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Query: UMLS:C0206061 (interstitial pneumonia)
 6,105 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied lungs at autopsy from 40 patients with cystic fibrosis (CF) to determine the structural and clinicopathologic features of pneumonia associated with Pseudomonas cepacia respiratory tract colonization. Three clinical groups were identified: group A included 11 patients exhibiting a fulminant course following P cepacia colonization; group B included 20 patients who declined slowly following colonization; and group C included nine patients without P cepacia colonization. Acute pneumonia occurred in all groups but was most extensive and necrotizing in group A. Chronic lobular pneumonia involved all groups equally, whereas interstitial pneumonia predominated in group B. Diffuse alveolar damage occurred infrequently in all groups. Combinations of structural patterns were frequently seen. We conclude that, although there is great overlap in the structural appearance of pneumonia among patients with CF with different bacterial colonization histories, the evidence suggests that P cepacia is a cause of necrotizing pneumonia in some patients. Factors that predispose to this fulminant lung infection are poorly understood.
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PMID:Pseudomonas cepacia-associated pneumonia in cystic fibrosis. Relation of clinical features to histopathologic patterns of pneumonia. 333 28

During a 4.4-year period, nonspecific interstitial pneumonitis was seen in 41 of 110 (38%) patients with the acquired immunodeficiency syndrome and accounted for 32% (48/152) of all episodes of clinical pneumonitis. Diffuse alveolar damage was typically a feature of nonspecific interstitial pneumonitis, but neither lung biopsy nor bronchoalveolar lavage detected a pathogen. Of these 41 patients, 13 had no associated pulmonary tumor and had not been exposed to pulmonary toxins, whereas 28 patients had either concurrent pulmonary Kaposi sarcoma, previous experimental therapies, or a history of pneumocystis pneumonia or drug abuse. Of these 41, 23 had normal chest radiographs. The clinical features of patients with nonspecific interstitial pneumonitis were similar to those of patients with pneumocystis pneumonia, although histologic findings showed less severe alveolar damage in patients with nonspecific interstitial pneumonitis (p less than 0.001). Pathologic evaluation and clinical follow-up suggest that many clinical episodes of pneumonitis in patients with the acquired immunodeficiency syndrome are due to nonspecific interstitial pneumonitis of unknown cause.
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PMID:Nonspecific interstitial pneumonitis: a common cause of pulmonary disease in the acquired immunodeficiency syndrome. 349 30

The concomitant treatment of hamsters with bleomycin and hyperoxia results in a synergistic development of pulmonary injury. We exposed hamsters for 72 hr to 70% oxygen following a single intratracheal instillation of bleomycin (0.16 U/100 g body weight). Groups of 10 animals were killed at 3, 6, 10, 30, 60, 90, and 120 days after instillation for histopathologic and morphometric assessment. Diffuse alveolar damage developed acutely. At 30 days, the intense acute cellular infiltrate had subsided, leaving a focal interstitial pneumonitis. Morphometric quantitation at 10 days revealed that 33.5 +/- 5.3% (x +/- SE) of the lung was diseased; there was apparent healing by 30 days, when 10.5 +/- 2.0% of the lung was diseased. However, progression to diffuse pneumonitis with fibrosis was seen at 60, 90, and 120 days, when 30.2 +/- 4.9%, 38.5 +/- 5.8%, and 38.8 +/- 4.5% of the lung was diseased, respectively. In vivo pulmonary function studies on treated animals at 25 and 55 days showed decreasing dynamic compliance and increased minute ventilation, which corroborates the presence of interstitial fibrosis. We conclude that simultaneous treatment of hamsters with bleomycin and hyperoxia results in interstitial fibrosis with a distribution and progression that mimics human pulmonary fibrosis. This model appears ideally suited for the study of progressive fibrosis and will be useful when development of a widely distributed lesion is crucial.
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PMID:Progressive pulmonary fibrosis in hamsters. 619 99

Polyarteritis nodosa (PAN) is characterized by necrotizing arteritis of medium-sized and small arteries in various organs. Pulmonary artery involvement in PAN has been considered rare. Previously, it also has been thought that patients with PAN do not have interstitial pneumonitis and fibrosis. A detailed pathologic analysis of pulmonary diseases associated with PAN was made in 10 autopsy cases of PAN. Arteritis affecting bronchial arteries was present in seven patients (70%). The data obtained suggest that arteritis in the lung in patients with PAN is more common than has been recognized previously. Diffuse alveolar damage (DAD) involving all lobes bilaterally was present in five patients; it was acute in two patients and organizing in three. In the patients with organizing DAD the degree of fibrosis in the interstitium differed among the lobes, and the fibrosis was more severe in the lower lobe than in the other lobes. Two patients presented with interstitial fibrosis with honeycomb lung of the posterior and lateral basal segments of the lower lobes of both lungs; in one of these patients interstitial fibrosis was present in an area of organizing DAD. Five patients died of respiratory failure resulting from DAD. In conclusion, it is important to consider DAD and interstitial fibrosis as complications of PAN.
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PMID:The lung in polyarteritis nodosa: a pathologic study of 10 cases. 810 May 52

Diffuse alveolar damage (DAD) and acute interstitial pneumonitis (AIP) often present clinically as the adult respiratory distress syndrome. To evaluate the usefulness of histochemical techniques and to better understand the histopathologic changes of these diffuse lung injuries, postmortem lung sections of 14 and 33 patients who had been diagnosed as having DAD in organizing stage and AIP, respectively, were studied with the use of lectins and monoclonal antibodies against surfactant apoprotein (PE-10) and collagen type IV. On hematoxylin-eosin stained sections, type II pneumocyte hyperplasia and hyaline membrane formation were the major histopathologic findings in both DAD and AIP. The binding rates of type II pneumocytes to Ulex europaeus agglutinin I (UEA-I) in both DAD (64%) and AIP (45%) cases were significantly higher than those of type I pneumocytes or alveolar macrophages (both P < 0.001). Reactions of type II pneumocytes to PE-10 varied from 40 to 44% in DAD and 0 to 100% in AIP cases depending on the use of respirator and steroid medication. Therefore, it may be said that UEA-I and PE-10 are useful methods for outlining hyperplastic type II pneumocytes in both DAD and AIP. Hyaline membrane coating alveolar septal surfaces and exudate in alveolar air spaces were also stainable with PE-10. Surfactant apoprotein remained demonstrable histochemically within type II pneumocytes and hyaline membrane despite severe inflammatory injuries of the lungs. The immunohistochemical stain using anti-collagen type IV antibody revealed discontinuous alveolar basement membrane in 50% of DAD patients with respirator use and 80% of AIP patients with steroid medication.
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PMID:Diffuse alveolar damage and acute interstitial pneumonitis: histochemical evaluation with lectins and monoclonal antibodies against surfactant apoprotein and collagen type IV. 834 71

We described a 65-year-old woman who died of acute interstitial pneumonia associated with dermatomyositis. Subcutaneous emphysema and pneumomediastinum simultaneously developed. The association of the pulmonary rupture with vasculitis has been assumed as the common cause in interstitial pneumonia. Diffuse alveolar damage, however, might have led to the pneumomediastinum and subcutaneous emphysema in our patient, who had no signs of cutaneous vasculitis.
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PMID:Pneumomediastinum and subcutaneous emphysema associated with fatal interstitial pneumonia in dermatomyositis. 926 11

Secondary interstitial pneumonia (SIP), a disease affecting patients immunocompromised by primary underlying diseases during their treatment in hospital, is frequently associated with cytomegalovirus (CMV) infection, a potentially treatable condition. However, in many cases, no infectious agent can be determined, and this clinical disease rapidly progresses to death. Theoretically, SIP could be caused by CMV, which may be present in such small amounts or such configuration that routine histopathological analysis or viral culture techniques cannot detect the virus. To test the hypothesis that immunohistochemistry (IH) and in situ detection by hybridization (ISH) provides more accurate results than the mere histological demonstration of CMV inclusions, these methods were applied to 37 autopsied lung sections obtained from children immunocompromised by primary underlying diseases and who died of SIP. As a result, the cases were subdivided into three groups: (1) children with SIP CMV inclusions (Diffuse alveolar damage-DAD-related) (n = 7); (2) children with SIP without classical viral inclusions (CMV-DAD-related) (n = 3); (3) children with SIP exhibiting nuclear cytopathic effect (not CMV-NSIP-related) (n = 27). In the first group, all three techniques yielded clearly positive results, whereas IH and ISH indicated that three of the children of the second group had CMV-related DAD without histological demonstration of CMV inclusions. In the third group, there were no positive CMV signals. These data indicate that DAD-related CMV infection is an important cause of SIP and of death in children immunosuppressed by primary underlying diseases, and that IH and in situ detection were more sensitive than the histological demonstration of CMV inclusions. A direct involvement of CMV in SIP exhibiting DAD is likely, but not in the non-specific interstitial pneumonia (NSIP) pattern. We conclude that all children with primary underlying diseases should be investigated for CMV SIP using sensitive IH and in situ tests in conjunction with histological routine procedures.
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PMID:Immunohistochemical and in situ detection of cytomegalovirus in lung autopsies of children immunocompromised by secondary interstitial pneumonia. 1515 47

A 55-year-old man was treated with gefitinib for disseminated pleural lesions, 1 year after resection of the left lower lobe for non-small cell lung cancer. After 6 weeks of continuous daily treatment with oral gefitinib, he developed dyspnoea on exertion and a non-productive cough. CXR and CT revealed focal areas of ground-glass opacity (GGO) in the right upper lobe. Despite gefitinib being discontinued, high-resolution CT revealed extension of GGO and restructuring of lung parenchyma, suggesting acute interstitial pneumonia. Transbronchial biopsy revealed acute-phase diffuse alveolar damage. After administration of methylprednisolone pulse therapy (1 g/day intravenously) for three consecutive days, the areas of GGO shrank on high-resolution CT and symptoms resolved. Diffuse alveolar damage caused by gefitinib can be successfully treated in the early phase with high-dose corticosteroids. Patients receiving gefitinib should be carefully examined for symptoms and undergo CT if their condition deteriorates.
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PMID:Gefitinib-induced lung injury successfully treated with high-dose corticosteroids. 1642 12

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

The classification scheme of interstitial lung diseases has undergone numerous revisions. The criteria for distinguishing seven distinct subtypes of idiopathic interstitial pneumonias are now well defined by consensus in the recently published ATS/ERS classification of these lung diseases. In our present review the histological patterns of the different types are described and the differential diagnosis of idiopathic interstitial pneumonias is discussed. Surgical lung biopsy remains the gold standard for the diagnosis of interstitial pneumonias, and sampling from at least 2 sites is recommended. Video-assisted thoracoscopic surgical biopsy is the preferred method for obtaining lung tissue as this procedure offers a similar yield as an open thoracotomy The most common histological subtype of chronic interstitial lung disease is the usual interstitial pneumonia [UIP] which makes up 47-71% of cases. The key histologic features include patchy subpleural and paraseptal distribution of remodeling lung architecture with dense fibrosis, frequent honeycombing, and large fibroblastic foci. Temporal and spatial heterogeneity are the hallmarks. Nonspecific interstitial pneumonia [NSIP] occurs primarily in middle-aged women who have never smoked, with more than 5-years survival rate in 80% of patients. The major feature of NSIP is a uniform interstitial thickening of alveolar septa by a fibrosing or cellular process. The cardinal histological feature in respiratory bronchiolitis and desquamative pneumonia is an excess of intraalveolar histiocytes. In both patterns, there is variable interstitial fibrosis and chronic inflammation, and a strong association with a history of smoking. Organizing pneumonia (idiopathic bronchiolitis obliterans-organizing pneumonia [BOOP]) is not strictly an interstitial process, because the alveoli and bronchioles are filled by intraluminal polyps of fibroblastic tissue and the expansion of the interstitium is mild. Lymphocytic interstitial pneumonia [LIP] is currently viewed as a pattern of diffuse reactive pulmonary hyperplasia associated in most cases with EB virus, immunosuppression, or a connective tissue disorder. Malignant transformation may rarely occur. A dense mixed interstitial lymphoid infiltrate is a typical histological finding. Diffuse alveolar damage [DAD] from unknown causes is termed acute interstitial pneumonia [AIP], and is synonymous with cases of Hamman-Rich disease. Hyaline membranes in the exsudative phase and marked expansion of the interstitium later are present.
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PMID:[Histopathological classification of idiopathic interstitial pneumonias]. 2128 Feb 74


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