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Query: UMLS:C0018801 (heart failure)
 72,216 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The radiological manifestations of asbestos-related visceral pleural changes are described. Generally, visceral pleural reactions follow the mesothelial cells response to various injurious substances, including asbestos, and even saline. The changes are nonspecific. They may occur subsequent to pleural reactions associated with many conditions, which include tuberculosis, viral pleurisy, malignancy and lymphoma, lupus, or rheumatoid-induced effusions, cardiac failure, and pulmonary embolism, among other etiologies. The failure to absorb the fibrinous exudate on the visceral pleural surface can lead to the development of diffuse fibrosis of the serosal surface, interlobar pleural thickening, localized pleural filaments (strands), subpleural wedge, and lenticular-shaped masses, and could be the forerunner of lobular atelectasis (pseudotumor) formation. Some of the features are recognized on posteroanterior chest radiographs and the counterparts corroborated with the use of routine and high-resolution computed tomography studies.
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PMID:Radiological features of asbestos-related visceral pleural changes. 200 21

Between April 1985 and July 1989, 125 cases with pleural effusion were admitted to our department. The causes of pleural effusion were carcinomatous pleurisy in 47 cases, infection without tuberculosis in 34 cases, tuberculous pleurisy in 17 cases, cardiac insufficiency and hypoproteinemia in 11 cases, trauma and pneumothorax in nine cases, collagen disease in two cases and unknown origin in five cases. Carcinomatous pleurisy and tuberculous pleurisy, the differential diagnosis of which is very important, comprised 37% and 14% of all cases, respectively. These diseases can be definitively diagnosed by pleural biopsy, effusion cytology and/or effusion culture. In July 1987, we introduced thoracoscopy to improve the ratio of definitive diagnoses. The ratio for carcinomatous pleurisy in the previous term, when thoracoscopy was not being used, was 59%, while that in the latter term, when it was used, was 73%. The ratio for all cases with tuberculous pleurisy was 47%. Prior to June 1987, pleural biopsies in our department were performed with a Cope needle. Using that procedure, a low positive ratio of 50% was obtained. For thoracoscopic pleural biopsies, a high positive ratio of 84% was achieved (in carcinomatous pleurisy, 13 out of 15 cases; in tuberculous pleurisy, three out of four cases). This procedure was performed with minimal patient discomfort and no serious complications. Therefore, thoracoscopic pleural biopsy is recommended as a diagnostic procedure for cases with pleural effusion.
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PMID:[The role of thoracoscopy in pleural biopsy in cases with pleural effusion]. 221 27

The authors report a case of bilateral hilar lymphoma of sarcoid origin associated with a pleural effusion. With the exception of pneumothorax, the pleural manifestations in the course of sarcoidosis amount to 115 published cases, including 49 with histopathological proof enabling us to speak of a pleural sarcoidosis. When the histopathological diagnosis is missing, it is preferable to speak of sarcoidotic pleurisy: the aetiopathogenesis in this case is venous obstruction and/or lymphatic obstruction by sarcoid involved lymph nodes. Exceptionally, it could be due to heart failure due to the fibrotic stage of sarcoidosis or to an autonomous sarcoidotic myocarditis.
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PMID:[Pleurisy and sarcoidosis. Apropos of a case]. 665 55

Pleuritis or pleural effusion frequently develops in patients with pneumonia or heart failure. Most of these pleural changes regress without intrapleural intervention. The detailed mechanisms of the regression of the pleural changes in humans are not well documented. We studied the parietal pleura of nine patients with lung cancer and two patients with coronary artery disease by scanning electron microscopy (SEM). All patients had neither radiographic nor gross evidence of pleural disease but all had mixed surface alterations by SEM. Focal denudation of mesothelial cells was common. Deeper injuries exposed thick and thin interweaving collagen bundles. Patchy depositions of amorphous or crystallized fibrin covered normal and damaged pleural surfaces, frequently admixed with macrophages, red blood cells, and tissue debris. Reactive mesothelial cells appeared to proliferate over the fibrin. Our findings suggest that subclinical pleural alterations occur often in patients with pulmonary or cardiac diseases and that an intact pleural surface in those patients is restored mainly by the proliferation of reactive mesothelial cells.
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PMID:Subclinical surface alterations of human pleura. A scanning electron microscopic study. 777 1

The Norwegian composer Edvard Grieg (1843-1907) suffered from pleurisy at the age of 17 years. The tuberculosis infection later also involved his lungs and columna. Throughout his whole life, his health was impaired by a destroyed left lung and considerable deformity of his thoracic columna. As complications to these sequelae, he suffered from numerous respiratory infections. Later he developed combined lung and heart failure. Grieg was admitted, many times to different spas and sanatoria both in Norway and abroad. In addition he was treated by many different doctors, and several of them became his personal friends. In this article, the author presents some of these physicians, and briefly describes Edvard Grieg's health problems.
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PMID:[Edvard Grieg's health and his physicians]. 827 65

An 80-year-old man was admitted with recurrent asphyxiating pleurisy, first attributed to heart failure. During the recurrent episodes, the patient presented fever, signs of inflammation, no signs of heart failure, and subnormal cardiac function, prompting further investigations which disclosed that the patient was a homozygous carrier of the severe type of periodic disease mutation. The patient's age at symptom onset and the clinical features of this case of periodic disease are exceptional. These points emphasize the usefulness of available genetic tests in difficult diagnostic cases. It also reflects current difficulties in trying to establish correlations between genotype and phenotype in periodic disease.
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PMID:[Recurrent bilateral pleurisy in an 80-year-old man]. 1036 15

Tuberculosis (TB) pleural disease is complicated by extensive tissue destruction. Matrix metalloproteinase (MMP)-1 and -9 are implicated in immunopathology of pulmonary and central nervous system TB. There are few data on MMP activity in TB pleurisy. The present study investigated MMP-1, -2 and -9 and their specific inhibitors (tissue inhibitor of metalloproteinase (TIMP)-1 and -2) in tuberculous effusions, and correlated these with clinical and histopathological features. Clinical data, routine blood tests, and pleural fluid/biopsy material were obtained from 89 patients presenting with pleural effusions in a TB-endemic area. MMP-1, -2 and -9 were measured by zymography or western blot, and TIMP-1 and -2 by ELISA. Pleural biopsies were examined microscopically, cultured for acid-alcohol fast bacilli and immunostained for MMP-9. Tuberculous pleural effusions contained the highest concentrations of MMP-9 compared with malignant effusions or heart failure transudates. MMP-9 concentrations were highest in effusions from patients with granulomatous biopsies: median (interquartile range) 108 (61-218) pg x mL(-1) versus 43 (12-83) pg x mL(-1) in those with nongranulomatous pleural biopsies. MMP-1 and -2 were not upregulated in tuberculous pleural fluid. The ratio of MMP-9:TIMP-1 was significantly higher in TB effusions. Tuberculous pleurisy is characterised by a specific pattern of matrix metalloproteinase-9 upregulation, correlating with the presence of granulomas and suggesting a specific role for matrix metalloproteinase-9 in inflammatory responses in tuberculous pleural disease.
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PMID:High MMP-9 activity characterises pleural tuberculosis correlating with granuloma formation. 1871 75

Acute pericarditis is usually a benign self-limiting condition, often of unexplained or viral aetiology, involving inflammation of the pericardial layers. It is often part of the differential diagnosis in patients admitted with acute chest pain and can be confused with acute myocardial infarction, acute pulmonary embolism and pleurisy. Occasionally it can result in cardiac tamponade and, if associated with myocarditis, in heart failure. This article sets out how to diagnose acute pericarditis, the common underlying causes, the possible treatment options and outcomes.
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PMID:The management of acute pericarditis. 2165 16

Malignant pleural mesothelioma (MPM) is a highly aggressive neoplasm primarily arising from surface serosal cells of the pleura and is strongly associated with asbestos exposure. Patients with MPM often develop pleural fluid as initial presentation. However, cytological diagnosis using pleural fluid is usually difficult and has limited utility. A useful molecular marker for differential diagnosis particularly with lung cancer (LC) is urgently needed. The aim of the present study was to investigate the diagnostic value of soluble mesothelin-related protein (SMRP) in pleural fluid. Pleural fluids were collected from 23 patients with MPM, 38 with LC, 26 with benign asbestos pleurisy (BAP), 5 with tuberculosis pleurisy (TP) and 4 with chronic heart failure (CHF), and the SMRP concentration was determined. All data were analyzed by using non-parametric two-sided statistical tests. The median concentration of SMRP in MPM, LC, BAP, TP and CHF were 11.5 (range 0.90-82.80), 5.20 (0.05-36.40), 6.65 (1.45-11.25), 3.20 (1.65-6.50) and 2.03 (1.35-2.80) nmol/l, respectively. The SMRP concentration was significantly higher in MPM than in the other diseases (P=0.001). The area under the ROC curve (AUC) values of the MPM diagnosis was 0.75 for the differential diagnosis from the other groups. Based on the cut-off value of 8 nmol/l, the sensitivity and specificity for diagnosis of MPM were 70.0 and 68.4%, respectively. These results indicate that the SMRP concentration in pleural fluid is a useful marker for the diagnosis of MPM.
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PMID:Soluble mesothelin-related protein in pleural effusion from patients with malignant pleural mesothelioma. 2299 44

Constrictive pericarditis is a rare and severe disease. A 37-year-old patient was admitted in the hospital for dyspnea, precordial pain, right-sided cardiac failure. Chest X-ray showed cardiac enlargement and an opacity suggestive for pleural effusion. Echocardiography revealed an adhesive-effusive-constrictive pericarditis, a very thickened pericardium and bilateral pleural effusion. After a pericardiectomy done to restore cardiac compensation and to identify etiological factors, a tuberculous pericarditis (TBP) was diagnosed. After surgery and starting anti-TB treatment, the patient presented altered clinical status, dyspnea, dry cough, fever and delayed callus formation at sternum level. Thoracic scan revealed mediastinal air collections, pericarditis and pleurisy. Thus, the TBP diagnosis was extended to mediastinal TB and anti-TB therapy was continued. After four months of treatment, another thoracic scan showed disappearance of the mediastinal air-leakage bubbles, multiple new micronodules in both lungs and lymph nodes of up to 15 mm; also increasing pericardial and pleural effusions. This case was interpreted as a TB treatment failure situation. A retreatment regimen was started, resulting in a slow favorable outcome. Pericardial TB is a rare condition, usually with delayed diagnosis and poor treatment benefits. Whenever possible, earlier diagnostic can contribute to better management of these cases.
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PMID:Tuberculous constrictive pericarditis complicated with tuberculous mediastinitis - case report. 2715 14


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