Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0476273 (respiratory distress)
 19,632 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 42-year-old, African-American man presented with a 2-month history of weight loss and fever for 2 weeks. Presumptive diagnoses of human immunodeficiency virus infection (HIV) and acquired immunodeficiency syndrome were made on the basis of a CD4 lymphocyte count of 23 lymphocytes/mL. Chest x-ray revealed right paratracheal adenopathy and a miliary pattern. The etiology of the patient's pulmonary infection was not known, but tuberculosis was an important consideration. Over 5 days, the pulmonary infection progressed and was complicated by acute respiratory distress syndrome (ARDS), septic shock, and death, despite vigorous antibiotic and supportive therapy. Serologic tests for HIV infection were reported as positive after the patient's demise. The etiology of the patient's pulmonary infection, ARDS, and sepsis was not known until autopsy study revealed enumerable yeast-like cells of Blastomyces dermatitidis in the extensively consolidated lungs and in disseminated foci of infection in most other major organs. Diffuse alveolar damage was closely associated with the pulmonary blastomycosis. Electron microscopic study of the yeast-like cells of B. dermatitidis in the autopsy lung obtained and fixed 5 days after the patient's death revealed excellent preservation of viable organisms.
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PMID:Disseminated blastomycosis and acquired immunodeficiency syndrome: a case report and ultrastructural study. 888 26

Initial trials of partial liquid ventilation (PLV), which is gas ventilation of perfluorocarbon-filled lungs, are underway in patients with severe respiratory failure. We report the first study of the effects of the perfluorocarbon, perflubron, on the lung. Necropsies were conducted in nine patients (seven adults and two neonates; mean adult age, 31 +/- 5 yr) managed with PLV (average number of doses, 4 +/- 1). All of the patients required extracorporeal life support. The patients had pneumonia with the acute respiratory distress syndrome (six patients), trauma/capillary leak syndrome (one patient), congenital diaphragmatic hernia (one patient), and primary pulmonary hypertension (one patient). Nine adult patients (mean age, 37 +/- 5 yr) with acute respiratory distress syndrome requiring extracorporeal life support served as a control. Pathologic findings were evaluated in both groups. Lung weights in the adult patients of both groups were elevated (mean weight of PLV-treated right lung, 1401 +/- 186 g; mean weight of PLV-treated left lung, 1131 +/- 177 g; mean weight of control right lung, 1018 +/- 91 g; mean weight of control left lung, 988 +/- 80 g). There was no significant difference between the two groups (right lung, P = .066; left lung, P = .436). Frequent gross findings included focal consolidation, patchy hemorrhage, and glassy cut surfaces. The histologic findings were similar in both groups. Diffuse alveolar damage (either proliferative phase or mixed proliferative and exudative phases) was seen in all nine of the study patients. Eight of the nine control patients had diffuse alveolar damage (five had proliferative phase only, one had mixed proliferative and exudative phases, and two had exudative phase only). One other patient had extensive parenchymal necrosis. Other frequent findings were intra-alveolar hemorrhage, numerous intra-alveolar macrophages, and organization of exudate. PLV with perflubron in patients with adult and neonatal respiratory distress syndromes is not associated with unique pathologic findings in the human lung.
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PMID:Pulmonary pathology of patients treated with partial liquid ventilation. 916 Mar 11

Diffuse alveolar damage (DAD) is a relatively nonspecific pattern of acute lung injury that can be observed in a wide range of clinical circumstances. DAD has often been recognized in association with various connective tissue diseases; however, to our knowledge, it has not been previously reported in the setting of progressive systemic sclerosis. Herein we describe two patients with established diagnoses of progressive systemic sclerosis who had development of the acute respiratory distress syndrome. Open-lung biopsy specimens from both patients showed a histologic pattern of DAD with no identifiable cause other than their progressive systemic sclerosis. Our results suggest that DAD should be added to the list of pleuropulmonary complications of progressive systemic sclerosis.
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PMID:Organizing diffuse alveolar damage associated with progressive systemic sclerosis. 921 65

Diffuse alveolar damage is the histopathological hallmark of acute respiratory distress syndrome (ARDS) and is a stereotypic response to a variety of etiologies. Moreover, a significant proportion of ARDS survivors have residual pulmonary fibrosis and compromised pulmonary function. This suggests that the pathogenesis of diffuse alveolar damage that ultimately leads to the chronic fibrosis of ARDS has features of dysregulated repair exemplified by exaggerated intra-alveolar angiogenesis and fibrogenesis (i.e., fibroproliferation and deposition of extracellular matrix), leading to progressive alveolar fibrosis and impaired lung function. We obtained bronchoalveolar lavage fluid (BALF) from patients with ARDS or ventilated control patients and assessed CXC chemokine levels by ELISA. We found an imbalance in the expression of ELR(+) as compared with ELR(-) CXC chemokines from BALF of patients with ARDS as compared with controls. This imbalance correlated with angiogenic activity as assessed by the corneal micropocket assay. Furthermore, these levels correlated with both procollagen I and procollagen III levels in BALF. In contrast, while BALF levels of vascular endothelial growth factor were elevated, vascular endothelial growth factor did not appear to be significantly contributing to the angiogenic activity. These findings suggest that CXC chemokines have an important role in the fibroproliferative phase of ARDS via the regulation of angiogenesis.
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PMID:Imbalance in the expression of CXC chemokines correlates with bronchoalveolar lavage fluid angiogenic activity and procollagen levels in acute respiratory distress syndrome. 1244 62

Diffuse alveolar damage is the histopathologic hallmark of acute respiratory distress syndrome (ARDS). A significant proportion of ARDS survivors have residual pulmonary fibrosis and compromised pulmonary function. On the other hand, heat shock protein 47 (HSP47) is a collagen-binding stress protein that is assumed to act as a collagen-specific molecular chaperone during the biosynthesis and secretion of procollagen in living cells. The synthesis of HSP47 has been reported to correlate with that of collagen in several cell lines. We examined the expression of HSP47 mRNA and protein during the progression of lipopolysaccharide (LPS)-induced ARDS in rat lung. Male Wistar rats were randomly divided into two groups: a control group with instillation of 0.9% NaCl solution alone, and a LPS group with instillation of LPS dissolved in 0.9% NaCl solution (10 mg/kg). Histologic changes thereafter appeared in the LPS-treated rats. Northern blot analysis revealed the expression of HSP47 mRNA to be markedly induced during the progression of lung damage in parallel with type I and type III collagen mRNA. These results suggest that the upregulation of HSP47 and collagen may play an important role in the fibrotic process of LPS-induced ARDS lung.
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PMID:Coexpression of HSP47 gene and type I and type III collagen genes in LPS-induced pulmonary fibrosis in rats. 2598 May 92

Diffuse alveolar damage represents the pathologic basis of most cases of the acute respiratory distress syndrome. Diffuse alveolar damage reflects injury to the pulmonary alveolar wall and microvasculature, leading to the exudation of water and plasma proteins that can overwhelm the local lymphatic drainage. Organizing pneumonia is a prominent histopathologic feature in some cases of diffuse alveolar damage. We examined whether diffuse alveolar damage-organizing pneumonia and changes in lymphatic architecture might be indicators of clinical outcome in acute respiratory distress syndrome. Formalin-fixed lung sections (n = 26) from thoracoscopic lung biopsies of patients with diffuse alveolar damage in the fibroproliferative phase, with or without organizing pneumonia, were immunostained with anti-CD31 and anti-D240, markers of vascular and lymphatic endothelium, respectively, and examined by morphometric analysis. Positively staining vessels were enumerated and maximal luminal diameters recorded in randomly selected low-power fields. Patients with diffuse alveolar damage-organizing pneumonia showed greater survival than those with diffuse alveolar damage (67% versus 33%, P = .03). The maximal luminal diameter of D240+ lymphatic vessels was larger for diffuse alveolar damage-organizing pneumonia than diffuse alveolar damage (28 +/- 4 versus 59 +/- 16 microm, P = .02). In addition, larger lymphatic luminal diameters (28 +/- 4 versus 47 +/- 11 microm) were associated with increased survival (P = .12). We conclude that lung biopsy histopathology and pulmonary lymphatic morphology may predict survival in acute respiratory distress syndrome.
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PMID:Organizing pneumonia and pulmonary lymphatic architecture in diffuse alveolar damage. 1860 71

A 62-year-old man, treated with corticosteroids and immunosuppressants for rheumatoid arthritis, visited hospital with high fever and dyspnea on exertion. A CT scan of the chest demonstrated bilateral diffuse ground glass opacities. On the basis of the findings of the CT scan, he was initially given a diagnosis of interstitial pneumonia. He was then referred to our hospital and admitted to the intensive care unit (ICU), where because of progressive respiratory failure, he was put on mechanical ventilation. A bronchoscopy specimen after intubation turned out to be positive for acid-fast bacilli, which were confirmed to be mycobacterium tuberculosis by a polymerase chain reaction test. He was given a diagnosis of miliary tuberculosis complicated with acute respiratory distress syndrome (ARDS). He died of respiratory failure despite treatment with antituberculosis drugs. The autopsy revealed necrotizing epithelioid granulomas in both lungs, mediastinal lymph nodes, the liver, both kidneys, vertebrae and other organs. Diffuse alveolar damage was also found in both lungs. It is often difficult to detect disseminated nodules in the miliary tuberculosis with ARDS. Miliary tuberculosis should be suspected in patients in an immunosuppressant state with rheumatoid arthritis, and who have respiratory symptoms or fever of unknown origin.
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PMID:[A case of miliary tuberculosis showing acute respiratory distress syndrome in rheumatoid arthritis]. 2038 30

Diffuse alveolar damage (DAD) is the underlying pathological finding in most cases of acute respiratory distress syndrome (ARDS). The objective of this study was to compare clinical criteria for ARDS secondary to community acquired pneumonia with autopsy findings of DAD and to determine the discrepancy rate between the two. We compared prospectively obtained clinical diagnosis of ARDS secondary to community acquired pneumonia with autopsy findings of DAD and pneumonia. Forty nine patients dead with a clinical diagnosis of ARDS secondary to pneumonia who underwent autopsy between 1986 and 2004 in our ICU were included with systematic histopathological analysis of all lung lobes. The discrepancy rate between the premortem clinical diagnosis of ARDS secondary to pneumonia and DAD at autopsy was determined. Seven patients were found to have neither infection nor DAD at autopsy. Six patients showed pathologic signs of DAD without evidence of infection. Out of 38 patients meeting clinical criteria for ARDS secondary to pneumonia and proven pneumonia at autopsy, 25 met criteria for DAD at autopsy. Therefore, 18 out of 49 patients who were clinically diagnosed with ARDS did not actually show pathological signs of DAD, resulting in a discrepancy rate of 37%. Despite an acceptable correspondence between clinical criteria for ARDS secondary to pneumonia and autopsy findings of DAD a significant number of patients had neither signs of DAD nor infection.
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PMID:Discrepancy between clinical criteria for diagnosing acute respiratory distress syndrome secondary to community acquired pneumonia with autopsy findings of diffuse alveolar damage. 2157 Feb 73

Diffuse alveolar damage (DAD) is the pathologic feature of rapidly progressive lung diseases, including acute respiratory distress syndrome, acute interstitial pneumonia, and acute exacerbation of idiopathic pulmonary fibrosis. The clinical significance and limitation of high-resolution computed tomography (HRCT) findings in these diseases were reviewed. The HRCT findings correlate well with pathologic phases (exudative, proliferative, and fibrotic) of DAD, although it cannot detect early exudative phase. Traction bronchiolectasis or bronchiectasis within areas of increased attenuation on HRCT scan is a sign of progression from the exudative to the proliferative and fibrotic phase of DAD. Extensive abnormalities seen on HRCT scans, which are indicative of fibroproliferative changes, were independently predictive of poor prognosis in patients with clinically early acute respiratory distress syndrome, acute interstitial pneumonia, and acute exacerbation of idiopathic pulmonary fibrosis.
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PMID:High-resolution computed tomography findings of acute respiratory distress syndrome, acute interstitial pneumonia, and acute exacerbation of idiopathic pulmonary fibrosis. 2448 Jan 42

Kao et al. have reported in Critical Care the histological findings of 101 patients with acute respiratory distress syndrome (ARDS) undergoing open lung biopsy. Diffuse alveolar damage (DAD), the histological hallmark of ARDS, was present in only 56.4% of cases. The presence of DAD was associated with higher mortality. Evidence from this and other studies indicates that the clinical criteria for the diagnosis of ARDS identify DAD in only about half of the cases. On the contrary, there is evidence that the clinical course and outcome of ARDS differs in patients with DAD and in patients without DAD. The discovery of biomarkers for the physiological (increased alveolocapillary permeability) or histological (DAD) hallmarks of ARDS is thus of paramount importance.
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PMID:Acute respiratory distress syndrome: does histology matter? 2598 98


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