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Biomedical subjects

A Churg

Publications and source records attributed to A Churg.

At least 145 records · Page 8Linked to original sources
PubMed1985

Immunohistochemical staining for vimentin and keratin in malignant mesothelioma.

Because tissue culture studies have suggested that mesothelial cells might produce large amounts of vimentin, I stained eight mesotheliomas (two fixed in alcohol) for vimentin using the Gown and Vogel monoclonal antibody 43 beta E8. The two tumors that had alcohol fixed blocks were strongly positive for vimentin, whereas one of the tumors fixed only in formalin showed moderately strong staining and two others showed very weak focal positivity; the remaining tumors were negative. In the mesotheliomas that did stain, both epithelial and spindled elements gave a positive reaction. Three alcohol-fixed lung cancers and two blocks of alcohol-fixed pleura failed to stain for vimentin. By contrast, all mesotheliomas and carcinomas, whether alcohol or formalin fixed, as well as sections of pleura, were strongly positive when stained with anticytokeratin antibody 35 beta H11. I conclude that the combination of staining for vimentin and keratin might be a useful diagnostic finding in malignant mesothelioma, but that specially fixed material is required for reliable vimentin staining.

Antibodies, Monoclonal↗
PubMed1985

Severe diffuse small airways abnormalities in long term chrysotile asbestos miners.

To determine the nature and extent of pathological changes in the small airways induced by asbestos, the pathological lesions of fibrosis and pigmentation of the membranous and respiratory bronchioles and alveolar ducts in lungs obtained from necropy from a group of 36 non-asbestotic long term chrysotile miners and 36 age, sex, and smoking matched controls who had no history of exposure to dust were compared. The airways were graded using a standard visual grading system. Appreciably greater airway fibrosis was found for all types of airway in the whole group of miners compared with the controls. Differences for pigmentation were generally similar but less pronounced. It is concluded that long term exposure to mineral dust as an asbestos miner produces severe diffuse pathological changes in the small airways; these findings may relate to the physiological observation of unusual degrees of airflow obstruction in this group of workers.

Aged↗
PubMed1985

Small airways disease and mineral dust exposure. Prevalence, structure, and function.

Previously we described a lesion of the small airways that appears related to mineral dust exposure and is found in asbestos and nonasbestos dust-exposed populations. To determine the usefulness of this lesion as a marker for mineral dust exposure, and to determine whether it produces functional consequences, we examined a group of 53 workers who had been either hard rock miners or in the asbestos, construction, and shipyard industries. The specific lesion (mineral dust airways disease (MDAD] consists of marked fibrosis and pigmentation of the respiratory bronchioles and was found in 13 of 53 workers with dust exposure, but only in 1 of 121 without dust exposure. Compared with age and smoking-matched dust-exposed control subjects, patients with this lesion had significant abnormalities of forced expiratory volume in one second (FEV1), forced expiratory flow during the middle half of the forced vital capacity (FEF25-75), vital capacity (VC), and nitrogen washout. In addition to fibrosis in the walls of respiratory bronchioles, these patients also had significant increases of fibrosis in the walls of membranous bronchioles, indicating that changes in the small airways are widespread in this subset of workers. We conclude that markedly abnormal small airways are present in some workers with mineral dust exposure; pathologic observation of this lesion is a good indicator of dust exposure, and its presence is associated with abnormalities of air flow greater than those induced by smoking alone. The presence of this lesion in only a portion of dust-exposed workers may account for contradictory results in past studies that attempted to demonstrate air flow abnormalities associated with mineral dust exposure.

Aged↗
PubMed1985

Pulmonary capillary hemangiomatosis.

We report a case of pulmonary capillary hemangiomatosis affecting a 35-yr-old Caucasian woman. Progressive pulmonary hypertension was documented by serial cardiac catheterizations, and pulmonary function studies showed changes suggestive of chronic pulmonary congestion. Although a difficult condition to diagnose during life as it may mimic veno-occlusive disease, capillary hemangiomatosis has a distinct histopathologic picture.

Adult↗
PubMed1985

Lymphocyte subpopulations in allergic granulomatosis and angiitis (Churg-Strauss syndrome).

We report a case of allergic granulomatosis and angiitis (Churg-Strauss syndrome) in which immunologic parameters, including lymphocyte subpopulations, were determined in the acute phase of the disease and during remission. Hyperimmunoglobulinemia E and immune complexes were present. A low proportion of suppressor/cytotoxic (T8+) lymphocytes and a high helper/suppressor ratio were seen throughout the course of the disease, although immunoglobulin levels and circulating immune complex levels decreased with therapy. We hypothesize that the deficiency of suppressor cells may play a role in the pathogenesis of this syndrome.

Aged↗
PubMed1985

Bronchiolitis obliterans complicating bone marrow transplantation.

A 19-year-old woman with extensive, persistent chronic graft versus host disease (GVHD), following an HLA-identical bone marrow graft for acute leukemia, developed rapidly progressive airflow obstruction 140 days post-transplantation (PT) and presented clinically with persistent cough, inspiratory rales, bronchospasm and exertional dyspnea. Pulmonary function tests (PFT) showed rapidly evolving severe airflow obstruction and hypoxemia without restrictive ventilatory defect. Open lung biopsy on the 204th day PT confirmed focal bronchiolitis obliterans. On the 381st day PT, she remained clinically stable. Chest x-ray film showed mild overinflation, but was otherwise unremarkable. PFT's continued to show very severe airflow obstruction without restrictive ventilatory defect. The etiology of the obliterative bronchiolitis might be explained on the basis of a direct immunologic reaction mediated by GVHD or possibly a joint viral-GVHD interaction. Awareness and further detailed documentation and analysis of this unusual respiratory syndrome associated with marrow transplant recipients may help clarify the role of GVHD in the development of lung disease in recipients of marrow grafts.

Adult↗
PubMed1985

Analysis of asbestos fibers and asbestos bodies in tissue samples from human lung. An international interlaboratory trial.

In order to compare methods of counting asbestos fibers in lung tissue, seven laboratories participated in an interlaboratory trial in which tissue samples from five human lungs were analyzed. In some laboratories, fiber concentrations were assessed with the light microscope and, in others, with either scanning or transmission electron microscopes. Within each laboratory the ranking of the results was similar, but there were marked differences in the absolute values obtained by the different laboratories. It is concluded that the laboratories participating in this trial appear to produce internally consistent results, but there is difficulty in directly comparing results from one laboratory to the next.

Aged↗
PubMed1985

Pathologic changes in the small airways of the guinea pig after amosite asbestos exposure.

To determine whether asbestos dust produces pathologic changes in the small airways, and to determine where the anatomic lesions of asbestosis commence, the authors examined lungs from guinea pigs exposed to 10 or 30 mg of amosite asbestos by intratracheal instillation and sacrificed 6 months later. Measurement of airway wall thickness revealed that membranous and respiratory bronchioles of all sizes in exposed animals were significantly thicker than those of controls. Amosite fibers were found embedded in the walls of bronchi and in membranous and respiratory bronchioles; where these fibers penetrated the airway walls, an interstitial inflammatory and fibrotic reaction (asbestosis) occurred. It is concluded that 1) amosite asbestos produces diffuse abnormalities throughout the noncartilagenous airways and possibly the cartilagenous airways as well; 2) this effect is independent of interstitial fibrosis of the parenchyma (classical asbestosis); 3) asbestosis, at least that induced by amosite, commences at any site in the parenchyma to which the asbestos fibers can gain access, either by deposition in alveoli and alveolar ducts or by direct passage of fibers through the walls of all types and sizes of small airways.

Animals↗
PubMed1984

Analysis of hyaluronic acid in the diagnosis of malignant mesothelioma.

Using a modified papain digestion cetylpyridinium salt precipitation method, glycosaminoglycans were isolated from 21 mesotheliomas, 34 primary lung carcinomas, 12 carcinomas of other sites, and 7 soft tissue sarcomas. Qualitatively, hyaluronic acid (HA) was present in 20 of 21 mesotheliomas, about half of the primary lung adenocarcinomas, and all of the soft tissue sarcomas. On the average, HA constituted 45% of the total glycosaminoglycans in the mesotheliomas and 28% of the total in the lung cancers. Quantitatively, mesotheliomas contained statistically greater amounts (mean value, 0.74 mg/g) of HA than primary lung adenocarcinomas (mean value, 0.08 mg/g), but were not statistically different from soft tissue sarcomas (mean value, 2.01 mg/g) or primary ovarian serous neoplasms (mean value, 0.92 mg/g). The study concludes that, contrary to previous reports, HA is neither the sole nor the predominant glycosaminoglycan in most mesotheliomas, but, given the proper clinical and histologic setting, the finding of sufficiently high levels (greater than 0.4 mg/g dry tissue extract) supports the diagnosis of mesothelioma when the alternative diagnosis is primary adenocarcinoma of lung.

Adenocarcinoma↗
PubMed1984

Morphology of small-airway lesions in patients with asbestos exposure.

The morphologic changes in the small airways of 15 patients who had been exposed to asbestos and had abnormalities of the respiratory bronchioles and alveolar ducts were examined and compared with changes in the small airways of a matched group of cigarette smokers. Lesions were evaluated using a visual grading scheme to determine pathologic severity of fibrosis, inflammation, and pigmentation in these airways. The membranous bronchioles of both asbestos-exposed and cigarette exposed patients showed the deposition of fibrous tissue and pigment; the lesions were morphologically identical, although more severe in the asbestos group (67 per cent of airways) than in the smoking group (19 per cent of airways). A distinctive lesion, consisting of fibrosis often accompanied by pigment, was found in 74 per cent of the respiratory bronchioles in the asbestos-exposed patients, compared with 6 per cent of respiratory bronchioles in the smokers. Similar changes were found in 49 per cent of alveolar ducts in the asbestos group and 1 per cent of the ducts in smoking group. Asbestos bodies were found in only 11 of 15 cases. The authors conclude that a distinctive lesion of small airways exists in some asbestos workers and that it can be identified by the finding of marked fibrosis in the walls of respiratory bronchioles and alveolar ducts. Because there is no proof that this lesion actually progresses to interstitial fibrosis (asbestosis), the authors suggest that it be termed "asbestos airways disease."

Asbestos↗
PubMed1984

Ferruginous bodies and the histologic evaluation of dust exposure.

Ferruginous bodies are frequently observed in histologic sections of lung from individuals with occupational or environmental exposure to asbestos and other mineral dusts. Analysis of large numbers of such ferruginous bodies has demonstrated that the types with asbestos cores can be differentiated by light microscopy from several chemically and morphologically distinct classes of nonasbestos ferruginous bodies, including those formed on sheet silicates (talc and mica), carbon, rutile, and fly ash. Light-microscopic screening of lung tissue sections for ferruginous bodies is a reliable, convenient, and economical method for documenting exposure to a variety of mineral dusts and can assist in determining the etiology of pneumoconiotic lesions. Because tissue sections are relatively insensitive detectors of particles, the finding of ferruginous bodies in section implies heavy dust exposure.

Asbestos↗
PubMed1984

Malakoplakia mimicking carcinoma metastatic to lung.

Malakoplakia is a rare inflammatory disorder which infrequently involves sites outside of the lower genitourinary or gastrointestinal tract. We report a case of malakoplakia in which the patient presented with a left renal mass and bilateral pulmonary nodules suggestive of metastatic renal carcinoma. Postmortem cultures of the lesions grew E. coli; macrophages at both sites contained gram-negative bacilli and numerous Michaelis-Gutmann bodies. X-ray spectroscopic analysis of the bodies showed wide variation in calcium, phosphorus, and iron content, suggesting that Michaelis-Gutmann bodies were formed in part by the deposition of amorphous salts.

Diagnosis, Differential↗
PubMed1984

Immunohistochemical staining for keratin and carcinoembryonic antigen in the diagnosis of malignant mesothelioma.

Using formalin-fixed, paraffin-embedded tissue and commercial antisera, we evaluated the usefulness of immunohistochemical staining for carcinoembryonic antigen (CEA) and keratin in the diagnosis of malignant mesothelioma. All 18 adenocarcinomas of lung examined stained for CEA, usually strongly, while only eight of 22 mesotheliomas stained for CEA and the staining was generally weak. Staining for keratin was observed in 10 of 22 mesotheliomas and 12 of 18 adenocarcinomas; there were no differences in intensity of staining between the groups. We conclude that strong diffuse staining for CEA favors a diagnosis of carcinoma, and negative staining for CEA is against a diagnosis of carcinoma, but these are relative and not absolute criteria. We find that staining for keratin is of no use in distinguishing these types of tumors.

Adenocarcinoma↗
PubMed1984

Lung asbestos content in chrysotile workers with mesothelioma.

The role of chrysotile asbestos in the genesis of mesotheliomas in humans is disputed. We analyzed the asbestos content of the lung in 6 long-term chrysotile miners and millers who had pleural mesotheliomas. In five patients, only chrysotile ore components (chrysotile and tremolite/actinolite/anthophyllite types of amphibole asbestos) were found, while the sixth patient presented both chrysotile ore components and amosite, a type of asbestos that is not derived from the mining process. The mean number of fibers/g dry lung for the 5 patients with mesothelioma containing only chrysotile ore components was higher (chrysotile 64 X 10(6) and tremolite group 540 X 10(6] than in a group of long-term chrysotile miner control subjects who had no asbestos-related disease (chrysotile 23 X 10(6), tremolite group 58 X 10(6], but some patients with mesothelioma had fiber burdens near the mean of the control range. Fiber sizes and aspect ratios in the mesothelioma group were approximately the same as those in the control subjects, and analysis of fiber distribution failed to show any preferential localization in the periphery of the lung. However, the concentration ratio of tremolite in the lungs of the mesothelioma cases compared to the control cases was 9.3, while the ratio of chrysotile was only 2.8. Our findings provide strong evidence that chrysotile mine dust (chrysotile and amphibole components) can produce mesotheliomas in humans; the greater relative amounts of tremolite group amphiboles present in the patients with mesothelioma raise the possibility that these fibers may be important in the pathogenesis of the tumors.

Aged↗
PubMed1984

Fiber size and number in amphibole asbestos-induced mesothelioma.

Numbers and sizes of fibers from the lungs of 10 patients who had an amphibole asbestos-induced malignant pleural mesothelioma were analyzed. Amosite was found in 10 lungs and crocidolite in 9; the average ratio of amosite to crocidolite was approximately 14:1. In the 8 patients who were not long-time asbestos insulators , the mean number of amosite fibers was 2.3 X 10(6) fibers/g dry lung, and of crocidolite fibers, 0.2 X 10(6)/g; these values represent an approximately 250-fold increase over those found in the general population. Crocidolite fibers were significantly narrower than amosite fibers (mean width, 0.13 versus 0.23 mu), were significantly shorter (mean length, 4.0 versus 5.8 mu), and had a significantly higher mean aspect (length to width) ratio (48 versus 34). Aspect ratios in general increased with increasing fiber length and decreasing fiber width, but the highest values were found for thin amosite fibers at about 13 mu in length, and thin crocidolite fibers at 8 or 15-17 mu in length. Comparison with data from other asbestos-exposed populations indicates that mesothelioma can be induced by relatively small numbers of amphibole fibers and also indicates that amosite is an effective mesothelial carcinogen in humans. Comparison of these data with epidemiologic and experimental predictions of carcinogenic size ranges for mesothelioma induction implies that either the carcinogenic size range is much broader than has been claimed (in particular, fibers considerably shorter than 8 mu and broader than 0.05 mu can produce mesothelioma), or, alternately, that extraordinarily small absolute numbers of fibers in certain size ranges can induce tumors in humans.

Aged↗
PubMed1983

Observations on the distribution of asbestos fibers in human lungs.

In an attempt to begin evaluating the distribution of mineral fibers within lung, multiple small adjacent samples were selected from peripheral portions of three normal and six asbestotic lungs, and analyzed for asbestos and nonasbestos fiber content. For both normal and fibrotic lungs there was marked variation in fiber concentration from site to site; the mean in-case ratio of maximum to minimum fiber concentration was 7.5 for amosite and crocidolite, 7.0 for tremolite, 3.8 for chrysotile, 4.0 for nonasbestos fibers, and 5.4 for asbestos bodies. In order to test the precision of the membrane filter method of quantitating particulates, multiple replicate samples of reference mineral standards were examined in a similar fashion; for these standard samples the ratio of maximum to minimum particle concentration varied from only 1.3 to 1.5. It is concluded that: (1) the membrane filter preparation technique used here for counting fibers provides reproducible results, and (2) there is marked variation in asbestos and nonasbestos fiber concentration from area to area within lung tissue. The latter finding implies that analysis of small subpleural lung biopsies may produce misleading results, and that larger pieces or several pieces should be analyzed when attempting to define total asbestos fiber content of the lung.

Asbestos↗