Giant Cell Interstitial Pneumonia In Native, Transplanted And Re-Transplanted Lungs 8 Years Apart Without Known Hard Metal Exposure.

Pneumoconioses are a group of non-neoplastic pulmonary disorders caused by inhaled inorganic particles. Well-described pneumoconioses include asbestosis, silicosis, coal worker's pneumoconiosis, chronic beryllium disease, and hard metal lung disease. Giant cell interstitial pneumonia (GIP) is a distinctive and rare pneumoconiosis most frequently found in workers exposed to hard metals, primarily cobalt and tungsten carbide. The pathologic picture is considered virtually pathognomonic for hard metal lung disease, although this dogma has been questioned by a few reports of giant cell interstitial pneumonia in patients without apparent hard metal exposure. Giant cell interstitial pneumonia is even rarer in lung transplant recipients. Here, we present a patient without known hard metal exposure who was found to have persistent giant cell interstitial pneumonia in native, transplanted and re-transplanted lungs 8 years apart.

Cobalt-related interstitial lung disease or hard metal lung disease: A case series of Chinese workers.

Hard metal lung disease (HMLD) is rarely diagnosed and is caused by the occupational inhalation of hard metal dust, mainly cobalt. The diagnosis of HMLD is based on a thorough occupational dust exposure combined with clinical-radiological-histological findings. We present a series of four Chinese workers who had occupational exposure to cobalt acid lithium or cobalt and tungsten dust. Four patients all complained of intermittent cough, chest tightness, or shortness of breath on exertion. High-resolution computed tomography scans presented bilateral ground-glass attenuation, consolidations, and/or reticular opacities with diffuse small nodules. Histologic findings showed that interstitial inflammation and fibrotic lesions distributed peribronchioles. The infiltrations by macrophages as well as visible multinucleated giant cells indicated giant cell interstitial pneumonia (GIP). Cobalt was detectable in the lung tissues of two patients measured by inductively-coupled plasma mass spectrometry. The first patient was diagnosed with cobalt-related interstitial lung disease (ILD), while the others were HMLD. GIP is the classic pathology of cobalt-related ILD or HMLD. One of the patients showed spontaneous remission after the cessation of exposure, while the other three recovered within 6-32 weeks after avoiding occupational exposure and using corticosteroids. At follow-up, all four patients showed no recurrence. A multidisciplinary diagnostic panel including occupational cobalt exposure evaluation is beneficial to recognize cobalt-related ILD or HMLD and to indicate the necessity of prevention.

Interstitial lung abnormality (ILA) and nonspecific interstitial pneumonia (NSIP).

This review article aims to address mysteries existing between Interstitial Lung Abnormality (ILA) and Nonspecific Interstitial Pneumonia (NSIP). The concept and definition of ILA are based upon CT scans from multiple large-scale cohort studies, whereas the concept and definition of NSIP originally derived from pathology with evolution to multi-disciplinary diagnosis. NSIP is the diagnosis as Interstitial Lung Disease (ILD) with clinical significance, whereas only a part of subjects with ILA have clinically significant ILD. Eventually, both ILA and NSIP must be understood in the context of chronic fibrosing ILD and progressive ILD, which remains to be further investigated.

Unusual pneumoconiosis in two patients with heavy print toner, and paper dust exposure.

Workers in a print shop are exposed to photocopier toner dust and paper dust over a prolonged period of time. However, there are only rare case reports of toner and paper dust induced lung damage in humans. We reviewed our consultation files for a period of 30 years from 1987 to 2018 to look for cases with a diagnosis of giant cell interstitial pneumonia (GIP), printer toner exposure and paper dust exposure resulting in lung disease. There were two cases which met our inclusion criteria. Slides, clinical histories and imaging were reviewed. Both the patients had worked in print shops, and had no history of exposure to hard metals. Patient 1 presented with shortness of breath and cough over several months, while patient 2 was asymptomatic at presentation. Both the patients underwent surgical lung biopsies. Histopathologic examination from both the cases showed a spectrum of pathology, including features of GIP, desquamative interstitial pneumonia, chronic bronchiolitis with lymphoid hyperplasia, and particulate matter consistent with toner. Energy dispersive spectroscopy was performed on one case, and it revealed no cobalt or tungsten particles. The unusual combination of findings is very suggestive that toner particles with or without paper dust exposure were responsible for the pathologic changes in the lungs of these patients. This possibility should be explored further with additional patients who work in print shops where they are exposed to paper dust and paper toner and have signs or symptoms of diffuse lung disease.

A case series describing common radiographic and pathologic patterns of hard metal pneumoconiosis.

INTRODUCTION: Hard metal pneumoconiosis is a rare but serious disease of the lungs associated with inhalational exposure to tungsten or cobalt dust. Little is known about the radiologic and pathologic characteristics of this disease and the efficacy of treating with immunosuppression. OBJECTIVE: We describe the largest cohort of patients with hard metal pneumoconiosis in the literature, including radiographic and pathologic patterns as well as treatment options. METHODS: We retrospectively identified patients from the University of Pittsburgh pathology registry between the years of 1985 and 2016. Experts in chest radiology and pulmonary pathology reviewed the cases for radiologic and pathologic patterns. RESULTS: We identified 23 patients with a pathologic pattern of hard metal pneumoconiosis. The most common radiographic findings were ground glass opacities (93%) and small nodules (64%). Of 20 surgical biopsies, 17 (85%) showed features of giant cell interstitial pneumonia. Most patients received systemic corticosteroids and/or steroid-sparing immunosuppression. CONCLUSIONS: Hard metal pneumoconiosis is characterized predominately by radiographic ground glass opacities and giant cell interstitial pneumonia on histopathology. Systemic corticosteroids and steroid-sparing immunosuppression are common treatment options.

Occupational hard metal lung disease: a case report / 中国职业医学

OBJECTIVE: To report the clinical manifestations,chest imaging,pathological changes,diagnosis and treatment on one case of hard metal lung disease( HMLD).METHODS: The occupational history,clinical manifestations,chest computed tomography and lung histopathological examinations of a case with pathologically confirmed HMLD were summarized.RESULTS: The patient began to cough and have dyspnea on exertion after 7 years of hard metal dust exposure of cobalt and tungsten, and pulmonary function test showed a restrictive ventilation dysfunction.Chest computed tomography showed bilateral areas of diffuse lesions,including ground-glass attenuation,areas of consolidation,diffuse small nodules, extensive reticular opacities and traction bronchiectasis.The lung histopathological changes include macrophage interstitial pneumonia,which is macrophages and a large number of multinucleated giant cells in the alveolar space.CONCLUSION: A clear history of hard metal dust exposure and the pathological examination of lung tissue are helpful for the diagnosis of HMLD.

Giant cell interstitial pneumonia in patients without hard metal exposure: analysis of 3 cases and review of the literature.

Giant cell interstitial pneumonia is a rare lung disease and is considered pathognomonic for hard metal lung disease, although some cases with no apparent hard metal (tungsten carbide cobalt) exposure have been reported. We aimed to explore the association between giant cell interstitial pneumonia and hard metal exposure. Surgical pathology files from 2001 to 2004 were searched for explanted lungs with the histopathologic diagnosis of giant cell interstitial pneumonia, and we reviewed the associated clinical histories. Mass spectrometry, energy-dispersive x-ray analysis, and human leukocyte antigen typing data were evaluated. Of the 455 lung transplants, 3 met the histologic criteria for giant cell interstitial pneumonia. Patient 1 was a 36-year-old firefighter, patient 2 was a 58-year-old welder, and patient 3 was a 45-year-old environmental inspector. None reported exposure to hard metal or cobalt dust. Patients 1 and 2 received double lung transplants; patient 3 received a left single-lung transplant. Histologically, giant cell interstitial pneumonia presented as chronic interstitial pneumonia with fibrosis, alveolar macrophage accumulation, and multinucleated giant cells of both alveolar macrophage and type 2 cell origin. Energy-dispersive x-ray analysis revealed no cobalt or tungsten particles in samples from the explanted lungs. None of the samples had detectable tungsten levels, and only patient 2 had elevated cobalt levels. The lack of appropriate inhalation history and negative analytical findings in the tissue from 2 of the 3 patients suggests that giant cell interstitial pneumonia is not limited to individuals with hard metal exposure, and other environmental factors may elicit the same histologic reaction.

Elemental analysis of occupational and environmental lung diseases by electron probe microanalyzer with wavelength dispersive spectrometer.

Occupational and environmental lung diseases are a group of pulmonary disorders caused by inhalation of harmful particles, mists, vapors or gases. Mineralogical analysis is not generally required in the diagnosis of most cases of these diseases. Apart from minerals that are encountered rarely or only in specific occupations, small quantities of mineral dusts are present in the healthy lung. As such when mineralogical analysis is required, quantitative or semi-quantitative methods must be employed. An electron probe microanalyzer with wavelength dispersive spectrometer (EPMA-WDS) enables analysis of human lung tissue for deposits of elements by both qualitative and semi-quantitative methods. Since 1993, we have analyzed 162 cases of suspected occupational and environmental lung diseases using an EPMA-WDS. Our institute has been accepting online requests for elemental analysis of lung tissue samples by EPMA-WDS since January 2011. Hard metal lung disease is an occupational interstitial lung disease that primarily affects workers exposed to the dust of tungsten carbide. The characteristic pathological findings of the disease are giant cell interstitial pneumonia (GIP) with centrilobular fibrosis, surrounded by mild alveolitis with giant cells within the alveolar space. EPMA-WDS analysis of biopsied lung tissue from patients with GIP has demonstrated that tungsten and/or cobalt is distributed in the giant cells and centrilobular fibrosing lesion in GIP. Pneumoconiosis, caused by amorphous silica, and acute interstitial pneumonia, associated with the giant tsunami, were also elementally analyzed by EPMA-WDS. The results suggest that commonly found elements, such as silicon, aluminum, and iron, may cause occupational and environmental lung diseases.

A Case of Giant Cell Interstitial Pneumonia without History of Exposure to Hard Metal / 결핵

A 44 year old man was admitted complaining of exertional dyspnea. The patient denied denied any occupational history of hard metal exposure. Chest radiography showed an increased interstitial marking at the peripheral po rtion of both lower lung fields. The spirometric values were within the normal ranges. However, the diffusion capacity of the lungs was lower. In the bronchial lavage fluid, the characteristic multinucleated giant cells were noticed, and the macrophage compartment was 96% and the neutrophils were 4%. Highresolution CT scan revealed ground glass opacities with emphysematous lung changes at the peripheral portion of the whole lung. An open lung biopsy confirmed the presence of numerous multinucleated giant cells (Define GIF) with an associated interstitial fibrosis throughout the lung. The radiographic abnormalities and symptoms subsequently improved following treatment with oral corticosteroids.

A Case of Giant Cell Interstitial Pneumonia without History of Exposure to Hard Metal / 결핵

A 44 year old man was admitted complaining of exertional dyspnea. The patient denied denied any occupational history of hard metal exposure. Chest radiography showed an increased interstitial marking at the peripheral po rtion of both lower lung fields. The spirometric values were within the normal ranges. However, the diffusion capacity of the lungs was lower. In the bronchial lavage fluid, the characteristic multinucleated giant cells were noticed, and the macrophage compartment was 96% and the neutrophils were 4%. Highresolution CT scan revealed ground glass opacities with emphysematous lung changes at the peripheral portion of the whole lung. An open lung biopsy confirmed the presence of numerous multinucleated giant cells (Define GIF) with an associated interstitial fibrosis throughout the lung. The radiographic abnormalities and symptoms subsequently improved following treatment with oral corticosteroids.

A Case of Giant Cell Interstitial Pneumonia / 결핵

Giant cell interstitial pneumonia, a synonym of (for) hard metal pneumoconiosis, is a unique form of pulmonary fibrosis resulting from an exposure to hard metal dust. A case of biopsy-proved giant cell interstitial pneumonia in the absence of appropriate history of exposure to hard metal dust is reported. The patient presented with clinical features of chronic interstitial lung disease or idiopathic pulmonary fibrosis. He worked in a chemical laboratory at a fertilizer plant(,)where he had been exposed to various chemicals such as benzene and toluene. He denied having any other hobby in his house or job at work which may have exposed him hard metal dust(.) High-resolution CT scan revealed multi-lobar distribution of ground glass opacity with peripheral and basal lung predominance. The retrieved fluid of bronchoalveolar lavage contained asbestos fiber and showed neutrophil predominance. Surgical lung biopsy was performed for a definite diagnosis. Lung specimen showed alveolar infiltration of numerous multinucleated giant cells with mild interstitial fibrosis. Upon detailed examination of the lung tissue, one asbestos body was found. An analysis for mineral contents in lung tissue was performed. Compared to with the control specimen, the amount of cobalt and several hard metal components in the lung tissue of this patient was ten times higher. We speculated that the inconsistency between occupational history and the findings of pathologic and mineralogical analyses could be explained by the difference in individual immunologic reactivity to hard metal dust despite the relatively small amount of unrecognized environmental exposure (ED: It's hard to understand what this phrase is trying to say).