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Query: UMLS:C0034069 (pulmonary fibrosis)
 7,050 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Exogenic allergic alveolitides are caused by organic dusts which contain bacteria, moulds or vegetable and animal antigens. The farmer's lung as a form of the exogenic allergic alveolitis is a rare disease. The uncharacteristic symptomatology in the initial phase and in particular the retarded beginning of the symptom after several hours handicap the timely recognition in an early phase of the disease so that curative therapeutic measures are rarely possible. The cases of the disease are found only at the chronic stage, at the stage of the pulmonary fibrosis. Then the prognosis is unfavourable. In the Central Clinic for Heart and Lung Diseases Bad Berka 1,110 patients with alveolitides and lung fibroses were diagnosed in the period from 1975 to 1988. 306 of them could be clarified as exogenic allergic alveolitis, 61 of them (19.8%) were farmer's lungs.
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PMID:[Farmer's lung--a form of exogenous allergic alveolitis]. 209 25

Communication between cells determines the steady-state composition of the lung in health and becomes a critical determinant of outcome in pathologic processes resulting in anatomic remodeling. This review presents the evolving concepts of the biology of cytokines (also known as peptide growth factors or biological response modifiers) in maintaining normal tissue growth and homeostasis. How these extracellular signaling proteins are involved in such pathologic disorders as spontaneous pulmonary fibrosis, sarcoidosis, pneumoconiosis, and the evolution and recovery from acute lung injury is also discussed. During the past decade the cytokines have come to the fore as important multifunctional mediators of cell behavior and cell-cell communication. A wide range of cellular responses are influenced or triggered when cytokines interact with cells. These include mitosis, chemotaxis, angiogenesis, cytoskeleton arrangement, immunomodulation, and extracellular matrix production. Cytokines influence cell behavior by binding to specific high affinity surface receptors on target cells. These receptors are linked in turn at the cell membrane to a complex array of intracellular signaling pathways. Individual cytokines may inhibit as well as promote cellular functions such as mitosis and thereby play a critical role in homeostasis of normal tissue elements. Hence, cytokines are intimately involved in normal tissue homeostasis as well as in processes eventuating in growth and remodeling. All cells produce and secrete cytokines at some time during their life. Each cytokine is capable of modulating more than one cellular function. Although produced by a variety of cell types, the triggers that induce a specific cytokine to be produced differ between cells. Many of the cytokines share regions of homologous nucleic acid sequences, suggesting that they are members of larger gene families. Given that tissues and cells are exposed to complex cytokine mixtures rather than to individual cytokines, recent attention has turned to understanding how cytokines interact. The combined effects of cytokine mixtures have proved to be both complex and unpredictable based on knowledge of the separate actions of the individual cytokines involved. In studies of the role of cytokines in lung disease, early research attention has focused on those cytokines released by alveolar macrophages (the so-called macrophage-derived growth factors). However, structural cells as well as immune effector cells of the lung are capable of cytokine production and release. The cytokines receiving the most attention to date in relation to pulmonary diseases include platelet-derived growth factor (PDGF), interleukin-1 (IL-1), transforming growth factor-beta (TGF-beta), tumor necrosis factor-alpha (TNF-alpha), insulinlike growth factor I (IGF-I), and, most recently, interleukin-6 (IL-6).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Cytokines of the lung. 224 Aug 51

The type of lung disease caused by metal compounds depends on the nature of the offending agent, its physicochemical form, the dose, exposure conditions and host factors. The fumes or gaseous forms of several metals, e.g. cadmium (Cd), manganese (Mn), mercury (Hg), nickel carbonyl (Nl(CO)4, zinc chloride (ZnCl2), vanadium pentoxide (V2O5), may lead to acute chemical pneumonitis and pulmonary oedema or to acute tracheobronchitis. Metal fume fever, which may follow the inhalation of metal fumes e.g. zinc (Zn), copper (Cu) and many others, is a poorly understood influenza-like reaction, accompanied by an acute self-limiting neutrophil alveolitis. Chronic obstructive lung disease may result from occupational exposure to mineral dusts, including probably some metallic dusts, or from jobs involving the working of metal compounds, such as welding. Exposure to cadmium may lead to emphysema. Bronchial asthma may be caused by complex platinum salts, nickel, chromium or cobalt, presumably on the basis of allergic sensitization. The cause of asthma in aluminium workers is unknown. It is remarkable that asthma induced by nickel (Ni) or chromium (Cr) is apparently infrequent, considering their potency and frequent involvement as dermal sensitizers. Metallic dusts deposited in the lung may give rise to pulmonary fibrosis and functional impairment, depending on the fibrogenic potential of the agent and on poorly understood host factors. Inhalation of iron compounds causes siderosis, a pneumoconiosis with little or no fibrosis. Hard metal lung disease is a fibrosis characterized by desquamative and giant cell interstitial pneumonitis and is probably caused by cobalt, since a similar disease has been observed in workers exposed to cobalt in the absence of tungsten carbide. Chronic beryllium disease is a fibrosis with sarcoid-like epitheloid granulomas and is presumably due to a cell-mediated immune response to beryllium. Such a mechanism may be responsible for the pulmonary fibrosis occasionally found in subjects exposed to other metals e.g. aluminium (Al), titanium (Ti), rare earths. The proportion of lung cancer attributable to occupation is around 15%, with exposure to metals being frequently incriminated. Underground mining of e.g. uranium or iron is associated with a high incidence of lung cancer, as a result of exposure to radon. At least some forms of arsenic, chromium and nickel are well established lung carcinogens in humans. There is also evidence for increased lung cancer mortality in cadmium workers and in iron or steel workers.
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PMID:Metal toxicity and the respiratory tract. 217 66

This report evaluates the histopathologic alterations of a series of 17 patients with the CREST syndrome and relates these alterations to clinical and functional abnormalities. Histologic abnormalities were classified into the following four distinct patterns: pulmonary vascular changes, primarily intimal fibroelastosis, associated with and without pulmonary hypertension; a pattern of fibrosis indistinguishable from usual interstitital pneumonia (UIP); small airways disease; and mixtures of these three patterns. Five patients (29%) had clinical and morphologic pulmonary hypertension, while five others showed mild reductions in diffusing capacity, presumably due to vascular compromise. Five patients had UIP-like interstitial fibrosis, with vascular alterations and restrictive lung disease. Only one patient had small airways disease exclusively. Concentric fibrointimal proliferation and occlusion of arterioles was worse in patients with clinical pulmonary hypertension and interstitial fibrosis of the UIP type, and was not always associated with pulmonary fibrosis. Twenty-one percent of patients developed primary lung carcinomas. The CREST syndrome is unique in the spectrum of pulmonary alterations seen in progressive systemic sclerosis for its high incidence of clinical pulmonary hypertension and propensity for the development of pulmonary carcinomas.
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PMID:The pulmonary pathologic manifestations of the CREST syndrome. 218 93

Between November 1983 and August 1989, we performed single-lung transplantation for end-stage pulmonary fibrosis in 20 patients. Nine patients (45 percent) who survived for more than one year form the basis of this report. Before surgery, the nine survivors had severe restrictive lung disease, with a mean (+/- SD) vital capacity (VC) of 43 +/- 9 percent, a forced expiratory volume in one second (FEV1) of 50 +/- 9 percent, and a single-breath diffusing capacity (DLCO) of 36 +/- 9 percent of predicted values. One year after transplantation, the patients' VC had reached 69 +/- 10 percent, FEV1 79 +/- 15 percent, and DLCO 62 +/- 16 percent of predicted values. Relative perfusion to the transplanted lung rose from 63 +/- 14 percent (three days after surgery) to 77 +/- 7 percent within three months and stayed constant or increased slightly thereafter. Before surgery, despite supplemental oxygen at flow rates varying from 1 to 9 liters per minute, none of the patients could exercise beyond stage 1/2 (2.7 km [1.7 miles] per hour, 5 percent grade) on a modified Bruce treadmill-exercise protocol. All eight patients tested one year or more after transplantation achieved at least stage 1 (2.7 km [1.7 miles] per hour, 10 percent grade), and usually a higher stage, without supplemental oxygen. Arterial oxygen tension returned to normal values in most patients (87 +/- 13 mm Hg), and supplemental oxygen, which all patients required before surgery, was no longer needed by any patient after transplantation. We conclude that in carefully selected patients with end-stage pulmonary fibrosis, single-lung transplantation is an effective treatment.
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PMID:Results of single-lung transplantation for bilateral pulmonary fibrosis. The Toronto Lung Transplant Group. 237 83

Between February 1988 and December 1989, 15 combined heart-lung, 2 double lung and 5 single lung transplants were performed at our institution for end stage lung disease. The indication for heart-lung transplantation was primary lung disease with associated secondary heart failure in 11 cases, diffuse pulmonary disease with extensive adenopathy of the hilum in 2 cases and profuse and antibiotic-resistant tracheobronchial infection due to Pseudomonas in 2 cases. A double lung transplant was performed in 2 patients with hypertensive emphysema. The indication for a single lung transplantation was emphysema in 2 cases and pulmonary fibrosis in 3 cases; in this last indication, transplantation should be performed on the right side with a slight lengthening of the main bronchus to avoid the side-effects of mediastinal shift. There were 2 early deaths, 7 secondary deaths (from the 2nd to the 5th month) due to viral or bacterial infectious complications, and 1 late death in the 7th month (infection due to a syncitial virus). All 12 surviving patients have an excellent functional result; the size of the tracheal or bronchial anastomosis ranges from 85% to 100% of normal. From this experience, we conclude that specificity and severity of lung hazards are mainly related to bronchial infection, dependence on steroids and pleural adhesions. Moreover, posttransplant pulmonary oedema, mucociliary dysfunction and the differential diagnosis between rejection and infection require careful endobronchial suction and periodical sampling.
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PMID:Lung and heart-lung transplantation for end-stage lung disease. The Bordeaux Lung and Heart-Lung Transplant Group. 236 Oct 20

Hard metal pneumopathy and hard metal asthma are two separate forms of hard metal lung disease. Cobalt is the probable causal agent involved. Bronchial provocation with hard metal powder induces obstruction within 2 hours of the challenge. Suspected hard metal pneumopathy, however, should be confirmed or excluded by a period of non-exposure followed by re-exposure, since the long-term exposure in patients suffering from hard-metal pneumopathy leads to pulmonary fibrosis.
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PMID:[Hard metal-induced lung changes. Hard metal asthma--interstitial hard metal pneumopathy]. 239 30

Sarcoidosis is a systemic granulomatous disorder of unknown genesis with an average annual incidence of 10/100,000 population in Denmark. The clinical picture and prognosis are dominated by the pulmonary changes in the majority of cases. The patho-anatomical picture consists of a T-lymphocyte-dominated interstitial inflammation with non-caseating epithelioid granulomas followed by fibrosis in varying degrees. The different types and courses of pulmonary disease are reviewed. Clinical examination, chest radiography, pulmonary function tests (especially the carbon dioxide diffusion capacity) and S-angiotensin-converting enzyme (S-ACE) are the most important measures of disease activity. The value of systemic corticosteroids is critically evaluated; most patients in this country can be observed without treatment because the spontaneous resolution rate is high. It is recommended that steroids should be administrated primarily in symptomatic and progressive parenchymal lung disease, or when critical or disabling extrathoracic sarcoidosis is present. If the pulmonary parenchymal infiltrates do not disappear within approximately 18 months, a course of prednisolone for at least one year should be considered to prevent disabling or even lethal pulmonary fibrosis.
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PMID:[Pulmonary sarcoidosis]. 240 53

The lungs are frequently affected in systemic sclerosis, and pulmonary disease may significantly influence morbidity and mortality. The clinical, radiographic, and physiologic features of scleroderma lung disease are discussed in this article, as are new approaches to the detection and study of interstitial pneumonitis. The pathogenesis of pulmonary fibrosis is discussed in the context of data derived from bronchoalveolar lavage studies. Pulmonary vascular disease and less common pulmonary features of systemic sclerosis are also discussed.
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PMID:Lung involvement in systemic sclerosis. 240 8

Bleomycin-induced lung disease is characterized by fibroblast proliferation and pulmonary fibrosis. In these studies, we demonstrate that fibroblasts are relatively resistant to clinically relevant amounts (below 10(-4) U/ml) of bleomycin and that these levels of bleomycin augment fibroblast proliferation in response to various fibroblast growth factors. These observations suggest that one mechanism by which bleomycin causes pulmonary fibrosis is augmentation of fibroblast proliferation.
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PMID:Augmentation of fibroblast proliferation by bleomycin. 242 90


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