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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adenocarcinomas of or in lung that clinically and pathologically mimic diffuse pleural mesotheliomas are rare. We reviewed selected clinical and pathologic features of 15 autopsy/surgical cases previously reported in the medical literature and of 15 additional cases from the files of the Armed Forces Institute of Pathology (AFIP). Ninety percent of the patients were men. The median age was 61 years. Sixty-three percent of the patients smoked, 17% of them had possible or definite occupational exposure to asbestos, and one patient had microscopically proven asbestosis. Most patients had chest pain, shortness of breath, or cough, and had unilateral pleural effusion in the chest x-ray. At thoracotomy or at autopsy, numerous nodules, plaques, or a continuous rind of tumor was present over the pleural surface. Microscopically, the tumors showed simplified glands, nests, cords, papillary, tubulopapillary or biphasic patterns of growth. The neoplasms contained mucin that stained with diastase-predigested periodic acid-Schiff (PAS), mucicarmine, and alcian blue (with or without hyaluronidase predigestion). All patients died with/of tumor, with a mean survival of 4.7 months for those reported in the medical literature and of 7 months for those in the AFIP files. These adenocarcinomas therefore mimic pleural mesothelioma not only in their clinical and gross and microscopic appearance, but also in their prognosis.
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PMID:Pseudomesotheliomatous adenocarcinoma: a reappraisal. 160 54

A 54-yr old male patient with a history of dyspnea and cough is presented. Due to the clinical course of disease and the radiological changes in the chest a diagnosis of sarcoidosis was established. However, the open lung biopsy revealed the true nature of the pulmonary disease: pulmonary adiaspiromycosis, only secondary to asbestosis, siderosis and silicosis as due to the well known occupational exposure to asbestos and other dusts.
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PMID:[Pulmonary adiaspiromycosis]. 176 90

Immunoblastic lymphadenopathy was diagnosed in a 71-year-old white man who had weakness, with weight loss, fever, cough, and generalized lymphadenopathy. The patient had a long occupational history of shipyard work. Diagnosis of asbestosis was made clinically by chest x-ray, and ferruginous bodies were found in the lung at autopsy. Recent reports have suggested a possible association between asbestos exposure and lymphoproliferative neoplasms. Chronic antigenic stimulation by asbestos could predispose one to the immunoproliferative disorder seen in this patient or be responsible for it. The possible significance of this relationship, previously unreported, is discussed for future consideration.
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PMID:Immunoblastic lymphadenopathy and asbestosis. 722 27

This presentation is the result of the survey of eight industries with asbestosis risk in the Barcelona area (two of fibro-cement, three of auto brakes, two of textiles, and one of insulation materials). Of 1,472 workers, 271 or 18.5% have asbestosis. Pleural involvement in asbestosis is twice as common as that of the lung, 15.7% versus 8.5%. Pulmonary asbestosis without pleural participation is seen in only 2.6% of cases. Pleural plaques, calcified and not calcified, are detected in only a few cases. There is a definite correlation between the incidence of asbestosis and the exposure time: from 1% in the group of workers with less than five years of exposure up to 64.58% for those with 30 or more years of exposure. Clinical symptoms (cough, and/or expectoration, and/or dyspnea) were present in 68% of the studied population. Pulmonary crepitations are the most significant physical sign detected, observed in one quarter to one third of the patients. Pulmonary function tests in asbestos workers revealed restrictive and mixed type syndromes in 17% of the cases and obstructive syndrome in 36%. The percentages for those workers without asbestosis are 9% and 16%, respectively. It seems, therefore, that a bronchial factor plays a role in asbestosis. The bronchial pathology would be manifested clinically by the appearance or the exaggeration of the chronic bronchitis symptoms, and physiologically by the presence of the obstructive syndrome. There is no doubt that smoking enhances the incidence of asbestosis, aggravates the respiratory symptoms in those affected, and is a cause of further deterioration of pulmonary function.
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PMID:Asbestosis in the industries of the Barcelona area. 734 62

A 68-year-old male presented with cough and sputum. He had suffered from these symptoms for ten years prior to admission. Chest roentgenogram revealed reticulonodular shadows in the lower fields of both lungs. CT scan of the chest revealed an interstitial pattern in the lower field of both lungs. Honeycombing and bullous pattern were also present in the subpleural area. The patient had a history of dust and asbestos inhalation while working as an electrician. Eosinophilia of the peripheral blood and BALF, and a slightly increased serum IgE concentration were noted. Open lung biopsy revealed interstitial fibrosis with intra-alveolar macrophage accumulation and asbestos bodies. The histopathological features resembled UIP and DIP, although DIP is uncommon in pulmonary asbestosis. The slightly increased serum IgE concentration was considered to be an additional effect of asbestos. This is a case of pulmonary asbestosis with intriguing immunological and histopathological features.
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PMID:[A case of pulmonary asbestosis with slightly increased serum IgE concentration and histopathological changes resembling DIP]. 851 2

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

Asbestosis is a diffuse interstitial pulmonary fibrosis, secondary to the inhalation of asbestos fibres. There is a dose-response relationship between exposure to asbestos and the risk of developing asbestosis, in such a way that the greater the exposure, the greater the risk of developing the disease. The time of clinical latency is inversely proportional to the level of exposure. Dyspnoea upon exertion and a dry cough together with end-inspiratory crackles are the most frequent symptoms and signs. Chest radiography is a basic tool in identifying the disease, however high resolution CAT has added greater sensitivity. Tests of the respiratory function show alterations and restrictive ventilations with a reduction of pulmonary spread. Determination of asbestos bodies in BAL is an indicator of exposure, although their absence does not rule out the disease. A histopathological diagnosis is the most reliable, although in the majority of cases the diagnosis is established on the basis of the existence of an antecedent of exposure to asbestos together with suggestive clinical, radiological and functional findings, and a suitable time of latency, without having recourse to a pulmonary biopsy.
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PMID:[Asbestosis]. 1591 70

The study included 318 asbestos exposed workers. The aim was to investigate the symptomatology and clinical findings over an average period of ten years. We took in cosideration quantitative data and analyzed them by statistical methodology of univariate and multivariate data analysis and chi2-test. Chest radiography, clinical and functional findings were used as a diagnostic tool. The most common finding was dyspnea, then cough and chest pain. Clinical symptoms were more common in workers exposed to crysotile asbestos than in those exposed to crocidolite asbestos. There is strong evidence for association between the symptoms and the duration of asbestos exposure. The symptoms were not specific for asbestosis. A significant positive correlation was found between physical examination and duration of asbestos exposure. Basal rales and pleural rub were recorded in 72% of exposed workers.
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PMID:[Asbestosis--physical examination and symptoms]. 1804 80

We encountered 19 patients of rounded atelectasis induced by exposure to asbestos from 2000 to 2007. All patients were men whose ages arranged from 60 to 89 years with a mean of 74.2 years. Twenty rounded atelectasis were present in the right lung and 5 in the left lung. Five patients had 2 rounded atelectasis. In 21 rounded atelectasis were found in Segment 10 and while other 2 found in S1 and each in S5 and 9. Eleven patients were diagnosed with no symptoms through medical examinations. Other 8 patients complained of dyspnea, chest pain and cough. Thirteen patients complicated with benign asbestos pleurisy and only 3 patients accompanied asbestosis. Eighteen patients (95%) displayed pleural plaques and 15 patients with calcified plaques. Ten patients had been exposed to asbestos in the shipyards and 4 in construction works and other 5 patients had also exposed by occupational exposure to asbestos. The mean period of exposure to asbestos was 26.6 years and the mean latency periods from the first asbestos exposure to the diagnosis of rounded atelectasis were 51.6 years. An autopsied patient had 18,100 asbestos bodies per 1 g of dry lung tissue which meant the heavy asbestos exposure. High incidence of pleural plaques and long period of latency from the first exposure to the appearance of rounded atelectasis in this study suggested that rounded atelectasis might appear less high-dose exposure to asbestos than former patients who were reported 6 years ago.
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PMID:[Evaluation of rounded atelectasis induced by exposure to asbestos]. 1893 12

Idiopathic pulmonary fibrosis (IPF) is a specific form of chronic interstitial lung pneumonia associated with the histologic pattern of usual interstitial pneumonia (UIP). Although UIP is a distinct histologic lesion, this histologic pattern is not specific for IPF and can also be found in other diseases (e.g., connective tissue disease and asbestosis). Clinical features of IPF include progressive cough, dyspnea, restrictive ventilatory defect, and progressive fibrosis and destruction of the lung parenchyma. IPF is rare (13-42 cases/100,000), and primarily affects older adults (>50 years of age). The diagnosis of IPF often requires surgical lung biopsy, but the diagnosis can be affirmed with confidence in some patients provided the results of computed tomographic (CT) scans and clinical features are consistent. The clinical course is variable, but inexorable progression (typically over months to years) is typical. Mean survival from the onset of symptoms approximates 3 to 5 years. Medical treatment is only modestly effective, primarily by slowing the rate of disease progression. Lung transplantation is the best therapeutic option.
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PMID:Idiopathic Pulmonary Fibrosis: Epidemiology, Clinical Features, Prognosis, and Management. 2723 59


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