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Diffuse Alveolar Damage (diffuse + alveolar_damage)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Diffuse alveolar damage in idiopathic pulmonary fibrosis: Does aetiology matter?

RESPIROLOGY, Issue 6 2010
Tamera J. Corte
No abstract is available for this article. [source]

The spectrum of pathological changes in severe acute respiratory syndrome (SARS)

HISTOPATHOLOGY, Issue 2 2004
O Y Cheung
Aims:, To analyse the lung pathology of severe acute respiratory syndrome (SARS) and correlate the findings with the time sequence of the disease. Methods and results:, Ten patients with a clinical diagnosis of SARS, and virological confirmation of SARS coronavirus infection were identified. Histology in most cases showed diffuse alveolar damage, from early to late phases, and the changes corresponded to the time sequence. Other variable features include multinucleated giant cells, pneumocytes with cytomegaly and variable amounts of inflammatory cells and foamy macrophages. One case showed superimposed bronchopneumonia. No viral inclusions were found. Coronavirus particles were identified in pneumocytes by electron microscopy. Conclusions:, The predominant pathological process of SARS is diffuse alveolar damage and, in patients who die from the disease, there is evidence of organization and fibrosis. There are apparently no histological features specific for this disease, and the aetiological diagnosis depends on virological and ultrastructural studies. [source]

Non-specific interstitial pneumonia as a manifestation of graft-versus-host disease following pediatric allogeneic hematopoietic stem cell transplantation

PATHOLOGY INTERNATIONAL, Issue 2 2010
Aya Miyagawa-Hayashino
Bronchiolitis obliterans (BO) is generally believed to be a marker of pulmonary manifestation of graft-versus-host disease (GVHD) in patients who have undergone bone marrow transplantation for hematological malignancy. Pulmonary manifestations reported as GVHD (other than BO) include lymphocytic bronchiolitis with cellular interstitial pneumonia, lymphoid interstitial pneumonia, veno-occlusive disease, and diffuse alveolar damage. Morphological reactions in the lungs of bone marrow transplant recipients associated with interstitial pneumonia have not been described systematically. Reported herein is a fibrosing non-specific interstitial pneumonia (NSIP) pattern together with BO in both lungs in an 8-year-old girl following a second allogeneic hematopoietic stem cell transplantation for relapsed neuroblastoma of adrenal origin. The course was complicated by bilateral pneumothoraces, and the patient underwent lung transplantation 3 years after the second stem cell transplantation. Because the patient had chronic GVHD of the skin and the liver preceeded by the development of pulmonary involvement, NSIP may represent one of the facets of pulmonary GVHD. [source]

Prognostic factors in rapidly progressive interstitial pneumonia

RESPIROLOGY, Issue 2 2010
Yasuhiro KONDOH
ABSTRACT Background and objective: The aim of the present study was to examine clinical and other features that might allow prognostic distinctions between histological patterns in presentations with rapidly progressive interstitial pneumonia (RPIP), and to assess prognostic factors for survival. Methods: Patients with RPIP among 425 consecutive patients with diffuse lung disease, who underwent surgical lung biopsy, were studied retrospectively. The discriminatory value of clinical and investigative features for identifying disease with a better outcome was evaluated. An a priori comparison was made between diffuse alveolar damage (DAD)/usual interstitial pneumonia with DAD pattern (Group A), and organizing pneumonia/non-specific interstitial pneumonia pattern (Group B). Results: Twenty-eight patients (6.6%) fulfilled the criteria for RPIP. The diagnosis was Group A disease in 15 (DAD in 10, usual interstitial pneumonia with DAD in 5), and Group B disease in 13 (organizing pneumonia in 8, non-specific interstitial pneumonia in 5). There were no significant differences in initial findings between the groups. Prognosis was significantly better for Group B patients than for Group A patients (P = 0.021). Neither BAL nor parenchymal high-resolution CT score was indicative of therapeutic responsiveness or outcome. Distinction between Group A and Group B on the basis of disease pattern was the only significant determinant of prognosis. Conclusions: RPIP included varied histological patterns with different outcomes, and in many cases these could not be predicted using baseline clinical data. Histology was the only significant predictor of ultimate prognosis. [source]

SARS: clinical virology and pathogenesis

RESPIROLOGY, Issue 2003
John NICHOLLS
Severe acute respiratory syndrome (SARS) is caused by a novel coronavirus, called the SARS coronavirus (SARS-CoV). Over 95% of well characterized cohorts of SARS have evidence of recent SARS-CoV infection. The genome of SARS-CoV has been sequenced and it is not related to any of the previously known human or animal coronaviruses. It is probable that SARS-CoV was an animal virus that adapted to human-human transmission in the recent past. The virus can be found in nasopharyngeal aspirate, urine and stools of SARS patients. Second generation reverse transcriptase polymerase chain reaction assays are able to detect SARS-CoV in nasopharyngeal aspirates of approximately 80% of patients with SARS within the first 3 days of illness. Seroconversion for SARS-CoV using immunofluorescence on infected cells is an excellent method of confirming the diagnosis, but antibody responses only appear around day 10 of the illness. Within the first 10 days the histological picture is that of acute phase diffuse alveolar damage (DAD) with a mixture of inflammatory infiltrate, oedema and hyaline membrane formation. Desquamation of pneumocytes is prominent and consistent. After 10 days of illness the picture changes to one of organizing DAD with increased fibrosis, squamous metaplasia and multinucleated giant cells. The role of cytokines in the pathogenesis of SARS is still unclear. [source]

Characterization and peripheral blood biomarker assessment of anti,Jo-1 antibody,positive interstitial lung disease

ARTHRITIS & RHEUMATISM, Issue 7 2009
Thomas J. Richards
Objective Using a combination of clinical, radiographic, functional, and serum protein biomarker assessments, this study was aimed at defining the prevalence and clinical characteristics of interstitial lung disease (ILD) in a large cohort of patients with anti,Jo-1 antibodies. Methods A review of clinical records, pulmonary function test results, and findings on imaging studies determined the existence of ILD in anti,Jo-1 antibody,positive individuals whose data were accumulated in the University of Pittsburgh Myositis Database from 1982 to 2007. Multiplex enzyme-linked immunosorbent assays (ELISAs) for serum inflammation markers, cytokines, chemokines, and matrix metalloproteinases in different patient subgroups were performed to assess the serum proteins associated with anti,Jo-1 antibody,positive ILD. Results Among the 90 anti,Jo-1 antibody,positive individuals with sufficient clinical, radiographic, and/or pulmonary function data, 77 (86%) met the criteria for ILD. While computed tomography scans revealed a variety of patterns suggestive of underlying usual interstitial pneumonia (UIP) or nonspecific interstitial pneumonia, a review of the histopathologic abnormalities in a subset of patients undergoing open lung biopsy or transplantation or whose lung tissue was obtained at autopsy (n = 22) demonstrated a preponderance of UIP and diffuse alveolar damage. Analysis by multiplex ELISA yielded statistically significant associations between anti,Jo-1 antibody,positive ILD and elevated serum levels of C-reactive protein (CRP), CXCL9, and CXCL10, which distinguished this disease entity from idiopathic pulmonary fibrosis and anti,signal recognition particle antibody,positive myositis. Recursive partitioning further demonstrated that combinations of these and other serum protein biomarkers can distinguish these disease subgroups at high levels of sensitivity and specificity. Conclusion In this large cohort of anti,Jo-1 antibody,positive individuals, the incidence of ILD approached 90%. Multiplex ELISA demonstrated disease-specific associations between anti,Jo-1 antibody,positive ILD and serum levels of CRP as well as the interferon-,,inducible chemokines CXCL9 and CXCL10, highlighting the potential of this approach to define biologically active molecules contributing to the pathogenesis of myositis-associated ILD. [source]