ECMO-dependent respiratory failure after snorting speed associated with anti-GBM antibodies.
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ABSTRACT:
SUBMITTER: De Rosa N
PROVIDER: S-EPMC4694606 | biostudies-other | 2015 Dec
REPOSITORIES: biostudies-other
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Project description:Death or hospital readmission are frequent among patients surviving acute hypercapnic respiratory failure (AHRF). Severity scores are not valid to predict death or readmission after AHRF. Gait speed, a simple functional parameter, has been associated with hospital admission and death in the general population. The purpose of this study is to highlight an association between gait speed at hospital discharge and death or readmission among AHRF survivors. Secondary analysis of a prospective cohort study. Single Swiss tertiary hospital, pulmonary division. Patients were prospectively recruited to form a cohort of patients surviving AHRF in the intensive care unit between January 2012 and May 2015. Gait speed was derived from a 6 min walking test (6MWT) before hospital discharge. All predictive variables were prospectively collected. Death or hospital readmission were recorded for 6 months. Univariate and multivariate analyses were performed to evaluate the association between predictive variables and death or hospital readmission. 71 patients performed a 6MWT. 34/71 (48%) patients died or were readmitted to the hospital during the observation period. Median gait speed was 0.7 (IQR 0.3-1.0) m/s. At 6 months, 66% (25/38) of slow walkers (gait speed <0.7 m/s) and 27% (9/33) of non-slow walkers died or were readmitted to the hospital (p=0.002). In univariate analysis, gait speed was associated with death or readmission (HR 0.41; 95% CI 0.19 to 0.90, p=0.025). In a multivariate model adjusted for age, gender, body mass index, forced expired volume, heart failure and home mechanical ventilation, gait speed remained the only variable associated with death or readmission (multivariate HR: 0.35; 95% CI 0.14 to 0.88, p=0.025). This study suggests that a simple functional parameter such as gait speed is associated with death or hospital readmission in patients surviving AHRF. NCT02111876.
| S-EPMC7304813 | biostudies-literature
Project description:BackgroundExtracorporeal membrane oxygenation (ECMO) is an important rescue therapy for patients with refractory respiratory or circulatory failure. High cost and associated complications warrant careful case selection. The aim of this study was to investigate the outcomes and factors associated with mortality in acute hypoxemic respiratory failure patients who received ECMO support, and to externally validate preexisting ECMO survival prediction scoring systems.MethodsThis retrospective study enrolled acute hypoxemic respiratory failure patients who received veno-venous (VV) or veno-arterial (VA) ECMO support at Siriraj Hospital (Bangkok, Thailand) from 2010 to 2020. All relevant baseline patient characteristics including ECMO survival prediction scores were recorded. The primary outcome was in-hospital mortality. Multivariate logistic regression analysis was employed to identify independent predictors of in-hospital mortality.ResultsOf a total of 65 patients, 34 (52%) were male, the median (IQR) age was 61 years (49-70 years), the median body mass index (BMI) was 22.6 kg/m2 (20.6-28 kg/m2), and the median Sequential Organ Failure Assessment (SOFA) score was 13 [11-16]. Forty-three patients (66%) received VV-ECMO, and 22 (34%) received VA-ECMO support. In-hospital mortality was 69%. Multivariate analysis identified a SOFA score >14, hospitalized >72 hours before ECMO initiation, PaO2/FiO2 ratio <60, and pH <7.2 as independent predictors of in-hospital mortality. These four parameters were combined to create the SHOP (S: SOFA >14, H: hospitalize >72 hours, O: PF ratio <60, and P: pH <7.2) score. Compared with three different preexisting ECMO survival prediction scoring systems, the SHOP score had the highest area under the curve (AUC) for predicting in-hospital mortality (overall: 0.873, VV-EMCO: 0.866, and VA-EMCO: 0.891).ConclusionsIn-hospital mortality among ECMO-supported patients was high at 69%. SOFA score >14, hospitalized >72 hours, PaO2/FiO2 ratio <60, and pH <7.2 were found to be independent predictors of in-hospital mortality. A SHOP score of 2 or higher significantly predicts in-hospital mortality in EMCO-supported patients.Trial registrationwww.clinicaltrials.gov (reg. No. NCT04031794).
| S-EPMC8902121 | biostudies-literature
Project description:BackgroundGlioblastoma (GBM) is a primary brain tumor with a 5-year survival rate of ≤5%. We have shown earlier that GBM-antibody-linked curcumin (CC) and also phytosomal curcumin (CCP) rescue 50-60% of GBM-bearing mice while repolarizing the tumor-associated microglia/macrophages (TAM) from the tumor-promoting M2-type to the tumoricidal M1-type. However, systemic application of CCP yields only sub-IC50 concentrations of CC in the plasma, which is unlikely to kill GBM cells directly. This study investigates the role of CC-evoked intra-GBM recruitment of activated natural killer (NK) cells in the elimination of GBM and GBM stem cells.MethodsWe have used an immune-competent syngeneic C57BL6 mouse model with the mouse-GBM GL261 cells orthotopically implanted in the brain. Using immunohistochemistry and flow cytometry, we have quantitatively analyzed the role of the intra-GBM-recruited NK cells by (i) injecting (i.p.) the NK1.1 antibody (NK1.1Ab) to temporarily eliminate the NK cells and (ii) blocking NK recruitment by injecting an IL12 antibody (IL12Ab). The treatment cohorts used randomly-chosen GL261-implanted mice and data sets were compared using two-tailed t-test or ANOVA.ResultsCCP treatment caused the GBM tumor to acquire M1-type macrophages (50-60% of the TAM) and activated NK cells. The treatment also elicited (a) suppression of the M2-linked tumor-promoting proteins STAT3, ARG1, and IL10, (b) induction of the M1-linked anti-tumor proteins STAT1 and inducible nitric oxide synthase in the TAM, (c) elimination of CD133(+) GBM stem cells, and (d) activation of caspase3 in the GBM cells. Eliminating intra-GBM NK cell recruitment caused a partial reversal of each of these effects. Concomitantly, we observed a CCP-evoked dramatic induction of the chemokine monocyte chemotactic protein-1 (MCP-1) in the TAM.ConclusionsThe recruited NK cells mediate a major part of the CCP-evoked elimination of GBM and GBM stem cells and stabilization of the TAM in the M1-like state. MCP-1 is known to activate peripheral M1-type macrophages to secrete IL12, an activator of NK cells. Based on such observations, we postulate that by binding to peripheral M1-type macrophages and IL12-activated NK cells, the brain-released chemokine MCP-1 causes recruitment of peripheral immune cells into the GBM, thereby causing destruction of the GBM cells and GBM stem cells.
| S-EPMC6058381 | biostudies-literature
Project description:Venous-arterial extracorporeal membrane oxygenation (VA-ECMO) treatment for acute cardiogenic shock in patients who also have acute lung injury predisposes development of a serious complication called "north-south syndrome" (NSS) which causes cerebral hypoxia. NSS is poorly characterized and hemodynamic studies have focused on cerebral perfusion ignoring the heart. We hypothesized in NSS the heart would be more likely to receive hypoxemic blood than the brain due to the proximity of the coronary arteries to the aortic annulus. To test this, we conducted a computational fluid dynamics simulation of blood flow in a human supported by VA-ECMO. Simulations quantified the fraction of blood at each aortic branching vessel originating from residual native cardiac output versus VA-ECMO. As residual cardiac function was increased, simulations demonstrated myocardial hypoxia would develop prior to cerebral hypoxia. These results illustrate the conditions where NSS will develop and the relative cardiac function that will lead to organ-specific hypoxia. Illustration of the impact of north-south syndrome on organ-specific oxygen delivery. Patients on VA-ECMO have two sources of blood flow, one from the VA-ECMO circuit and one from the residual cardiac function. When there is no residual cardiac function, all organs are perfused with oxygenated blood. As myocardial recovery progresses, blood supply from the two sources will begin to mix resulting in non-homogeneous mixing and differential oxygenation based upon the anatomical site of branching vessels.
| S-EPMC7901681 | biostudies-literature
Project description:In September 2010, a 75-year-old hepatitis B virus (HBV)-positive man was admitted to our hospital because of fever, persistent cough, general fatigue, and leg edema. The patient was a hepatitis B surface antigen carrier with detectable HBV DNA level. On admission, laboratory examination revealed severe inflammatory signs, decreased serum albumin, and renal insufficiency with proteinuria. The patient had rapidly progressive renal insufficiency without pulmonary involvement over the few days after admission. Renal biopsy showed membranous nephropathy (MN) with crescent formation. Further serological study revealed a high titer of anti-glomerular basement membrane (GBM) antibody, suggestive of anti-GBM glomerulonephritis superimposed on HBV-associated MN. For both preventing HBV reactivation during immunosuppressive therapy and treating HBV-associated MN, the administration of entecavir was immediately initiated, and then treatment with plasma exchange (PE) and intravenous methylprednisolone administration was performed. Both HBV DNA level and an anti-GBM titer became undetectable, and clinical remission of MN was subsequently achieved. This was a rare case of an elderly patient with anti-GBM glomerulonephritis superimposed on HBV-associated MN, who was successfully treated with PE, corticosteroid, and entecavir combination therapy.
| S-EPMC5411555 | biostudies-literature
Project description:BackgroundAutoantibodies are common in glomerulonephritis, but the clinical benefit of rapid elimination has not been determined, even in anti-glomerular basement membrane (GBM) disease. Even less is known about the importance of autoantibody characteristics, including epitope specificity and immunoglobulin G (IgG) subclass distribution. We aimed to address this by characterizing the autoantibody profile in anti-GBM patients: we utilized samples from the GOOD-IDES-01 (treating GOODpasture's disease with Imunoglobulin G Degrading Enzyme of Streptococcus pyogenous) (ClinicalTrials.gov identifier: NCT03157037) trial , where imlifidase, which cleaves all IgG in vivo within hours, was given to 15 anti-GBM patients.MethodsIn the GOOD-IDES-01 trial, plasmapheresis was (re)started if anti-GBM antibodies rebounded. Serum samples were collected prospectively for 6 months and analyzed for anti-GBM epitope specificity using recombinant constructs of the EA and EB epitopes, IgG subclass using monoclonal antibodies, and anti-neutrophil cytoplasmic antibodies (ANCA). The results were correlated with clinical data.ResultsPatients with a rebound (n = 10) tended to have lower eGFR at 6 months (11 vs 34 mL/min/1.73 m2, P = .055), and patients with dialysis at 6 months had a higher EB/EA ratio at rebound (0.8 vs 0.5, P = .047). Moreover, two patients demonstrated increasing epitope restriction and several patients displayed a shift in subclass distribution at rebound. Six patients were double positive for ANCA. ANCA rebound was seen in 50% of patients; only one patient remained ANCA positive at 6 months.ConclusionsIn this study, rebound of anti-GBM antibodies, especially if directed against the EB epitope, was associated with a worse outcome. This supports the notion that all means should be used to eliminate anti-GBM antibodies. In this study ANCA was removed early and long-term by imlifidase and cyclophosphamide.
| S-EPMC10730795 | biostudies-literature
Project description:Objective: Autoantibodies to the α3 chain noncollagen 1 domain of type IV collagen (α3(IV)NC1) are a serological hallmark in the diagnosis of anti-glomerular basement membrane (GBM) disease. The objective of our study was to compare the performance of anti-glomerular basement membrane (GBM) antibody detection by chemiluminescence immunoassay (CIA) and by enzyme-linked immunosorbent assays (ELISAs).Methods: Sera from outpatients who were suspected to have anti-GBM disease and 31 patients with biopsy-proven anti-GBM disease were collected. Thirty normal controls were also included. All samples were tested for anti-GBM antibodies by CIA and commercial ELISA. The anti-GBM antibody-positive samples were confirmed by a homemade ELISA coated with recombinant human α3(IV)NC1.Results: Compared with detection of anti-GBM antibodies with ELISA, detection of anti-GBM antibodies with CIA showed a positivity agreement of 70% and a negativity agreement of 98.6%. Among the 4 patients with different results, the anti-GBM antibody detection by CIA was in agreement with the homemade ELISA coated with recombinant human α3(IV)NC1 and the clinical diagnosis. In 31 patients with anti-GBM disease, good agreement was achieved in the detection of anti-GBM antibodies with CIA, commercial ELISA and the homemade ELISA (100%, 100%). The AUC for CIA and commercial ELISA was 0.987 and 0.966, respectively.Conclusions: The detection of anti-GBM antibodies with CIA demonstrated good sensitivity and specificity and was in good agreement with our homemade ELISA, which seems better than the commercial ELISA in suspected anti-GBM disease patients. The three assays performed in parallel in the diagnosis of anti-GBM disease patients.
| S-EPMC6968565 | biostudies-literature
Project description: Not available
| S-EPMC10644522 | biostudies-literature
Project description:RationalePatients with ventilator-dependent respiratory failure have improved outcomes at centers with greater expertise; yet, most patients are not treated in such facilities. Efforts to align care for respiratory failure and hospital capability would necessarily require interhospital transfer.ObjectivesTo characterize the prevalence and the patient and hospital factors associated with interhospital transfer of adults residing in Florida with ventilator-dependent respiratory failure.MethodsWe performed a retrospective, observational study using Florida Healthcare Cost and Utilization Project data. We selected patients 18 years of age and older with International Classification of Diseases, Ninth Revision, codes of respiratory failure and mechanical ventilation during 2012 and 2013, and we identified cohorts of patients that did and did not undergo interhospital transfer. We obtained patient sociodemographic and clinical variables and categorized hospitals into subtypes on the basis of patient volume and services provided: large, medium (nonprofit or for-profit), and small.ResultsInterhospital transfer was our primary outcome measure. Patient sociodemographics, clinical variables, and hospital types were used as covariates. We identified 2,580 patients with ventilator-dependent respiratory failure who underwent interhospital transfer. Overall, transfer was uncommon, with only 2.9% of patients being transferred. In a hierarchical model, age less than 65 years (odds ratio [OR], 2.09; 95% confidence interval [CI], 1.77-2.45) and tracheostomy (OR, 3.19; 95% CI, 2.80-3.65) were associated with higher odds of transfer, whereas having Medicaid was associated with lower odds of transfer than having commercial insurance (OR, 0.65; 95% CI, 0.56-0.75). Additionally, care in medium-sized for-profit hospitals was associated with lower odds of transfer (OR, 1.37 vs. 2.70) than care in medium nonprofit hospitals, despite similar hospital characteristics.ConclusionsIn Florida, interhospital transfer of patients with ventilator-dependent respiratory failure is uncommon and more likely among younger, commercially insured, medically resource-intensive patients. For-profit hospitals are less likely to transfer than nonprofit hospitals. In future studies, researchers should test for geographic variations and examine the clinical implications of selectivity in interhospital transfer of patients with ventilator-dependent respiratory failure.
| S-EPMC5427742 | biostudies-literature
Project description:Background Complement-fixing antibodies against donor HLA are considered a contraindication for kidney transplant. A modification of the IgG single-antigen bead (SAB) assay allows detection of anti-HLA antibodies that bind C3d. Because early humoral graft rejection is considered to be complement mediated, this SAB-based technique may provide a valuable tool in the pretransplant risk stratification of kidney transplant recipients.Methods Previously, we established that pretransplant donor-specific anti-HLA antibodies (DSAs) are associated with increased risk for long-term graft failure in complement-dependent cytotoxicity crossmatch-negative transplants. In this study, we further characterized the DSA-positive serum samples using the C3d SAB assay.Results Among 567 pretransplant DSA-positive serum samples, 97 (17%) contained at least one C3d-fixing DSA, whereas 470 (83%) had non-C3d-fixing DSA. At 10 years after transplant, patients with C3d-fixing antibodies had a death-censored, covariate-adjusted graft survival of 60%, whereas patients with non-C3d-fixing DSA had a graft survival of 64% (hazard ratio, 1.02; 95% confidence interval, 0.70 to 1.48 for C3d-fixing DSA compared with non-C3d-fixing DSA; P=0.93). Patients without DSA had a 10-year graft survival of 78%.Conclusions The C3d-fixing ability of pretransplant DSA is not associated with increased risk for graft failure.
| S-EPMC6115667 | biostudies-literature