Magnetic resonance appearance of asbestos-related benign and malignant pleural diseases. (1/296)

OBJECTIVES: This study describes the magnetic resonance findings of benign and malignant pleural diseases in asbestos-exposed subjects. METHODS: Thirty patients with a history of asbestos exposure and pleural lesions in chest X-rays and computed tomography scans were examined with a 0.5- and a 1.5-T magnetic resonance unit. The examination protocol included cardiac-gated proton density and T2-weighted images, unenhanced and enhanced (Gd-DTPA; 0.1 mmol/ kg) T1-weighted images in the axial plane and sometimes in another orthogonal plane (sagittal or coronal or both). All the magnetic resonance images were reviewed by 3 experienced observers, who visually evaluated morphologic features, signal intensity, and contrast enhancement of pleural lesions. The diagnosis was established by means of percutaneous biopsy, thoracotomy, and combined clinical and radiological follow-up for at least 3 years. RESULTS: Eighteen patients affected with multiple pleural plaques showed low signal intensity on both unenhanced and enhanced T1-weighted and proton density and T2-weighted images. In 2 of these patients an acute pleural effusion was observed. All the malignant lesions (11 mesotheliomas) and a solitary benign pleural plaque revealed high signal intensity on the proton density and T2-weighted images and inhomogeneous contrast enhancement in the postcontrast T1-weighted images. The sensitivity, specificity, and diagnostic accuracy of the magnetic resonance imaging in classifying a lesion as suggestive of malignancy were 100%, 95% and 97%, respectively. CONCLUSIONS: The results point out 2 magnetic resonance signal intensity patterns for asbestos-related pleural lesions: (i) low-signal intensity on unenhanced and enhanced T1-weighted and proton density and T2-weighted images for benign plaques and (ii) nonhomogeneous hyperintensity in T2-weighted and enhanced T1-weighted images for malignant mesotheliomas.  (+info)

Suction curettage for removal of retained intrathoracic blood clots and pleural lesions. (2/296)

OBJECTIVE: To develop a thoracoscopic technique for correcting and/or removing an intrathoracic disease process using our existing operating room equipment and without a "small thoracotomy." METHODS AND PROCEDURES: Fifty-eight patients from October 1994 to April 1998 were prospectively studied. All were undergoing procedures involving the removal of a suspected benign (or infectious) pleural process or a retained blood clot. Three or four thoracic ports were used in all cases. Straight and curved suction curettage cannulae (with finger valve attachment) ranging from 8 to 16 French were available for use. Intermittent variable suction (between zero and 60 mm Hg) was used in all cases. Dependent upon the size and adherence of the lesion to be removed, the pressure was determined by the surgeon and regulated by the circulating nurse in the room. In each case, a trap system was used for retrieval of the specimen. One lung ventilation was used in every case, and when suction was used one of the ports was kept "open" to allow room air to enter the chest cavity. RESULTS: All patients in our series had their procedures completed without the need for any kind of open thoracotomy. Pre and postoperative diagnosis concurred in all 10 patients, and no complications occurred (specifically, no injury to the lung tissue or chest wall structures). Operative time ranged from 45 minutes to 180 minutes with a mean of 75 minutes. In all cases of a hemothorax, a cell saver system was used for an average of one unit of blood autotransfused per case. CONCLUSIONS: New techniques do not always require the purchase of new equipment. Tight hospital budgets are forcing surgeons to rely on redefining uses of instrumentation already available in solving surgical problems. We believe that the use of this instrumentation will provide another avenue for surgeons to successfully complete a procedure thoracoscopically without the need for a thoracotomy. It is through multidisciplinary conferences such as the Society of Laparoendoscopic Surgeons that ideas such as this are propagated.  (+info)

Increased serum concentrations of growth factor receptors and Neu in workers previously exposed to asbestos. (3/296)

OBJECTIVES: Epidermal growth factor receptor (EGFR) and oncogene Neu belong to a family of growth factor receptors which may play a part in carcinogenesis. Although increased serum concentrations of Neu and EGFR have been shown in several patients with asbestosis who later developed cancer, serum concentrations have not been studied in workers exposed in the past to asbestos but without asbestos related diseases. METHODS: Serum concentrations of secreted growth factor receptors were studied in 300 workers exposed in the past to asbestos and the results were compared with those of 70 controls. RESULTS: In the controls 4.3% (3/70) had EGFR values > 912 units/ml, compared with 39% (117/299) of the exposed group (p < 0.001). The difference in high values was even more pronounced for Neu with 4.3% of controls having Neu values > 2580 fmol/ml compared with 72% (216/299) of the exposed workers (p < 0.001). Pleural plaques predicted lower serum concentrations of EGFR but not lower Neu concentrations, and this finding remained significant after adjustment for age, exposure time, smoking, and time from initial exposure. CONCLUSIONS: Enhanced secretion of EGFR and Neu was found in a large cohort of retired asbestos workers with a wide range of exposure and latency periods. They did not have asbestosis or cancer and their EGFR values were higher in those without plaques. Further studies are needed to confirm our results, to determine the source of the secreted growth factor receptors, and to study their possible value as risk factors in the development of cancer.  (+info)

Carboxyterminal propeptide of type I procollagen in ELF: elevation in asbestosis, but not in pleural plaque disease. (4/296)

Markers of collagen metabolism may possibly be used in the assessment of pulmonary involvement in asbestosis-related pulmonary diseases. In this study the levels of the carboxyterminal propeptide of type I procollagen (PICP) and the aminoterminal propeptide of type III procollagen (PIIINP) were evaluated in bronchoalveolar lavage fluid (BALF), epithelial lining fluid (ELF) and serum from patients with asbestos related pulmonary and pleural involvement. Forty-two consecutive patients with occupational exposure to asbestos fibres, who underwent bronchoscopy and bronchoalveolar lavage (BAL) at the time of the diagnosis were investigated. Five patients were diagnosed as having asbestosis, while 37 showed no parenchymal involvement. Of the latter group, 25 had pleural plaques, while 12 had no detectable changes in chest radiographs. The patients were followed-up for an average of 7 yrs. The PICP in BALF and ELF was detectable in all patients with asbestosis and in 8/37 subjects without parenchymal involvement. The levels of PICP in BALF and ELF were significantly higher in the asbestosis group compared to the patients without asbestosis (9.8+/-1.8 microg x L(-1) versus 0.6+/-1.3 microg x L(-1), p<0.001 and 488.9+/-208.8 microg x L(-1) versus 22.6+/-50.6 microg x L(-1), p<0.001, respectively). Only 1 patient with asbestosis and 3 patients without parenchymal involvement had detectable levels of PIIINP in BALF. The serum levels of PICP and PIIINP did not differ between the patients with asbestosis and those with exposure to asbestos fibres without asbestosis and were within the normal range. None of the 37 patients exposed to asbestos fibres without parenchymal involvement at the baseline developed asbestosis during the follow-up period of 7 yrs. In conclusion, the data show that the carboxyterminal propeptide of procollagen type I, but not the aminoterminal propeptide of type III procollagen is highly elevated in bronchoalveolar lavage fluid and epithelial lining fluid in patients with asbestosis, but not in those without parenchymal involvement. This suggests that the determination of carboxyterminal propeptide of procollagen type I in bronchoalveolar lavage fluid could be used as a marker of parenchymal involvement in patients exposed to asbestos fibres.  (+info)

Familial extensive idiopathic bilateral pleural fibrosis. (5/296)

The authors report three sisters with bilateral isolated apical pleural fibrosis of unknown origin, which did not respond to empirical antituberculosis therapy and oral corticosteroids. The disease evolved in an unrelenting fashion producing pleural fibrosis at the lung bases and leading to the death of two sisters and to lung transplantation in the other one. There was no history of other familial disease or consanguinity. The particular features of these cases and the differences from other reports of apparently cryptogenic pleural fibrosis are outlined.  (+info)

Mortality due to asbestos-related causes among railway carriage construction and repair workers. (6/296)

The objective of this study was to further clarify the cancer risk associated with asbestos exposure in railway carriage construction and repair. The cohort included 734 subjects employed between 1 January 1945 and 31 December 1969. Vital status was ascertained at 31 December 1997. Mortality was investigated in the time span 1970-97. Forty-two subjects (6%) were lost to follow-up and eight causes of death (4%) could not be ascertained. The overall mortality was not above the expected value. Among neoplastic diseases, excesses were observed for lung standardized mortality ratio (SMR) = 124; 90% confidence interval (CI) = 87-172; 26 obs), pleura (SMR = 1,327; CI = 523-2,790; 5 obs), larynx (SMR = 240; CI = 95-505; 5 obs), liver (SMR = 241; CI = 126-420; 9 obs), pancreas (SMR = 224; CI = 98-443; 6 obs) and multiple myeloma (SMR = 429; CI = 117-1,109; 3 obs). The observed excess of lung and pleural neoplasms can be causally related to asbestos exposure in the manufacture of railway carriages. A causal role of asbestos exposure in the raised SMRs from laryngeal and pancreatic neoplasms and multiple myeloma cannot be conclusively proven.  (+info)

High-resolution computed tomography in cases with environmental exposure to asbestos in Turkey. (7/296)

BACKGROUND AND OBJECTIVES: Although all parts of the lung can be affected as a consequence of asbestos exposure, most CT protocols tend to scan only the middle and lower parts of the thorax. The aim of this study was to investigate parenchymal and pleural lesions of persons exposed to environmental asbestos, using a high-resolution computed tomography (HRCT) protocol scanning the whole thorax. METHODS: We analyzed the chest radiographs and HRCT scans of 26 patients who presented bilaterally with multiple pleural plaques related to environmental asbestos exposure. RESULTS: Twenty-four cases (92%) had an abnormal HRCT suggestive of asbestosis. Apart from common HRCT changes related to asbestosis, we detected apical pleural thickening (APT) in 9 cases as well as a coarse honeycomb pattern adjacent to APT in 7 of these cases. Cavitary lesions due to pulmonary tuberculosis were observed on HRCT scans from 4 patients in total. Neither apical pulmonary fibrosis nor cavitary lesions were visible on chest radiographs. CONCLUSIONS: We suggest that the HRCT protocol for examining asbestos-exposed individuals with pleural plaques on chest X-rays should include the whole thorax, since the asbestos-related pathologies may involve all parts of the lung.  (+info)

Pulmonary calcifications: a review. (8/296)

Pulmonary calcification is a common asymptomatic finding, usually discovered on routine chest X-ray or at autopsy. Pulmonary calcifications are caused mainly by two mechanisms: the dystrophic form and the metastatic form (1). Despite the different aetiologies, the pulmonary function and clinical manifestations are quite similar in both forms. We present a review of the clinical and radiology findings of the different aspects of pulmonary calcifications according to its pathogenesis and its anatomic distribution: parenchymal, lymphe node and pleural.  (+info)