Clément Picard

Life-threatening hemoptysis in adults with community-acquired pneumonia due to Panton-Valentine leukocidin-secreting Staphylococcus aureus

Three new consecutive cases of life-threatening hemoptysis in adults with community-acquired pneumonia due to Panton-Valentine leukocidin-secreting Staphylococcus aureus are presented, focusing on the particular clinical presentation of this new entity. Between December 1999 and March 2001, three adults aged from 23 to 67 years were admitted to our respiratory intensive care unit for massive hemoptysis and septic shock associated with community-acquired Staphylococcus aureus pneumonia. Isolates were sent to the Centre National de Référence des Toxémies Staphylococciques in Lyon, France, where they were found to secrete Panton-Valentive leukocidin. The clinical course was similar in the three patients, with massive hemoptysis and septic shock necessitating mechanical ventilation. Two patients died rapidly; necropsy showed pulmonary vascular necrosis in one of them. The third patient recovered after appropriate antibiotic therapy. Leukocidin/neutrophil interactions in the pulmonary vasculature may cause severe hemoptysis in patients with community-acquired Staphylococcus aureus pneumonia secreting Panton-Valentine leukocidin. Adult patients with massive hemoptysis and suspected community-acquired pneumonia should receive antibiotic regimens covering Staphylococcus aureus.

Massive hemoptysis due to Rasmussen aneurysm: detection with helicoidal CT angiography and successful steel coil embolization.

ObjectiveTo present the successful management of two cases of massive hemoptysis related to pulmonary aneurysms in patients with active tuberculosis.Design and settingRetrospective study in the respiratory intensive care unit (ICU) of a university hospital.PatientsBetween July 1996 and January 2002, 46 cases of hemoptysis related to active tuberculosis needed ICU admission. In two cases, pulmonary aneurysm was the source of bleeding.ResultsDiagnosis was suspected on enhanced CT scan and confirmed by pulmonary angiograms. Transcatheter occlusion of pulmonary arterial circulation was successful. Both patients were alive at 1-year follow-up.ConclusionsMassive hemoptysis occurring in patients with active tuberculosis could arise from pulmonary aneurysms. In such cases, bronchial artery embolization is ineffective. Before referring those patients for emergency surgery, an alternative strategy using angiographic study and transcatheter occlusion of pulmonary arterial circulation might be of interest.

Diffuse alveolar hemorrhage in immunocompetent patients: Etiologies and prognosis revisited

BACKGROUND Diffuse alveolar hemorrhage (DAH) represents a diagnostic challenge of acute respiratory failure. Prompt identification of the underlying cause of DAH and initiation of appropriate treatment are required in order to prevent acute respiratory failure and irreversible loss of renal function. More than 100 causes of DAH have been reported. However, the relative frequency and the differential presentation of those causes have been poorly documented, as well as their respective prognosis. METHODS We retrospectively reviewed the charts of 112 consecutive patients hospitalized for DAH in a tertiary referral center over a 30-year period. RESULTS Twenty-four causes of DAH were classified into four etiologic groups: immune (n = 39), congestive heart failure (CHF; n = 33), miscellaneous (n = 26), and idiopathic DAH (n = 14). Based on this classification, clinical and laboratory features of DAH differed on hospital admission. Patients with immune DAH had more frequent pulmonary-renal syndrome (p < 0.001), extra-pulmonary symptoms (p < 0.01), and lower blood hemoglobin level than others (p < 0.001). Patients with CHF-related DAH were older and received more anticoagulant treatments than others (p < 0.05). Those with miscellaneous causes of DAH exhibited a shorter prodromal phase (p < 0.001) and had more frequent hemoptysis >200 mL (p < 0.05). Patients with idiopathic DAH had more bronchoalveolar lavage siderophages (p < 0.01). In-hospital mortality was 24.1%, ranging from 7.1% in patients with idiopathic DAH to 36.4% in those with CHF. CONCLUSIONS Arbitrary classification of DAH in four etiologic groups gives the opportunity to underline distinct presentations and outcomes of various causes of DAH.

Diffuse alveolar haemorrhage: factors associated with in-hospital and long-term mortality

Diffuse alveolar haemorrhage (DAH) is a feature of several immune and nonimmune disorders. Reported prognosis is poor, with in-hospital mortality ranging from 20% to 100%. Early identification of prognostic factors may be useful in the initiation of appropriate treatment. We retrospectively analysed the charts of all patients referred to a university hospital for DAH between 1980 and 2008. Variables associated with in-hospital and long-term mortality were determined using a logistic regression model and the Kaplan–Meier method, respectively. Immunosuppressed patients were excluded. Overall, 97 patients were included in the study. In-hospital mortality was 24.7%. Factors associated with in-hospital mortality were shock (OR 77.5, 95% CI 8.9–677.2), glomerular filtration rate <60 mL·min−1 (OR 11.2, 95% CI 1.8–68.4) and plasmatic lactate dehydrogenase level more than twice the normal value (OR 12.1, 95% CI 1.7–84.3). Mortality among discharged patients was 16.4% with a median follow-up duration of 34 months. Factors associated with increased long-term mortality in univariate analysis were age over 60 yrs (p = 0.026), cardiovascular comorbidity (p = 0.027) and end-stage renal failure with dependence on haemodialysis (p = 0.026). Patients with immune and nonimmune DAH had similar outcomes. Early outcome depended on nonpulmonary organ failures. Conversely, late outcome was related to age, cardiac comorbidities and the need for haemodialysis.

Prevalence and characteristics of TERT and TERC mutations in suspected genetic pulmonary fibrosis

Telomerase reverse transcriptase (TERT) or telomerase RNA (TERC) gene mutation is a major monogenic cause of pulmonary fibrosis. Sequencing of TERT/TERC genes is proposed to patients with familial pulmonary fibrosis. Little is known about the possible predictors of this mutation and its impact on prognosis. We retrospectively analysed all the genetic diagnoses made between 2007–2014 in patients with pulmonary fibrosis. We evaluated the prevalence of TERT/TERC disease-associated variant (DAV), factors associated with a DAV, and the impact of the DAV on survival. 237 patients with pulmonary fibrosis (153 with familial pulmonary fibrosis, 84 with telomere syndrome features without familial pulmonary fibrosis) were tested for TERT/TERC DAV. DAV was diagnosed in 40 patients (16.8%), including five with non-idiopathic interstitial pneumonia. Prevalence of TERT/TERC DAV did not significantly differ between patients with familial pulmonary fibrosis or with only telomere syndrome features (18.2% versus 16.4%). Young age, red blood cell macrocytosis, and low platelet count were associated with the presence of DAV; the probability of DAV was increased for patients 40–60 years. Transplant-free survival was lower with than without TERT/TERC DAV (4.2 versus 7.2 years; p=0.046). TERT/TERC DAV were associated with specific clinical and biological features and reduced transplant-free survival. Pulmonary fibrosis patients with TERT/TERC disease-associated variants show reduced transplant-free survival http://ow.ly/EmYs304atGl

Alveolar haemorrhage in the immunocompetent host: a scale for early diagnosis of an immune cause.

Background: Diffuse alveolar haemorrhage (DAH) is a life-threatening condition due to immune and non-immune causes. Early identification of an underlying immune disorder is essential in order to initiate appropriate treatment. Objective: The purpose of this study was to identify early predictive factors of an immune cause of DAH. Methods: We conducted a retrospective study of 76 immunocompetent patients with DAH to identify early predictive factors of immune-related DAH using clinical, radiological and routine biological data available in the first 24 h after hospital admission. Results: Multivariate analysis identified 4 parameters which were independently associated with immune-related DAH: (1) onset of first respiratory symptoms ≧11 days, (2) fatigue and/or weight loss during the month prior to presentation, (3) arthralgias or arthritis and (4) proteinuria ≧1 g/l. A simplified scale was constructed using these variables, with an area under the receiver operating characteristic curve of 0.913, for the diagnosis of immune-related DAH. Conclusions: A simple diagnostic scale can be used to identify an immune-related cause of DAH in immunocompetent patients and may help guide treatment decisions such as initiation of steroid therapy on the day of admission.

Hémorragies alvéolaires en dehors des situations d’immunodépression : prise en charge diagnostique et thérapeutique

Diffuse alveolar hemorrhage is a bleeding originating from the pulmonary acinus. Number of causes are possible, that can be divided in immune and non immune causes. Immune mediated diffuse alveolar hemorrhages are mainly due to small vessels vasculitis (Wegener granulomatosis, microscopic polyangiitis), systemic lupus erythematosus and antiglomerular basement membrane antibody disease. Early immunosuppressive treatment is required, mostly with pulse methylprednisolone and cyclophosphamide. Plasmapheresis are added in antiglomerular basement membrane antibody disease and refractory systemic lupus erythematosus. Non immune mediated diffuse alveolar hemorrhages are mainly due to cardiac failure, severe dyscrasia and idiopathic diffuse alveolar hemorrhage. Barotrauma, cancer microangiopathy, toxic or drug-induced diffuse alveolar hemorrhage are other rare causes. Whatever is the cause, diffuse alveolar hemorrhage is an emergency associated with an intrahospital mortality rate of approximately 20 percent.

Mise au pointHémorragies alvéolaires en dehors des situations d’immunodépression : prise en charge diagnostique et thérapeutiqueDiffuse alveolar hemorrhage in the immunocompetent host: diagnostic and therapeutc management

Diffuse alveolar hemorrhage is a bleeding originating from the pulmonary acinus. Number of causes are possible, that can be divided in immune and non immune causes. Immune mediated diffuse alveolar hemorrhages are mainly due to small vessels vasculitis (Wegener granulomatosis, microscopic polyangiitis), systemic lupus erythematosus and antiglomerular basement membrane antibody disease. Early immunosuppressive treatment is required, mostly with pulse methylprednisolone and cyclophosphamide. Plasmapheresis are added in antiglomerular basement membrane antibody disease and refractory systemic lupus erythematosus. Non immune mediated diffuse alveolar hemorrhages are mainly due to cardiac failure, severe dyscrasia and idiopathic diffuse alveolar hemorrhage. Barotrauma, cancer microangiopathy, toxic or drug-induced diffuse alveolar hemorrhage are other rare causes. Whatever is the cause, diffuse alveolar hemorrhage is an emergency associated with an intrahospital mortality rate of approximately 20 percent.

High Emergency Lung Transplantation: dramatic decrease of waiting list death rate without relevant higher post-transplant mortality

Many candidates for lung transplantation (LT) die on the waiting list, raising the question of graft availability and strategy for organ allocation. We report the experience of the new organ allocation program, “High Emergency Lung Transplantation” (HELT), since its implementation in our center in 2007. Retrospective analysis of 201 lung transplant patients, of whom 37 received HELT from 1st July 2007 to 31th May 2012. HELT candidates had a higher impairment grade on respiratory status and higher Lung Allocation Score (LAS). HELT patients had increased incidence of perioperative complications (e.g., perioperative bleeding) and extracorporeal circulatory assistance (75% vs. 36.6%, P = 0.0005). No significant difference was observed between HELT and non‐HELT patients in mechanical ventilation duration (15.5 days vs. 11 days, P = 0.27), intensive care unit length of stay (15 days vs. 10 days, P = 0.22) or survival rate at 12 (81% vs. 80%), and 24 months post‐LT (72.9% vs. 75.0%). Lastly, mortality on the waiting list was spectacularly reduced from 19% to 2% when compared to the non‐HELT 2004–2007 group. Despite a more severe clinical status of patients on the waiting list, HELT provided similar results to conventional LT. These results were associated with a dramatic reduction in the mortality rate of patients on the waiting list.

Characteristics of Donor-Specific Antibodies Associated With Antibody-Mediated Rejection in Lung Transplantation

Although donor-specific anti-human leukocyte antigen (HLA) antibodies (DSAs) are frequently found in recipients after lung transplantation (LT), the characteristics of DSA which influence antibody-mediated rejection (AMR) in LT are not fully defined. We retrospectively analyzed 206 consecutive LT patients of our center (2010–2013). DSAs were detected by using luminex single antigen beads assay and mean fluorescence intensity was assessed. Within the study population, 105 patients had positive DSA. Patients with and without AMR (AMRPos, n = 22, and AMRNeg, n = 83, respectively) were compared. AMRPos patients had significantly greater frequencies of anti-HLA DQ DSA (DQ DSA) than AMRNeg patients (95 vs 58%, respectively, p < 0.0001). Compared to AMRNeg patients, AMRPos patients had higher DQ DSA sum MFI [7,332 (2,067–10,213) vs 681 (0–1,887), p < 0.0001]. DQ DSA when associated with AMR, had more frequent graft loss and chronic lung allograft dysfunction (CLAD). These data suggest (i) that DSA characteristics clearly differ between AMRPos and AMRNeg patients and (ii) the deleterious impact of DQ DSA on clinical outcome.