Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032273 (pneumoconiosis)
 1,578 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 57 year old man, receiving compensation for talc pneumoconiosis since 1977, was admitted to hospital for the first time in 1987, with symptoms of weight loss, fever, dyspnoea and productive cough. A chest roentgenogram showed bilateral cavitation. Two years later, Mycobacterium xenopi was found in sputum cultures. Despite specific oral antibiotherapy, the patient's health deteriorated and he died in 1990. To the best of our knowledge, this is the first reported case of an association of talcosis with a M. xenopi pneumonia. The relative timing of the two diseases suggests that talc pneumoconiosis predisposed to the infection by M. xenopi.
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PMID:Atypical mycobacteriosis as a complication of talc pneumoconiosis. 886 7

The Erasmus syndrome describes the association of generalised progressive scleroderma following exposure to silica with or without silicosis. This is a case report on four patients presenting with the Erasmus syndrome who were admitted to hospital. The analysis of the four cases enables an assessment of the cause of the dyspnoea during the course of the Erasmus syndrome. The dyspnoea presents more as scleroderma (pulmonary fibrosis in two cases, pulmonary artery hypertension in one case and localised thoracic skin disease in one case) than of pneumoconiosis. Pulmonary fibrosis should be considered where there is an association of progressive effort dyspnoea, fine crackles on auscultation and a radiological appearance either of honeycombing and/or a ground glass appearance predominantly in the posterior regions which does not exist in isolated cases of silicosis. The functional repercussion of the fibrosis is evident by a restrictive ventilatory defect which is not specific but more severe than in a case of silicosis alone. Bronchoalveolar lavage showed, in two cases of pulmonary fibrosis, an unusual polymorphonuclear neutrophilia during the course of the silicosis. The presence of ausculatory anomalies, the atypical aspects of pneumoconiosis on computed tomography and an unusual form of LBA should suggest the existence of pulmonary fibrosis associated with pneumoconiosis.
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PMID:[Erasmus syndrome: clinical, tomographic, respiratory function and bronchoalveolar lavage characteristics]. 908 2

A 35 year old man heavily exposed to polyvinylchloride (PVC) polymer dust developed dyspnoea and a mild restrictive lung disorder consistent with PVC pneumoconiosis. Clinical and radiological abnormalities cleared on removal from exposure, suggesting that in its early stages PVC pneumoconiosis is reversible.
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PMID:Regression of polyvinylchloride polymer pneumoconiosis. 933 40

It is well known that silica exposure leads in an experimental model to the development of an acute fibrotic process. In human beings two main observations have already been done: (1) silica exposure is frequently associated with the development of connective tissue disease (CTD), especially progressive systemic sclerosis; (2) 10 to 20% patients with CTD developed pulmonary fibrosis. In this context we report 26 cases of coal miners who presented with clinical, radiological, biological and functional characteristics mimicking idiopathic pulmonary fibrosis (IPF), with or without associated coal worker's pneumoconiosis (CWP). All were men; mean age was 68 +/- 9.2 years. Twenty-three were smokers. Duration of exposure was 28.8 +/- 9.1 years. All the patients had dyspnea (stage III, IV in the NHYA classification) and diffuse crackles. Eleven out of 26 had finger clubbing. Computed tomography showed honeycombing (23 cases), and/or ground glass opacities (6 cases) with bronchiectasis (3 cases) predominant in the lower lobes; 19 had radiological signs of CWP, micronodules (n = 16) and nodules (n = 3) predominant in the upper lobes. BAL exhibited an increased % of neutrophils (11.9 +/- 16.1%). Lung function demonstrated a restrictive pattern (TLC = 73 +/- 15.6% and VC = 80 +/- 18% of predicted values) associated with a decreased DLCO (51.8 +/- 23.6% of predicted values) and hypoxemia (at rest = 66.5 +/- 11.2 mmHg, upon effort = 56 +/- 12 mmHg). Lung biopsies were performed in four cases and demonstrated interstitial fibrosis of intraalveolar septum with an accumulation of immune and inflammatory cells similar to the one described in IPF. The association between IPF and silica exposure with or without associated CWP points out the problem of legal recognition of idiopathic-like pulmonary fibrosis as a complication of the occupational exposure of coal workers.
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PMID:["Primary" diffuse interstitial fibrosis in coal miners: a new entity? Study Group on Interstitial Pathology of the Society of Thoracic Pathology of the North]. 941 11

The authors report a case of an employee in the wood processing industry. The clinical presentation was respiratory with dyspnoea on effort. The chest x-ray showed bilateral interstitial changes. Following bronchioalveolar lavage electron microscopic studies showed evidence of silica particles. Respiratory function tests showed pulmonary performance of 51%-64% of theoretical values depending on the test used. His working position involved the up keep of the boilers and also the drainage of the silos for wood dust. The wood used was corupixa, a brazilian wood containing crystalline silica; 0.1% in fresh wood dust. Numerous analyses have specified the percentage of silica in the ashes in magma. The diagnosis of pneumoconiosis of the silicotic type was sustained. The occupational risk linked to using this type of wood should be understood and the need to take protective measures for the employees concerned.
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PMID:[Pneumoconiosis and exposure to wood]. 949 9

This article illustrates problems in diagnosis and treatment of an atypical form of bronchial carcinoid. We described the case of a 49-year old man, exposed to granite dust and noise for 25 years who had suffered from frequent bronchitis inflammations and pneumonias for 5 years prior to the diagnosis. He was admitted to our clinic because of supposed occupational nature of hearing deficiency. Although a pneumoconiosis was excluded before the admission, we found clinical and X-ray features of the right lung emphysema with medium restrictive ventilation disturbances. Bronchoscopy was performed because of "bright" right lung and ventilation disturbances and it showed presence of the carcinoid. Unusual in this case were tiny anamnestical findings (mild dyspnea attacks after physical effort or nervousness) plus increasing frequency of reported from the childhood bronchitis and pneumonias and uncharacteristic "bright" right lung in X-ray. Therapeutical difficulties resulted from atypical histological form of the tumor, its diameter, polypous-infiltrative character, and inconvenient localization. In spite of late diagnosis of carcinoid and significant acceleration of respiratory decompensation symptoms after the diagnosis the attempt of surgical therapy was appropriate but unsuccessful. After the operation the patient was suffering long lasting lowering of arterial pressure (what was corrected with catecholamine infusions) probably as a result of serotonin secretion. However it was not established because of technical reasons.
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PMID:[Atypical case of bronchial carcinoid]. 959 57

Histiocytosis X (HX), also referred as Langerhans cell granulomatosis is a disorder characterized by the presence of destructive granulomas containing Langerhans cells, lymphocytes, eosinophils and fibroblastes in the involved organs. Three presentations are commonly observed: 1) nonproductive cough or effort dyspnea, 2) spontaneous pneumothorax 3) incidental pulmonary infiltrates on chest X-ray in asymptomatic patients. HRCT may be helpful in the initial diagnosis of pulmonary HX. HRCT scans show nodules, cysts and estimate the extent of disease. But the final diagnosis of histiocytosis X requires the histologic demonstration of specific histiocytosis X cell in biopsy specimens of the lung. The aim of this study was to define the importance of the detection of Langerhans cells in bronchoalveolar lavage fluid (BALF) for the diagnosis of HX. The searched cells express a specific CD1 antigen, recognized by the monoclonal antibody OKT-6. In our study the demonstration of more than 5% of CD1 positive cells was defined to confirm HX. We have studied the BALF in 21 patients with suspected histiocytosis X. In BALF of 4 patients more than 5% of CD1 positive cells were found. In 1 of them HX was confirmed with open lung biopsy. Two patients displayed 5% of CD1 positive cells. The final diagnosis of the first patient was hypersensitivity pneumonitis and of the second one was bronchitis chronica. In 5 patients out of 15 patients in whom less than 5% of CD1 positive cells were found histiocytosis X was histologically proven. In other 10 patients the following disorders were histologically recognised: pulmonary emphysema 3 cases, pneumoconiosis-3, LMA-BOOP-1, sarcoidosis-1 and pleuritis eosinophilica-1. The estimation of Langerhans cells in BALF can be a useful method among the diagnostic procedures for histiocytosis X. It is necessary to remember that demonstration of less than 5% of CD1 positive cells do not exclude histiocytosis X.
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PMID:[Usefulness of CD1 expression on surfaces of cells in bronchoalveolar fluid for diagnosis of histiocytosis X--our experience]. 1064 82

Asbestosis is a rare pneumoconiosis secondary to inhalation of asbestos fibers. It follows sufficient professional exposures (more than 25 fibers x years/ml). The mean latency is 20 years. Clinical symptoms include exertion dyspnea, crackles and clubbing. Chest radiography the performances of which have been enhanced by the use of the ILO score shows fine reticular or reticulonodular opacities which predominate in pulmonary bases often in association with benign pleural abnormalities. An ILO score equal or higher than 1/1 is suggestive of asbestosis in the context of a compatible professional history. Pulmonary function is typical of diffuse interstitial lung disease. High resolution CT is the most performance investigation in particular in presence of asbestosis either minimal or of recent origin. The diagnosis of asbestosis is based on the professional exposure, a compatible interstitial lung and pleural disease and the exclusion of alternative hypothesis. The diagnosis can be comforted by bronchoalveolar lavage (cytology and biometeorology). Various evolutions are possible: stability, progression to respiratory insufficiency, increased incidence of bronchial carcinoma. Life expectancy is reduced in severe cases. There is no efficient medical treatment. Asbestosis is recognized as a professional disease. A better recognition of asbestosis necessitates a performance policy of depistage in populations with significant present or past exposure and an appropriate diagnostic strategy including high-resolution-CT.
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PMID:[Asbestosis]. 1089 51

This study aims to provide further understanding of physiologic and symptomatic changes and radiographic abnormalities due to exposure to silica, asbestos, and coal dusts. Questionnaires and pulmonary function tests were given to 220 silica, 277 asbestos, and 511 coal workers from three different industries in China. Posteroanterior chest radiographs were classified as stages 0, I, II, and III according to degree of parenchymal fibrosis. Significantly poorer pulmonary function and a higher prevalence of dyspnea and chronic cough were observed in workers with pneumoconiosis than those without, irrespective of dust type. Workers with stages II and III silicosis had worse pulmonary function and more common symptoms relative to workers with equivalent coal workers' pneumoconiosis or asbestosis. After adjusting for relevant confounders, reductions in the spirometric parameters and single breath diffusing capacity for carbon monoxide (DLCO) and the occurrence of respiratory symptoms were associated with increasing stage of silicosis, whereas lower DLCO and the occurrence of symptoms were associated with increasing stage of asbestosis and coal workers' pneumoconiosis. The study suggests that despite the differences in degree and pattern due to exposure to different fibrogenic dusts, respiratory impairments of all of the workers are associated with the presence and progression of parenchymal fibrosis and smoking.
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PMID:Respiratory symptoms and functional status in workers exposed to silica, asbestos, and coal mine dusts. 1109 86

Inhalation of dusts is an important cause of interstitial lung disease in the tropical countries such as India. While dusts of organic origin, such as the cotton dust causing byssinosis, generally cause bronchial or bronchiolar involvement and hypersensitivity pneumonitis, inorganic metallic dusts cause progressive pulmonary fibrosis. Silicosis, coal workers' pneumoconiosis, and asbestosis are the three most commonly recognized forms of pneumoconiotic pulmonary fibrosis. Pulmonary tuberculosis is an important complication seen in up to 50% of patients of silicosis in some reports from India. The presentation is generally chronic, although acute and accelerated forms of silicosis are known when the exposures are heavy. Breathlessness, dry cough, and general constitutional symptoms are commonly seen. Patients with silicotuberculosis or other forms of infection may also have significant expectoration, hemoptysis, fever, and rapid progression. Respiratory failure and chronic cor pulmonale occur in the later stages. The diagnosis is easily established if the occupational history is available. Dense nodular opacities on chest roentgenograms, which may be large in patients with massive pulmonary fibrosis, are characteristic. Emphysematous changes generally appear in advanced stages or in patients who smoke. Bronchoalveolar lavage and/or lung biopsy may occasionally be required to establish or exclude other causes of interstitial lung disease. Treatment is largely palliative, although a variety of drugs including corticosteroids and procedures such as whole lung lavage have been tried. None of these methods has yet been found successful in the treatment. Preventive safety steps, including removal of the patient from the site of exposure, are the only effective strategies to control disease progression.
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PMID:Dust-induced interstitial lung disease in the tropics. 1158 75


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