Why walking by a main road is as bad for you as smoking
William Phin, six, from Whitley Bay, north of Newcastle, has obliterative bronchiolitis - which may be triggered by pollution. A lung transplant is the only cure.
Long-term outcomes after lung transplantation (LTx) remain inferior to other solid organs such as heart transplantation. This is largely a result of a high prevalence of chronic lung allograft dysfunction (CLAD), affecting approximately 50% of transplanted patients at 5 years post-transplant.1 Although Bronchiolitis Obliterans Syndrome (BOS) is the major clinical phenotype of CLAD (occurring in 70% of CLAD patients), Restrictive Allograft Syndrome (RAS), the other CLAD phenotype (30%), has a worse survival following diagnosis.
Chronic lung allograft dysfunction (CLAD) is the principal obstacle to improved long-term survival after lung transplantation.1 CLAD is a condition of sustained lung function impairment recognized by a persistent decline in the forced expiratory volume in one second (FEV1) relative to the highest posttransplant baseline after exclusion of confounding conditions.2,3 Previously bronchiolitis obliterans syndrome (BOS) was the most widely described CLAD phenotype; however, accumulating evidence suggests CLAD takes on at least two phenotypes conferring distinct prognoses.
In this report, 3 transbronchial biopsies showed viral inclusions on histologic examination and were evaluated for anti-SV40 large T antigen (SV40 T Ag) by immunohistochemistry (IHC), in situ hybridization, and viral genome sequencing by polymerase chain reaction. Patients 1 and 2 were immunosuppressed lung transplant recipients. Patient 1 presented with diffuse pruritic rash and respiratory failure, and patient 2 with PyV viremia. Patient 3 had chronic lymphocytic leukemia/small lymphocytic lymphoma and presented with cough and shortness of breath. Histologic examination of all 3 lung biopsies were similar and revealed pr...
This study investigated whether changes in serum KL-6 levels over time were associated with CLAD. Twenty-one lung transplant recipients had serum KL-6 measured (NANOPIA®) at baseline and after 7 years. Changes in serum KL-6 levels from baseline were determined. Receiver operating characteristic curves and Kaplan-Meier analysis were used to test the predictive value of changes in serum KL-6 over time. The average increase in KL-6 in patients with CLAD was 15% versus a 28% decrease in non-CLAD patients (p = .042). An 11% decrease in serum KL-6 level was determined as the best cut-off value to be associated with the...
CONCLUSIONS Everolimus might be beneficial in heart and lung transplant patients with leukopenia or neutropenia and lead to modest, short-term renal function improvement. Patient selection is crucial because adverse effects frequently lead to everolimus discontinuation. PMID: 30348935 [PubMed - in process]
This article is protected by copyright. All rights reserved. PMID: 30303525 [PubMed - as supplied by publisher]
AbstractPurpose of ReviewSynthesize recent developments in the understanding of chronic lung allograft dysfunction (CLAD) epidemiology, pathophysiology, outcomes, and treatments with a focus on the classification of CLAD into restrictive allograft syndrome (RAS) and from bronchiolitis obliterans syndrome (BOS).Recent FindingsChronic lung allograft dysfunction (CLAD) remains the leading cause of long-term morbidity and mortality in lung transplant recipients. Despite the lack of progress on improving outcomes, significant progress has been made in better characterizing the disease ’s clinical and pathologic diversity....
Lung transplant (LTx) recipients have low long-term survival and a high incidence of bronchiolitis obliterans syndrome (BOS). However, few long-term, multicenter, and precise estimates of BOS-free survival (a composite outcome of death or BOS) incidence exist.
Lung transplantation (LTx) recipients have 1-, 5-, and 10-year unadjusted survival rates of 80%, 54%, and 32%, respectively.1 Chronic lung allograft dysfunction (CLAD) causes most deaths after the first post-transplant year,1 –3 and most CLAD has an obstructive phenotype known as bronchiolitis obliterans syndrome (BOS).4 Obliterative bronchiolitis (OB), the histologic hallmark of BOS, consists of a fibrotic luminal obliteration of the respiratory and terminal bronchioles.5 The patchy nature of OB reduces the diagnostic sensitivity of transbronchial lung biopsies.
Pulmonary compromise has been shown to significantly contribute to nonrelapse mortality after hematopoietic stem cell transplantation (HSCT) [1-4]. The etiology of these pulmonary complications includes intrapulmonary causes of fibrosis and toxicities from treatment regimens or infections (ie, restrictive lung disease), graft-versus-host disease (GVHD) or bronchiolitis obliterans syndrome (BOS) (ie, obstructive lung disease), and vascular abnormalities (eg, pulmonary hypertension), as well as extrapulmonary causes, such as weakness or sclerodermatous GVHD.