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1.
Ann Thorac Surg ; 60(3): 710-2, 1995 Sep.
Article in English | MEDLINE | ID: mdl-7677514

ABSTRACT

Fibrous histiocytomas are uncommon pulmonary tumors. They generally involve only the lung parenchyma. Endobronchial involvement is extremely rare. Usually, surgical resection of the mass is required for definitive diagnosis and therapy. We report a case of benign atypical fibrous histiocytoma visualized during fiberoptic bronchoscopy and review the clinical findings and pathologic features of this tumor.


Subject(s)
Bronchial Neoplasms/pathology , Histiocytoma, Benign Fibrous/pathology , Adult , Airway Obstruction/pathology , Airway Obstruction/surgery , Bronchial Neoplasms/surgery , Bronchoscopy , Female , Fiber Optic Technology , Histiocytoma, Benign Fibrous/surgery , Humans , Pneumonectomy
3.
Chest ; 102(6): 1672-5, 1992 Dec.
Article in English | MEDLINE | ID: mdl-1446470

ABSTRACT

Random assessments of SaO2 were performed via pulse oximetry in 274 hospitalized non-ICU patients prescribed supplemental O2 in a large tertiary care university hospital. In 507 assessments performed in patients inspiring the prescribed O2, 426 were receiving excessive amounts of O2 to maintain a SaO2 > or = 92 percent. In 233 of these assessments, SaO2 was > or = 92 percent while breathing ambient air. In an additional 193 assessments, the concentration of inspired supplemental O2 was excessive to maintain a SaO2 > or = 92 percent. However, in 81 assessments performed in patients inspiring O2, the prescribed amount was insufficient to maintain SaO2 > or = 92 percent. These results indicate that O2 prescription in hospitalized non-ICU patients is excessive or not required in the majority of cases. Furthermore, routine use of pulse oximetry in hospitalized patients prescribed O2 may be useful in determining the continued need for supplemental O2 and adjusting the proper concentration needed to avoid hypoxemia.


Subject(s)
Hospitals, University/statistics & numerical data , Oxygen Inhalation Therapy/statistics & numerical data , Baltimore/epidemiology , Clinical Protocols , Cost Control , Cost Savings , Costs and Cost Analysis , Hospitals, University/economics , Humans , Insurance, Health, Reimbursement , Intensive Care Units , Oximetry , Oxygen/blood , Oxygen Inhalation Therapy/economics , Patient Compliance , Reimbursement Mechanisms , Respiratory Therapy Department, Hospital/economics , Respiratory Therapy Department, Hospital/statistics & numerical data , Time Factors , Workforce
4.
Am J Med ; 87(6): 664-8, 1989 Dec.
Article in English | MEDLINE | ID: mdl-2686434

ABSTRACT

A variety of pulmonary complications related to the use of freebase cocaine have been reported in the medical literature. Pulmonary barotrauma, hypersensitivity pneumonitis, pulmonary hemorrhage, obliterative bronchiolitis, asthma, and pulmonary edema have all recently been described. The number of reports are few, reflecting either the low incidence of these complications or the lack of recognition of these phenomena as cocaine-related illnesses. The mechanism by which freebase cocaine can injure the lung is not well defined. Whether an abnormal immunologic response to cocaine freebase can result in hemorrhage, pneumonitis, bronchiolitis, or asthma remains speculative. Whether cardiogenic or non-cardiogenic factors play a role in the development of pulmonary edema in freebase smokers has not yet been determined. Likewise, the roles of either cocaine, tobacco, or adulterants in producing the observed abnormalities of lung function remain controversial. Further reporting of freebase-related pulmonary complications, as well as the development of appropriate animal models, is needed.


Subject(s)
Cocaine/pharmacology , Lung Diseases/chemically induced , Substance-Related Disorders , Administration, Inhalation , Barotrauma/chemically induced , Bronchiolitis Obliterans/chemically induced , Hemorrhage/chemically induced , Humans , Pulmonary Alveoli/injuries , Pulmonary Edema/chemically induced , Respiratory Hypersensitivity/chemically induced
5.
Chest ; 96(5): 1050-3, 1989 Nov.
Article in English | MEDLINE | ID: mdl-2805835

ABSTRACT

A reduction in the DCO has been reported among "free-base" cocaine smokers. We reviewed the pulmonary histopathology in 20 deaths due to cocaine intoxication for either parenchymal or vascular abnormalities which might explain this physiologic finding. Pulmonary artery medical hypertrophy in the absence of foreign particle microembolization was present in four of 20 cases (20 percent). Hemosiderin-laden macrophages were found in seven of 20 cases (35 percent). These abnormalities were not seen in a matched control group. We conclude that in the absence of foreign particle microembolization, pulmonary artery medial hypertrophy occurs among cocaine users, although the mechanism of these vascular changes is unknown. In addition, occult alveolar hemorrhage occurs more frequently among cocaine users than is clinically recognized.


Subject(s)
Cocaine , Foreign Bodies , Lung , Pulmonary Artery/pathology , Substance-Related Disorders/pathology , Adult , Cocaine/poisoning , Female , Humans , Hypertrophy , Lung/pathology , Male , Pulmonary Artery/drug effects , Pulmonary Circulation/drug effects , Pulmonary Diffusing Capacity/drug effects , Pulmonary Embolism
6.
Clin Nucl Med ; 14(5): 341-3, 1989 May.
Article in English | MEDLINE | ID: mdl-2656040

ABSTRACT

Hepatic hydrothorax is a complication in approximately 5% of patients with cirrhosis. Ascites is almost always present and helps to suggest the correct diagnosis. However, when ascites is absent, radionuclide imaging has proven to be helpful in establishing that the pleural effusion originated from ascitic fluid. When pleural fluid is rapidly removed, such as by thoracostomy tube drainage, the radioisotope may accumulate outside the thorax and produce a negative scan of the chest. When the radionuclide scan is nondiagnostic and the pleural space is being rapidly drained, the pleural fluid collecting system should always be imaged before rejecting a diagnosis of hepatic hydrothorax.


Subject(s)
Drainage , Hydrothorax/diagnostic imaging , Liver Cirrhosis/complications , Thoracostomy , Female , Humans , Hydrothorax/etiology , Hydrothorax/surgery , Middle Aged , Organometallic Compounds , Pentetic Acid , Radionuclide Imaging , Technetium , Technetium Tc 99m Pentetate
7.
J Immunol ; 141(12): 4306-12, 1988 Dec 15.
Article in English | MEDLINE | ID: mdl-2848893

ABSTRACT

Collagenase catalyzes the initial and rate-limiting step in interstitial collagen degradation. Human alveolar macrophages produce both a fibroblast-like procollagenase and tissue inhibitor of metalloproteinases (TIMP). To define the potential of macrophages to express collagenase and TIMP, we have studied the effects of certain cell culture variables and LPS on in vitro production of these proteins. Our data indicate: 1) human macrophages cultured in a 1/1 (v/v) mixture of HAM F-12:DME produce two- to three-fold greater quantities of procollagenase (but not TIMP) as compared to HAM F-12, DME, or alpha-MEM alone; 2) maximal collagenase expression requires the further addition of LPS, whereas TIMP production is optimized by 5% fetal bovine serum alone; 3) the up-regulation of macrophage procollagenase by LPS represents a highly selective biologic response when compared to changes induced in other secreted and intracellular proteins; 4) measurements of steady state procollagenase mRNA by Northern blot analysis suggest that the LPS effect is mediated at a pre-translational level; and finally 5) on a per cell basis, human alveolar macrophages cultured under optional conditions secrete approximately 20% of the collagenase and approximately 10% of the TIMP elaborated by stimulated human fibroblasts. We conclude that procollagenase and TIMP secretion by human alveolar macrophages in vitro is strikingly responsive to variations in cell culture conditions and that an especially noteworthy selective upregulation of procollagenase secretion by LPS is probably modulated by a transcriptional mechanism. The macrophage synthetic potential for procollagenase suggests a potentially important role for these cells in directly mediating collagen turnover.


Subject(s)
Collagenases , Fibroblasts/enzymology , Lipopolysaccharides , Macrophages/enzymology , Microbial Collagenase/biosynthesis , Pulmonary Alveoli , Adult , Cells, Cultured , Culture Media , Enzyme Inhibitors/immunology , Enzyme Inhibitors/metabolism , Enzyme Precursors/biosynthesis , Enzyme Precursors/metabolism , Fetal Blood , Fibroblasts/drug effects , Humans , Macrophages/drug effects , Microbial Collagenase/antagonists & inhibitors , Microbial Collagenase/immunology , Microbial Collagenase/metabolism , Protein Biosynthesis , Tissue Inhibitor of Metalloproteinases
8.
Chest ; 94(1): 193-5, 1988 Jul.
Article in English | MEDLINE | ID: mdl-3383632

ABSTRACT

Interstitial pneumonitis in sarcoidosis is rare. When present, it confined to areas of active granuloma formation. We report finding widespread interstitial pneumonitis and fibrosis in a patient with sarcoidosis. Due to the focal sampling of pulmonary tissue by transbronchial biopsy, a finding of interstitial pneumonitis does not exclude a diagnosis of sarcoidosis.


Subject(s)
Lung Diseases/pathology , Lung/pathology , Pulmonary Fibrosis/pathology , Sarcoidosis/pathology , Adult , Biopsy , Female , Humans
9.
Chest ; 93(2): 427-9, 1988 Feb.
Article in English | MEDLINE | ID: mdl-3338316

ABSTRACT

Previous reports of respiratory complications from cocaine abuse have focused on pulmonary barotrauma or a reduction in carbon monoxide diffusing capacity. We report a patient who developed life-threatening alveolar hemorrhage following repeated inhalation of alkaloid cocaine.


Subject(s)
Cocaine , Hemorrhage/chemically induced , Lung Diseases/chemically induced , Substance-Related Disorders/complications , Adult , Female , Hemorrhage/pathology , Humans , Lung Diseases/pathology , Pulmonary Alveoli/pathology
10.
Am Rev Respir Dis ; 135(6): 1281-5, 1987 Jun.
Article in English | MEDLINE | ID: mdl-2438967

ABSTRACT

Elastase activity directed against lung extracellular matrix is currently believed to be important in the pathogenesis of pulmonary emphysema. Although human alveolar macrophages degrade elastin when in direct contact with this substrate in vitro, studies of free elastase activity in medium conditioned by human alveolar macrophages have yielded variable results. As human alveolar macrophages secrete the tissue inhibitor of metalloproteinases (TIMP), an inhibitor of collagenase and of other connective-tissue-derived mammalian metalloproteinases, we speculated that this inhibitor's effects might extend to macrophage elastase. Using metalloproteinase elastase from the murine macrophagelike cell line P388D1, we observed that human alveolar macrophage conditioned medium inhibits metalloproteinase elastase and that this inhibitory activity could be blocked by specific antibody to TIMP. Alpha 2-macroglobulin, another proteinase inhibitor secreted by alveolar macrophages, also inhibited metalloproteinase elastase, but its inhibitory capacity was not blocked by antibody to TIMP. Because detergents are often included in elastase assays, we examined the effects of sodium dodecyl sulfate (SDS). Buffers containing SDS and SDS-treated elastin were found to exert diverse effects on metalloproteinase elastase, TIMP, and alpha 2-macroglobulin activities, including a marked inhibition of metalloproteinase elastase activity by SDS-containing buffers. These findings suggest that detection of secreted metalloproteinase elastase activity by human alveolar macrophages is complicated by the concomitant release by these cells of inhibitors of metalloproteinases, and that assay conditions can markedly influence the results.


Subject(s)
Enzyme Inhibitors/metabolism , Macrophages/metabolism , Metalloendopeptidases , Protease Inhibitors , Pulmonary Alveoli/cytology , Antibodies/immunology , Endopeptidases/metabolism , Enzyme Inhibitors/immunology , Enzyme Inhibitors/pharmacology , Humans , In Vitro Techniques , Matrix Metalloproteinase 12 , Sodium Dodecyl Sulfate/pharmacology , Tissue Inhibitor of Metalloproteinases , alpha-Macroglobulins/pharmacology
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