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)

There are different categories of non-infectious antigenic contaminants capable of provoking pulmonary reactions: thermophilic actinomycetales, fungi, vegetable particles, protein antigens, arthropods, drugs; their identification is based on their isolation, culture, and the study of their biochemical composition. The pulmonary reactions depend on the size and number of antigenic particles inhaled and by the underlying background. The immunological mechanisms brought into play a complex Arthus's phenomenon: in addition to the IgGs, the IgEs and the different factors of complement intervene; the recent acquisitions of immunomorphology enable better comprehension of the histogenesis of the pulmonary granuloma. The diagnosis of extrinsic allergic alveolitis is founded on well defined criteria of clinical, radiological, respiratory functional, immunological and histophthological order. These conditions are met with in agricultural, industrial and urban environments or are related to iatrogenic diseases. Many problems still remain obscure with regards to the pathogenesis and integration within the framework of immunological pneumonia of various conditions, and especially certain sarcoidosis.
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PMID:[Pulmonary reactions to non-infective antigenic contaminants]. 13 75

The air bronchogram classically signals an end-air-space or "alveolar" filling process such as alveolar proteinosis and bronchioloalveolar-cell carcinoma. However, it can also occur in interstitial diseases, possibly leading to compressive atelectasis and causing crowding of tissue around open airways. In addition, such disease processes may encroach on distal airways, producing obstructive pneumonia which may then surround open proximal airways, as in sarcoidosis and lymphoma. In mixed "alveolar" and interstitial processes such as Pneumocystis carinii pneumonia and the late stages of hemosiderosis, "alveolar" filling may mask the interstitial disease.
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PMID:The air bronchogram in interstitial disease of the lungs. A radiological-pathological correlation. 16 9

A patient who had undergone amputation and adjuvant chemotherapy with methotrexate doxorubicin hydrochloride for osteosarcoma of the femur later developed granulomatous hilar and paratracheal lymphadenopathy and multiple pulmonary nodules. Biopsy of the nodules showed noncaseating granulomas typical of sarcoidosis. Hilar adenopathy and granulomatous pneumonitis have been reported following methotrexate therapy, but a roentgenographic pattern of isolated, discrete pulmonary nodules has not been described. Treatment with immunosuppressive chemotherapy may have inhibited the development of sarcoidosis, which became manifest only after cessation of the chemotherapy.
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PMID:Sarcoidosis following adjuvant high-dose methotrexate therapy for osteosarcoma. 27 65

The results of 97 autopsy cases of lymphogranulomatosis showed the causes of death to be either progression of the disease (78 cases), complications of treatment (12) or other diseases (7). The immediate causes of death in the progression of the disease were toxicity (29%), pulmonary insufficiency (22%), pulmonary-cardial insufficiency (12%), hepatic insufficiency (21%), peritonitis (3.4%), sepsis (5.8%), uremia (3.4%), posthemorrhagic anemia (1.7%), cerebral edema (1.7%). The immediate causes of death in complications of therapy were secondary infection (5 cases), posthemorrhagic anemia (3), pulmonary insufficiency (3), cerebral edema (1). In 7 observations death was not due to lymphogranulomatosis: in 2 cases it was caused by disseminated hematogenic tuberculosis, in 2 pneumonia (with cured lymphogranulomatosis, in 1 myocardial infarction, in 1 uremia (aterosclerotic nephrosclerosis) and 1 patient died accidentally.
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PMID:[Causes of death in lymphogranulomatosis]. 45 24

In vitro production of interferon by blood leukocytes from patients with lymphosarcoma, lymphogranulomatosis, leukemia, cancer tumours, pneumonia, as well as by leukocytes of mice with Rauscher leukemia, and mice in the condition of hyporeactivity to interferon inducer was studied. Alongside with quantitative differences in interferon production, biological differences in the properties of interferons produced of normal and sick humans and animals were revealed. The biological differences consist in that the interferon produced by leukocytes from cancer and leukemia patients interacting with homologous cell culture is conducive to more rapid formation of resistance to the indicator virus than the interferon produced by normal leukocytes. Thus, resistance of the homologous cell culture to the infection with the indicator vesicular stomatitis virus developed within 1--2 hours after contact with leukocyte interferon from patients and only within 5--6 hours after contact with that of normal subjects. This finding is not specific for cancer and leukemia, as the same was observed with specimens from patients with pneumonia and from mice hyporeactive to interferon inducer. It is suggested that patients with cancer and leukemia have a state of interferon hyporeactivity.
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PMID:[Differences in the properties of the interferons produced by the leukocytes of healthy persons and of cancer and leukemia patients]. 50 7

Electron microscopic studies of lung were made and compared in 17 patients with lung disease (10 with idiopathic pulmonary fibrosis, 3 with collagen--vascular diseases, 3 with sarcoidosis, and 1 with chronic eosinophilic pneumonia) and in 5 control patients. In control patients, the alveolar epithelial cells were normal, and no hemidesmosomes were present between the plasma membranes and the basal laminae. In comparison, cuboidal alveolar epithelial cells were present in 15 of the patients with fibrotic lung disease; in 9 of these the alveolar epithelial cells were multilayered. In 7 of the latter 9 patients (5 with idiopathic pulmonary fibrosis and 2 with collagen-vascular diseases), the basal laminae of the alveolar epithelial cells were attached to the plasma membranes by hemidesmosomes and to the underlying interstitial connective tissue by "anchoring fibrils." These fibrils measured from 4000 to 6000 A in length and from 200 to 600 A in width. One or both ends of the anchoring fibrils inserted into thebasal lamina, often forming arcs through which collagen fibrils and connective tissue microfibrils penetrated. Anchoring fibrils showed a complex pattern of transverse banding, which differed from that of collagen and appeared to be symmetric about the center of the fibril. These anchoring fibrils, which resemble those in normal skin and other tissues, were not found in lungs of control patients. In addition, there was a significant correlation between the severity of the pulmonary fibrosis and the presence of anchoring fibrils. These observations suggest that in severe fibrotic lung disease, anchoring fibrils reinforce the attachment of the basal lamina of multilayered alveolar epithelial cells to interstitial connective tissue.
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PMID:Anchoring fibrils. A new connective tissue structure in fibrotic lung disease. 67 68

Destruction of intra-alveolar stroma in regions of tuberculous pneumonia is described. This destruction is associated with phagocytosis of argentophilic granules and fibre fragments by macrophages. The specific features of stromal destruction consist of sequestration, fragmentation, lysis, and other, less obvious, changes in reticulin and collagen fibres found in the air spaces. These findings have important implications in chronic fibrosing pneumonitis where similar intra-alveolar stromal changes occur. Destructive stromal changes have also been noted within granulomatous nodules of sarcoidosis in the region of giant cells. Some of the latter also contain argentophilic fibre fragments.
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PMID:The morphology of alveolar tissue destruction. 70 88

Reccurrent abnormalities of polymorphonuclear leukocyte and monocyte bactericidal activity were demonstrated in a patient with sarcoidosis. Defective function occurred during hypercalcemia complicating recovery from Listeria meningitis, and during separate, unrelated episodes of erythema nodosum, staphylococcal cellulitis, and pneumococcal pneumonia. Leukocyte morphology, oxidative metabolism, degranulation, and content of myeloperoxidase and lysozyme were normal, but low leukocyte alkaline phosphatase activity was demonstrable on one occasion. Despite defective bactericidal function of monocytes, the patient's macrophages killed bacteria normally. The relationship between an intermittent leukocyte bactericidal defect and sarcoidosis is unclear; however, further studies of leukocyte function in sarcoidosis patients with opportunistic infection are indicated.
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PMID:Intermittent neutrophil-monocyte bactericidal defects in a patient with sarcoidosis. 80 91

Intercellular adhesion molecule-1 (ICAM-1), a member of immunoglobulin supergene family with a five-domain structure, is known to play an important role in inflammatory diseases. An ELISA was developed using two MoAbs against human ICAM-1 in order to detect the soluble shedding ICAM-1 antigen in sera. We measured levels of circulating ICAM-1 antigen in sera of patients with idiopathic pulmonary fibrosis (IPF), pulmonary sarcoidosis, hypersensitive pneumonitis, bacterial and mycoplasmal pneumonia, and inflammatory diseases of other organs. The results clearly demonstrated that IPF had significantly high levels of circulating ICAM-1 in sera as compared with other disorders or normal controls. Moreover, immunohistochemical analysis with MoAb against human ICAM-1 disclosed that in IPF, the expression of ICAM-1 was intensively enhanced on alveolar epithelial cells. These results suggest that ICAM-1 may contribute to the pathogenesis of IPF.
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PMID:Circulating intercellular adhesion molecule-1 (ICAM-1) antigen in sera of patients with idiopathic pulmonary fibrosis. 135 47

We evaluated the levels of bradykinin, albumin, TAME-esterase activity, histamine, PGD2 and LTC4 in bronchoalveolar lavage fluid from asthmatics and from patients with pneumonia, sarcoidosis, fibrosis, and chronic bronchitis. Compared with the results of healthy volunteers and atopic asymptomatic asthmatics the bradykinin levels and TAME-esterase activity were significantly elevated. In all other groups, histamine was additionally elevated in asymptomatic asthmatics, whereas albumin was elevated in symptomatic asthmatics and fibrosis patients, and decreased in chronic bronchitis and pneumonia patients. Following local intrabronchial allergen challenge of mild grass pollen asthmatics out of season bradykinin levels increased significantly, correlated with albumin, histamine and TAME-esterase activity. In contrast to the increased mediator concentrations in the early phase reaction there was no change of BAL cells in asthmatics compared to baseline and healthy volunteers. The presence of bradykinin in the bronchoalveolar space of patients with active pulmonary inflammations and bradykinin generation in asthmatics as a result of intrabronchial allergen challenge provides strong evidence that kinins are involved in inflammatory disorders of the lower airways.
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PMID:Bradykinin and other inflammatory mediators in BAL-fluid from patients with active pulmonary inflammation. 146 81


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