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Original Report |
1 Department of Radiology and Center for Imaging Science, Samsung Medical
Center, Sungkyunkwan University School of Medicine, 50, Ilwon-Dong,
Kangnam-Ku, Seoul 135-710, Korea.
2 Division of Pulmonary and Critical Care Medicine, Department of Medicine,
Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul
135-710, Korea.
3 Department of Diagnostic Pathology, Samsung Medical Center, Sungkyunkwan
University School of Medicine, Seoul 135-710, Korea.
4 Department of Radiology, Soonchunhyang University Bucheon Hospital, Bucheon,
Kyungki-Do 420-853, Korea.
Received March 30, 2004;
accepted after revision May 11, 2004.
Address correspondence to K. S. Lee
(kyungs.lee{at}samsung.com).
Abstract
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CONCLUSION. GIP appears on high-resolution CT as ground-glass and irregular linear opacities in both lungs. These CT findings correspond histopathologically to areas of interstitial thickening caused by fibrosis and inflammatory cell infiltration and to areas of intraalveolar accumulation of macrophages and multinucleated giant cells.
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All patients had experienced coughing and dyspnea on exertion for periods ranging from 1 month to 5 years (mean, 20 months). One patient worked in a chemical laboratory in a fertilizer plant and had handled benzene and toluene for 22 years, another had worked in a tungsten alloy company for 20 years, the third had worked in a saw manufacturing company for 15 years, and the fourth had worked as a coal worker for 8 years. Three of the four patients were smokers (range of tobacco use, 15-45 pack years; mean, 27 pack years). Pulmonary function tests showed a mild reduction in carbon monoxide diffusing capacity in two patients, moderate reduction in one, and severe reduction in one. A mixed obstructive and restrictive pattern was seen in one patient, and a restrictive pattern, in another. In the remaining two patients, the spirometric flow-volume curve showed a normal pattern.
Chest radiographs and CT scans were available for all patients. Follow-up chest radiographs were available for two patients (with follow-up periods of 33 months and 24 months). Posteroanterior chest radiographs were obtained using a computed radiography system (FCR 9501, Fuji) (120 kVp; nominal focus, 0.6 or 1.2 mm; film-focus distance, 183 cm; oscillating grid, 12:1; exposure, phototimed). Observers assessed the presence of reticular opacities, nodules, ground-glass opacities, and air-space consolidation on radiographs. For the purposes of analysis, each lung was divided into upper and lower zones. Lesions were considered to be in the upper lung zone if located cephalad to the hilum, the lower lung zone if located caudad to the hilum, or random if located in both zones. In patients whose follow-up radiographs were available, changes in the extent of parenchymal lesions were assessed.
CT scans were obtained using a HiSpeed Advantage scanner (GE Healthcare).
High-resolution CT scans were obtained throughout the thorax with 1-mm
collimation at 10-mm intervals. Image data were reconstructed using bone
algorithms. Images were printed with both lung (width, 1500 H; level,
–700 H) and mediastinal (width, 400 H; level, 20 H) window settings. The
scanning parameters used were 120 kVp and 170
200 mA.
Two thoracic radiologists reached decisions on CT findings by consensus. CT images were reviewed for the presence of ground-glass opacities, irregular linear opacities, honeycombing, consolidation, nodules, emphysema, associated pulmonary abnormalities, mediastinal lymphadenopathy, and pleural effusion. If present, the extent and distribution of each pattern of parenchymal abnormality were recorded. The extent of each pattern was semiquantified visually to the nearest 5% of lung volume by estimating the percentage of the whole lung volume involved by the abnormality. Distributions were classified as central, subpleural, random, or diffuse in the transverse plane and as upper, lower, random, or diffuse in the cephalocaudal plane. Honeycombing was diagnosed if the air space was cystic, with a diameter of approximately 0.3-1.0 cm (but as large as 2.5 cm), usually subpleural, and characterized by thick well-defined walls. Nodules were classified as small if their diameter was 10 mm or less or as large if their diameter ranged from larger than 10 mm through 30 mm. Interlobular septal thickening, when present, was classified as smooth or nodular.
Patterns (ground-glass or irregular linear opacity; consolidation; small, poorly defined centrilobular nodule; and emphysema) of lung lesions on high-resolution CT at the site of the video-assisted thoracoscopic surgery and open lung biopsy were compared with the microscopic structures of the histopathologic specimens by one chest radiologist and by the pathologist who evaluated all pathologic specimens. CT-pathologic correlations were feasible because biopsy sites were chosen on the basis of high-resolution CT findings. A metallic analysis was performed on the surgical specimen from one patient.
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On high-resolution CT, the most common findings were ground-glass opacities and irregular linear opacities (Figs. 1A, 1B, 1C, 1D, 1E, 2A, 2B, and 2C), both of which were seen in all patients. Ground-glass opacities, which always appeared as a mixed pattern with irregular linear opacities, showed lower lung zone predominance in the cephalocaudal plane in two patients and random distribution in the remaining two. It showed a random distribution in transverse plane in three patients and a subpleural distribution in the remaining patient. The extent of ground-glass opacities, involvement ranged from 15% to 75% of lung volume (mean, 44%). Irregular linear opacities, seen in both lungs always as a mixed pattern with ground-glass opacity, were present in lower lung zone and showed subpleural predominance (n = 4). The extent of involvement ranged from 5% to 20% of lung volume (mean, 13%). Honeycombing (Figs. 2A, 2B, and 2C) was seen in one patient. The honeycombing was bilateral, subpleural, and located in the lower lung zone; it occupied 10% of lung volume. Small centrilobular nodules were present in one patient and were bilateral, subpleural, and located in both the upper and lower lung zones; they involved less than 1% of lung volume. Extensive pulmonary emphysema involving approximately 40% of the lung volume was observed in one patient.
Histopathologic examinations of pathologic specimens, obtained from the areas that on high-resolution CT showed ground-glass and irregular linear opacities, found interstitial thickening caused by fibrosis and mononuclear inflammatory cell infiltration. These findings were accentuated around the peribronchiolar interstitium, and the accumulation of macrophages and multinucleated giant cells was noted in alveolar spaces (Figs. 1A, 1B, 1C, 1D, and 1E). In one patient in whom honeycombing was observed on high-resolution CT, areas of interstitial fibrosis and cysts with dense fibrotic wall also were found. In another patient, several small bronchiolocentric microfibrotic nodules with surrounding emphysema were noted.
Pathologic specimens contained concentrations of metals that were at least 10 times greater than those of standard values found in the lungs of control subjects (i.e., aluminum, 225.8 µg/g, cobalt, 0.3 µg/g, chromium, 93.3 µg/g, and magnesium, 444 µg/g). The concentrations were determined by atomic absorption spectrophotometry or ionic coupled plasma emission spectrometry.
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The diagnostic criteria for hard-metal lung disease include a history of exposure to metal dust; characteristic clinical features of shortness of breath, cough, and dyspnea on exertion over a prolonged period; radiologic findings of interstitial lung disease; histologic findings of interstitial lung disease (a GIP pattern; presence of a large number of giant cells filling the air spaces and thickening of the interstitium and alveolar walls by mononuclear cells); and a pathologic finding of constituents of metal in lung tissue [6].
The histopathologic manifestations of hard-metal disease range from bronchitis to subacute fibrosing alveolitis to interstitial fibrosis [2]. Obliterative bronchiolitis is reportedly the earliest manifestation of hard-metal disease. Subacute fibrosing alveolitis is characterized by desquamation of epithelial cells and accumulation of macrophages and multinucleated giant cells in alveolar spaces, which develop within a few years of hard-metal exposure, whereas chronic diffuse mural fibrosis with honeycombing can occur either a few or many years after exposure [7]. Pathologic specimens showed subacute fibrosing alveolitis accompanied by a variable degree of interstitial fibrosis in three of our patients and chronic mural fibrosis in one. In the patient with mural fibrosis, chronic interstitial fibrosis and honeycombing predominated, with findings of subacute fibrosing alveolitis.
Kakugawa et al. [3] observed diffuse ground-glass opacities in both lungs with lower lung zone predominance associated with enlarged mediastinal lymph nodes on CT in a patient with GIP, and microscopic examination of lung biopsy specimens revealed marked cellular interstitial infiltration and prominent intraalveolar macrophages and giant cells. Akira [8] described high-resolution CT findings of hard-metal pneumoconiosis in two patients and observed bilateral consolidation or ground-glass opacities associated with parenchymal distortion. The typical honeycomb appearance was not found, rather patients showed traction bronchiectasis and bronchiolectasis in areas of intense lung attenuation. According to Akira's description, the areas of consolidation corresponded to areas of marked intraalveolar desquamation, intramural mononuclear cell infiltrate, and multinucleated giant cells. Although consolidation was not seen in our patients, irregular linear opacities were observed in all patients and honeycombing was seen in one patient. In our study, main patterns of parenchymal abnormalities were ground-glass and irregular linear opacities, which were noticed in all patients. These patterns of abnormalities are similar to those of other idiopathic interstitial pneumonias including idiopathic pulmonary fibrosis and nonspecific interstitial pneumonia [5]. Therefore, meticulous history taking on the occupational history of patients is important for the diagnosis of GIP.
Recent studies have suggested that most GIP cases are caused by exposure to metals and their derivatives, such as cobalt and tungsten carbide [2]. Animal models have shown the development of pulmonary fibrosis after the intratracheal instillation of cobalt. Although tungsten carbide alone is not believed to play a crucial role in interstitial pneumonia, the combination of cobalt and tungsten carbide may be worse than cobalt alone [9]. It has also been noted that cobalt and tungsten carbide interact with oxygen, resulting in the augmented production of toxic activated oxygen species [10].
However, the mechanism by which exposure to metal causes GIP is unknown. Moreover, a few confirmed cases of GIP in unexposed individuals have been reported [3, 11]. Two of four of our patients had a history of apparent exposure to metals, but two patients did not. The patient who worked as a coal miner showed a histopathologically overt GIP pattern. Another patient without a history of metal exposure had been exposed to solvents like benzene and toluene for 22 years while working in a chemical laboratory in a fertilizer plant. In addition, his workplace contained many pipelines that had been coated with insulating materials. As in the case of the coal miner, the histopathologic findings in this patient were consistent with metal-induced pneumoconiosis with associated pulmonary asbestosis. In this particular patient, biopsy specimen tissue analysis showed concentrations of metals that were at least 10 times greater than standard values found in normal lungs [12].
Our study is limited by the small number of patients involved. Therefore, our results cannot be taken to be representative of GIP.
In summary, GIP appears on high-resolution CT scans as ground-glass and irregular linear opacities. These findings represent histopathologically interstitial thickening caused by interstitial fibrosis and inflammatory cell infiltration, and intraalveolar accumulation of macrophages and multinucleated giant cells found at pathologic examination.
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