Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 27-year-old nonsmoking woman complained of cough and chest oppression for two years since an episode of pneumonia. Clinical tests showed decrease in FEV1.0 during attacks of coughing and evidence of bronchial hypersensitivity. While these events fitted the picture of bronchial asthma, the nonwheezing cough suggested cough variant asthma. Antinuclear antibody and anti-ds DNA antibody were increased and leukopenia was recognized, suggesting the diagnosis of systemic lupus erythematosus (SLE). Bronchoalveolar lavage showed lymphocytic alveolitis and decreased T4/T8. These results were suggestive of collagen lung induced by SLE. Inhalation challenge with capsaicin and rapid intravenous injection of lobelin and alinamin indicated that peripheral c-fiber receptors were involved in the induction of coughing. We conclude that the peripheral lesion of collagen lung stimulates the peripheral c-fiber receptors, leading to cough variant asthma.
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PMID:[Case report of collagen lung in SLE presenting with cough variant asthma: relation between the localization of responsible receptors and cough]. 156 25

A light and electron microscopy study was performed on endothelial cells of alveolar capillaries in biopsied lung tissues obtained from 28 patients with interstitial fibrotic lung diseases, including idiopathic pulmonary fibrosis, sarcoidosis, hypersensitivity pneumonitis, chronic eosinophilic pneumonia, collagen vascular diseases and acute interstitial pneumonia. In the relatively early stages of acute interstitial pneumonia, hypersensitivity pneumonitis and other diseases, the cytoplasms of the endothelial cells appeared swollen and electron-lucent and occasionally showed degeneration and necrosis. Although mitosis was not evident in the endothelium at any disease stage, some capillary endothelial cells showed regeneration. Furthermore, although rarely, they showed obvious phenotypic transformation into diaphragmed fenestrae in some limited segments of fibrotic lungs in the 20 of the 28 patients examined. The frequency of endothelial fenestration seemed to be correlated with the degree of interstitial fibrosis along the alveolar walls. In such fibrotic lung tissues, cuboidal metaplastic cells of bronchiolar origin proliferated on the luminal side. The mechanism of endothelial fenestration in the alveolar capillaries is assumed to be comparable with cuboidal metaplasia of alveolar epithelial cells. The alveolar capillary endothelium is recruited from the bronchiolar capillaries via bronchopulmonary anastomoses unless endothelial repair occurs in situ. Regenerating endothelial cells move into the alveolar capillary tubes along the remnant sleeves of the basement membrane. New endothelial processes finally display their original fenestrated structure while secreting irregular fragments of basement membrane during implantation in the capillary beds.
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PMID:Endothelial fenestration of the alveolar capillaries in interstitial fibrotic lung diseases. 157 Jul 40

We studied the clinico-pathological correlation of collagen disease-related pulmonary lesions to examine the pathological and radiological features of collagen lung, and the effect of steroid therapy. Ten open lung biopsy cases were examined; 4 male, and 6 female. The mean age was 55 years old. Seven cases developed pulmonary shadows after the diagnosis of collagen disease, and 3 cases showed pulmonary shadow prior to diagnosis. Pathologically, 6 cases proved to be bronchiolitis obliterans organizing pneumonia (BOOP), 3 cases were chronic interstitial pneumonia (UIP), and 1 case was acute interstitial pneumonia. All cases had inflammatory thickening of the interstitium involving the pleura, bronchial wall, and perivascular connective tissue. Half of the cases had bronchiolar inflammatory lesions. Radiologically BOOP cases showed either localized ground glass shadows, or diffuse reticulonodular shadows predominantly in the lower lung fields with shrinkage of affected areas. UIP cases showed reticulonodular shadows, and active UIP cases showed overlapping ground glass shadows. Steroids were administered in cases of BOOP and active UIP, and all cases showed improvement. We consider that open lung biopsy is of use in the diagnosis of some cases and in assessing whether steroid therapy is indicated.
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PMID:[Clinico-pathological study of collagen-related pulmonary lesions in cases of open lung biopsy]. 160 60

Collagen types and ultrastructural features of the stroma and scar extracellular matrix in the peripheral lung carcinoma, post-tuberculosis and post-pneumonia pneumosclerosis foci, fibrosing alveolitis interstitium were studied on the material of operational and transbronchial lung biopsies. It is established that by the collagen composition the scars in the peripheral carcinoma are identical to the pneumosclerosis foci and are distinguished from the carcinoma stroma by a higher concentration of type IV and V collagens (p less than 0.05). Accumulation of type III collagen in the lung carcinoma stroma reflects anaplasia of the tumour as the domination of type III collagen is characteristic of the embryonal tissue. The decrease of collagen type IV in the cancer stroma correlates with an increase of its malignancy. Pneumosclerosis in the fibrosing alveolitis is distinct from the focal forms of pneumosclerosis by a higher content of collagen I and a lower content of collagen V this being probably due to the character of sclerosis morphogenesis in this disease.
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PMID:[The extracellular matrix of peripheral lung cancer in the scar and of pneumosclerosis of different origins (the immunohistochemistry and electron microscopy of the collagens)]. 165 27

One form of idiopathic pulmonary fibrosis (IPF), usual intersitial pneumonia (UIP) is characterized pathologically by patchily distributed fibrotic areas in apparently normal parenchyma. Excessive accumulation of collagen and fibroblasts in fibrotic areas are shown histologically. Fibroblast proliferation is generally evaluated as a process following alveolitis. However, substantial alveolitis with increased inflammatory and immune cells were not observed in our UIP cases. To evaluate the possibility that fibroblasts in UIP are controlled by mechanisms other than normal paracrine regulation, proliferative features of lung fibroblast lines from UIP lung with regular growth medium, platelet derived growth factor (PDGF) and prostaglandin E2 (PGE2) were investigated. Ten fibroblast lines from open lung biopsy specimens of patients with IPF (UIP) and 10 control fibroblast lines from surgically resected lung tissues of patients with limited lung disease were established. The doubling time of fibroblast lines with regular growth medium was UIP:32.0 +/- 6.0 hrs. (mean +/- S.D.), normal control: 33.2 +/- 10.4 hrs. There was no difference between the groups. To examine growth promotion activity by PDGF and growth inhibition by PGE2, lung specimens from 4 patients with IPF were subdivided into tissue with high intensity fibrotic lesion (H) and low intensity fibrotic lesion (L), and the fibroblast lines were established separately. 3H-thymidine uptake with or without PDGF and PGE2 was examined, and results were expressed as the stimulation index. Growth promotion by PDGF was H: 1.97 +/- 1.19, L: 1.89 +/- 0.78, normal control: 2.29 +/- 0.55. There were no differences between groups. Growth inhibition by PGE2 was H: 0.88 +/- 0.24, L: 0.69 +/- 0.49, normal control: 0.44 +/- 0.33. Growth inhibition for H was significantly lower than control (p less than 0.05). Growth inhibition for L was lower than controls, but the difference was not statistically significant.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Proliferative characteristics of fibroblast lines derived from open lung biopsy specimens of patients with the usual interstitial pneumonia form of idiopathic pulmonary fibrosis]. 175 41

The histologic findings of BOOP are nonspecific, and the diagnosis of idiopathic BOOP is one of exclusion. We studied the clinicopathologic features of various lung diseases with histopathological appearance of bronchiolitis obliterans organizing pneumonia (BOOP) pattern in open lung biopsy specimens. The 17 patients with BOOP pattern studied included idiopathic BOOP (n = 7), unclassified interstitial pneumonia (n = 1), collagen vascular disease (n = 3, RA 1, PM/DM 2), hypersensitivity pneumonitis (HP, n = 2), eosinophilic pneumonia (EP, n = 1), multiple lung abscesses (n = 1), limited form of Wegener's granulomatosis (n = 1), and pneumocystis carinii pneumonia associated with adult T cell leukemia (n = 1). There were no differences in clinical symptoms, laboratory data, respiratory function, and cytological findings in bronchoalveolar lavage fluid (BALF) between cases of idiopathic BOOP and other lung diseases. The duration of clinical symptoms was less than one year in 16 patients (one case had no symptoms). Chest X-rays showed bilateral patchy, nodular, or reticular shadows in all cases. Multiple patchy migratory shadows were only observed in cases of idiopathic BOOP or EP. Organizing pneumonia was recognized in the transbronchial lung biopsy specimens of all patients with idiopathic BOOP, HP or EP. Regarding prognosis, relapses occurred in idiopathic BOOP (n = 5), polymyositis, EP, limited form of Wegener's granulomatosis, and Pneumocystis carinii pneumonia. Four patients with idiopathic BOOP relapsed when steroid therapy was decreased or stopped. These findings indicate that idiopathic BOOP should be differentiated from other lung diseases, and these patients should be followed for a long period of time.
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PMID:[Clinicopathologic study of various lung diseases with bronchiolitis obliterans organizing pneumonia (BOOP) pattern in open lung biopsy]. 180 81

The interstitial lung diseases are comprised of a group of pulmonary disorders characterized clinically by diffuse infiltrates on the chest radiograph and histologically by distortion of the gas exchanging portion of the lung. The physiologic correlates are restriction of lung volumes and impaired oxygenation. The term "interstitial" when applied to these diseases is actually a misnomer because it implies that the inflammatory process is limited specifically to the area between the alveolar epithelial and capillary endothelial basement membranes. The diseases currently grouped as "interstitial" also frequently involve the alveolar epithelium, alveolar space, pulmonary microvasculature, and less commonly, the respiratory bronchioles, larger airways, and even the pleura. The enormous differential diagnosis of interstitial lung disease can be made manageable by understanding that pneumoconiosis, drug-induced disease, and hypersensitivity pneumonitis account for over 80% of the responsible entities and can usually be identified from the patient's history. The nine remaining diseases/disease categories include: sarcoidosis, idiopathic pulmonary fibrosis, bronchiolitis obliterans-organizing pneumonia, histiocytosis X, chronic eosinophilic pneumonia, collagen vascular disease-associated interstitial lung disease, granulomatous vasculitis (Wegener's granulomatosis, Churg-Strauss syndrome, lymphomatoid granulomatosis), Goodpasture's syndrome, and pulmonary alveolar proteinosis. The diagnosis of a specific interstitial lung disease can be made via various means including the patient's history, specific serologies, bronchoalveolar lavage, transbronchial biopsy, and biopsy of extrathoracic tissues or open lung biopsy. A directed diagnostic approach can be formulated based on an understanding of these techniques and a thorough knowledge of the clinical presentations and specific diagnostic criteria for each of the major diseases. This monograph will serve as a guide for the clinician to use in evaluating and treating patients with interstitial lung disease. We begin by reviewing the clinical presentation, diagnostic criteria, and management of specific interstitial lung diseases excluding pulmonary infection, neoplasm, and sarcoidosis. Pneumoconiosis and drug-induced syndromes are not discussed in detail, but the agents responsible and pertinent exposures are presented in tabular form in the discussion of the general diagnostic approach.
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PMID:Interstitial lung disease. 199 45

The synthesis of collagen and EIIIA-containing cellular fibronectin in certain forms of pulmonary fibrosis occurs in discrete locations: in the Masson bodies in bronchiolitis obliterans with organizing pneumonia and in focal clusters of fibroblasts (fibroblastic foci) within airspaces in usual interstitial pneumonia. These sites were examined by electron microscopy and immunohistochemistry using antibodies against cytoskeletal markers and extracellular matrix components in biopsies from three patients with bronchiolitis obliterans with organizing pneumonia and four patients with usual interstitial pneumonia. Fibroblasts of both Masson bodies and fibroblastic foci expressed vimentin and alpha smooth muscle actin but not desmin, distinguishing them from true smooth muscle. In both structures fibroblasts with well-formed actin filament bundles were aligned parallel to one another, enmeshed in a matrix of fibronectin-containing fibrils (microtendons) that linked cells and collagen bundles. Similar features characterize the phase of contraction during the healing of skin wounds. This suggests that active contractions of fibroblasts plays a role in the remodeling of the lung in pulmonary fibrosis.
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PMID:The roles of the myofibroblast in idiopathic pulmonary fibrosis. Ultrastructural and immunohistochemical features of sites of active extracellular matrix synthesis. 202 10

The authors established an easy fluorescent microscopy method to measure the ratio of CD4 (helper/inducer T lymphocytes) to CD8 (suppressor/cytotoxic T lymphocytes) (CD4/CD8 ratio) in bronchoalveolar lavage fluid (BALF) in patients with diffuse pulmonary diseases and measles pneumonia. The CD4/CD8 ratio determined by this method strongly correlated with the CD4/CD8 ratio obtained by flow cytometry in both peripheral blood lymphocytes and BALF lymphocytes. When the proportion of lymphocytes in BALF nuclear cells is more than 6%, the CD4/CD8 ratio in BALF was measurable. The CD4/CD8 ratio in peripheral blood was not significantly different among hypersensitive pneumonitis (HP), sarcoidosis (SAR), collagen vascular disease (CVD), idiopathic interstitial pneumonitis (IIP), and measles pneumonia (MP). However, the BALF CD4/CD8 ratio was 0.61 +/- 0.37 in HP, 6.83 +/- 2.73 in SAR, 0.77 +/- 0.40 in CVD, 1.49 +/- 0.29 in IIP. These results were consistent with previously published data. The CD4/CD8 ratio in patients with MP was as low as 0.39 +/- 0.34. In patients with summer type HP, this ratio was low in the acute phase, but became within normal range after moving or reconstructing their homes, accompanied with the improvement of subjective symptoms and the disappearance of inflammation. These data indicate that our method is very simple and useful in the diagnosis and the monitoring of diffuse pulmonary diseases.
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PMID:[Establishment of a simple fluorescent microscopy method for measurement of the CD4/CD8 ratio in BALF]. 212 Apr 96

Parainfluenza 1 (Sendai) and influenza A virus pneumonitis cause severe lung damage, which, upon resolution, is followed by persistent alveolitis and parenchymal changes characterized by patchy consolidation and collagen deposition in the affected areas. To determine whether these long-term sequelae of the virus pneumonias are cumulative, mice were infected by aerosol inhalation with Sendai virus, influenza A virus, or Sendai followed 30 days later by influenza virus infection. At 90 days after the initial infection, mice were killed for assay of long-term parenchymal changes as quantitated lung hydroxyproline (Hpr) content, morphometric analysis, and total and differential lavage cell counts. Sendai virus infection did not alter the proliferation of influenza virus in the lungs as quantitated by infectious virus titers on Day 1, 3, 5, 7, 9, and 11 of influenza infection. At Day 90, lung Hpr content was cumulative in dual-infected mice, with a concomitant increase in the persistent alveolitis. To determine whether bacterial infections played a similar role in these long-term pulmonary sequelae, mice were infected by aerosol inhalation with either Staphylococcus aureus or Klebsiella pneumoniae or, during the course of influenza virus infection, superinfected with each of the bacteria. Sixty days after infection with K. pneumoniae alone, lung Hpr levels were significantly increased over those in noninfected control mice. Infection with S. aureus had no effect on the quantitated parameters of long-term lung damage. In influenza-infected mice superinfected with K. pneumoniae, lung Hpr content was significantly increased over that of S. aureus did not elevate any quantitated parameter of lung damage when compared with the virus alone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Sequential virus infections, bacterial superinfections, and fibrogenesis. 216 56


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