Algeria was identified. The seven isolates were genetically indistinguishable, belonging to ST85. The blaNDM-1 carbapenemase gene was part of the chromosomally located composite transposon Tn125. This report underscores the growing concern about the spread of NDM-1-producing A. baumannii in Europe.
Jayol A.,University of Fribourg |
Nordmann P.,University of Fribourg |
Desroches M.,University Hospital Henri Mondor |
Desroches M.,French Institute of Health and Medical Research |
And 3 more authors.
Antimicrobial Agents and Chemotherapy | Year: 2016
An extended-spectrum β-lactamase (ESBL)-producing and colistin-resistant Klebsiella pneumoniae clinical isolate was recovered from a patient who was treated with cefotaxime. This isolate harbored a blaCTX-M-15 ESBL gene that was associated with an ISEcp1 insertion sequence. Transposition of that tandem occurred within the chromosomal mgrB gene, leading to inactivation of the mgrB gene and consequently to acquired resistance to colistin. We showed here a coselection of colistin resistance as a result of a broad-spectrum cephalosporin selective pressure. Copyright © 2016, American Society for Microbiology. All Rights Reserved.
De Leval L.,University of Lausanne |
Gaulard P.,University Hospital Henri Mondor
Blood | Year: 2014
In this issue of Blood, Iqbal et al,1 having compiled gene expression profiles from .300 peripheral T-cell lymphomas, expand previous findings on the diagnostic value of molecular signatures that correlate with different histological types of T-cell lymphomas. They report the discovery of 2 molecular subgroups of peripheral T-cell lymphomas, not otherwise specified (PTCL, NOS), characterized by high expression of either GATA-binding protein 3 (GATA-3) or t-box 21 (TBX21) transcription factors and corresponding target genes, with the GATA3 subgroup being associated with distinctly worse prognosis. In an independent study, Wang et al2 also show that GATA3 expression in a subset of PTCL, NOS identifies a subgroup of patients with inferior survival. © 2014 by The American Society of Hematology.
Plante-Bordeneuve V.,University Hospital Henri Mondor
Journal of Neurology | Year: 2014
Transthyretin familial amyloid polyneuropathy (TTR-FAP) is a progressive neurodegenerative and systemic genetic disease first identified in Portugal, now reported worldwide. During the past few years our knowledge on the phenotypic presentation of this devastating condition has remarkably expanded including a wide variation in age of onset, different neuropathic patterns and patients presenting with isolated or predominant cardiac involvement. Liver transplantation, the first therapeutic approach, although invasive, has been shown to halt the progression of the neuropathy in young onset patients. Fortunately, several disease-modifying treatments are now available or in clinical development including TTR stabilizers and gene therapy. Their efficacy is higher if administered at the earliest disease stage. Thus, management of TTR-FAP patients is a moving field with need for early diagnosis using new diagnostic tools and new therapeutic options. © 2014 Springer-Verlag Berlin Heidelberg.