Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034069 (pulmonary fibrosis)
 7,050 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 61-year-old man was admitted to our hospital because of persisting cough, sputum and shortness of breath for four months. Brushing specimens and BALF bronchoscopically obtained revealed acid-fast bacilli and TBLB showed pathological findings consistent with interstitial pneumonia. Based on these results, clinical symptoms, chest roentgenograms on admission and identification of M. kansasii, a diagnosis of M. kansasii lung infection occurred in idiopathic pulmonary fibrosis was made. The patient's symptoms consistent with M. kansasii lung infection and his sputum became negative 6 weeks after antituberculosis chemotherapy with INH, SM and RFP. Because of an increasing dyspnea due to pulmonary fibrosis, however, the patient received oxygen therapy. This case suggested an increasing tendency of compromised hosts associated with M. kansasii lung infection.
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PMID:[M. kansasii lung infection occurring in a compromised host with idiopathic pulmonary fibrosis]. 258 49

Establishing the diagnosis of drug-induced pneumonitis is always difficult and requires that the following criteria be met: administration of the drug on a long-term basis; knowledge that the drug is able to induce pulmonary disorders; occurrence during therapy of interstitial pneumonitis with clinical, radiological and functional characteristics of this type of lung disease; exclusion of all other causes of interstitial pneumonitis (cardiac failure, infections, collagen vascular diseases, malignancies); bronchoalveolar lavage specimen, revealing lymphocytosis with an inverted CD4/CD8 lymphocyte ratio, isolated or associated with neutrophil and/or eosinophil alveolitis; finally, full recovery within several weeks or months after drug withdrawal unless irreversible pulmonary fibrosis has occurred. Certain specific characteristics correspond to the therapeutic class of the drug, i.e. antimicrobial, cardiovascular, antiinflammatory, neurological, metabolic, antiallergy or some other drugs.
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PMID:[Drug-induced pneumopathies (excluding cytostatic drugs)]. 261 Apr 52

To evaluate the usefulness of anti-T6 monoclonal antibody cell analysis in the assessment of diffuse lung disease, 77 bronchoalveolar lavages (BAL) were performed on 70 subjects: 18 normal smokers, 14 normal nonsmokers, 30 patients with chronic interstitial lung diseases (15 sarcoidosis, 12 idiopathic or associated pulmonary fibrosis, 3 histiocytosis X) and 8 patients with diffuse lung neoplastic disorders. The percentage of T6-positive cells was significantly higher in normal smokers than in normal nonsmokers (p less than 0.05). Positive T6 cells were absent or less than 1% in normal subjects, in patients with interstitial lung diseases and in patients with diffuse lung cancer, except in a case of desquamative interstitial pneumonitis, who had 2% of reacting cells. In contrast, such cells were always 3% or higher in the 6 BAL performed in histiocytosis X patients (p less than 0.05).
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PMID:Bronchoalveolar lavage analysis with anti-T6 monoclonal antibody in the evaluation of diffuse lung diseases. 263 45

An electron microscopic study was undertaken to investigate pulmonary ultrastructural changes in mice following exposure to an aerosolized Periodontal Pack Powder (PPP), and to determine if the asbestos fiber, which contains 7% PPP, is respirable. One hundred and sixty-five animals were used in this study. Seventy-two of the animals were exposed to the powder twice weekly for a minimum of two weeks and a maximum of four weeks. Fifty animals were exposed to the PPP (without asbestos), with the same exposure sequence used. Forty-three animals served as nonexposed controls. Randomly selected groups of exposed and control mice were killed at designated intervals between two and 12 weeks. Microscopic examination of the lungs revealed early interstitial pneumonia. These changes were seen in both treatment groups. Late changes included a generalized resolution of the pneumonia (seen in both treatment groups) with residual diffuse interstitial fibrosis, persistence of asbestos fibers within the tissue, and early asbestos body formation (seen only in animals exposed to asbestos-containing PPP). This study documents that the asbestos in Periodontal Pack Powder is both respirable and potentially pathogenic. Dentists who have used this product could conceivably be a population at risk for pulmonary fibrosis and/or obstructive airways disease.
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PMID:Ultrastructural pulmonary changes in mice exposed to aerosolized Periodontal Pack Powder. 263 15

A 20-year-old Chinese male given an HLA-identical sibling bone marrow transplant for severe aplastic anemia, who had previously had chronic graft-versus-host disease (GVHD) of the mouth, developed myasthenia gravis and widespread pulmonary infiltrates with cough and exertional dyspnea at day 820 post-transplant. There was nothing to suggest aspiration pneumonia. Lung histology at day 940 showed some areas of dense pulmonary fibrosis, some areas of normal parenchyma, and some areas of widening of the interstitium and a mild lymphocytic infiltrate. Evidence of infection was not found. Treatment with cyclosporin and prednisone resulted in slow partial resolution of the infiltrates over 5 months. The myasthenia gravis was controlled with pyridostigmine. In view of the association with myasthenia gravis, of the absence of infectious agents and the response to immunosuppression, we conclude that widespread pulmonary fibrosis can be a major clinical manifestation of chronic GVHD. Examination of lung tissue to distinguish this from infective interstitial pneumonitis is essential.
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PMID:Widespread pulmonary fibrosis as a major clinical manifestation of chronic graft-versus-host disease. 264 79

Interstitial pneumonitis and biopsy-proven pulmonary fibrosis developed in a 35-year-old man with acute myeloblastic leukemia 4 months after conditioning with total body irradiation, etoposide and cyclophosphamide and allogeneic marrow transplantation from an HLA-identical sister. The patient had no evidence of graft-versus-host disease. Under treatment with cyclosporine and prednisone the patient became asymptomatic and radiographic changes of the chest normalized. Following discontinuation of immunosuppressive treatment the patient again became dyspneic, and chest radiographs showed bilateral diffuse interstitial infiltrates. Concurrently there was a rise in serum transaminases. Treatment with prednisone again resulted in resolution of all symptoms and normalization of radiographic and hepatic function abnormalities. This case indicates that late onset interstitial pneumonitis may respond to immunosuppressive therapy. Conceivably, such pulmonary disease may represent the first or only manifestation of chronic graft-versus-host disease.
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PMID:Pulmonary fibrosis after bone marrow transplantation responsive to treatment with prednisone and cyclosporine. 265 Jul 91

Thoracoscopy was performed under local anesthesia in 419 patients suffering from a diffuse lung disease. In 85% of the cases diagnosis was clarified by thoracoscopy. All other cases were confirmed by means of an open lung biopsy. The best results were obtained in sarcoidosis of the stages II and III, the sensitivity being 0.98. Tumour-conditioned diffuse lung diseases were clarified in 88% of the cases; proof of an interstitial pulmonary fibrosis or interstitial pneumonia was established in 85% of the patients. Results regarding histiocytosis X were poor: thoracoscopic-bioptic proof was successful in only 42% of the patients. In 419 examinations we only detected a severe complication (air embolism). Drainage times were on the average between 4 and 5 days. On the whole, the method was characterised in the field of diagnosis of diffuse lung diseases by a high degree of sensitivity and satisfactory specificity. Both in respect of the invasiveness of the examination and its sensitivity it occupies an intermediate position between peripheral bronchoscopically obtained biopsy and surgical open lung biopsy, representing a valuable extension of the diagnostic instrumentarium if the indication is carefully considered.
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PMID:[Thoracoscopy in diffuse lung diseases]. 271 51

Two cases of Hermansky-Pudlak syndrome with interstitial pneumonia were reported. Both patients had evidence of pulmonary involvement characterized by diffuse bilateral infiltrates. They had oculocutaneous albinism. Case 1 was a 55 year-old female who had a history of easy bruising. Her two sisters were albino and had died of pulmonary fibrosis. One of them was diagnosed as Hermansky-Pudlak syndrome on autopsy. Bone marrow aspirate disclosed typical macrophages with ceroid-like pigment. Transbronchial lung biopsy showed alveolar wall thickening. Lumi-aggregometer showed a decrease of platelet aggregation and an absence of ATP release. Case 2 was a 43 year-old female and had a bleeding tendency during a surgical procedure. Lumi-aggregometer showed normal platelet aggregation but an absence of ATP release. BALF analysis did not disclose macrophages with ceroid-like pigment.
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PMID:[Two cases of Hermansky-Pudlak syndrome with interstitial pneumonia]. 281 Sep 74

An autopsy case of sarcoidosis followed up for 27 years in a 48-year-old woman with pulmonary fibrosis is presented. Chest roentgenography demonstrated an interstitial pneumonia-like pattern with gradual contraction of the upper lobes. Focal and extending fibrosis and hyalinization were observed in various organs including the lung, lymph nodes, heart and liver. Most of the fibrosis was thought to be derived from solitary or confluent granuloma, showing hyalinized nodular, stellate or band-like fibrosis. There was also another type of fibrosis, not derived from granuloma, manifested as fibrosing alveolitis in the lung, and diffuse fibrosis extending throughout the other organs. In the lymph nodes, chromogenic bodies (Hamazaki-Wesenberg bodies) were seen. The process of fibrosis and the significance of chromogenic bodies in cases of chronic sarcoidosis are discussed.
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PMID:An autopsy case of sarcoidosis followed up for 27 years, with special reference to pulmonary fibrosis. 284 79

An autopsy case of smoldering adult T-cell leukemia (ATL) is presented. 67 year-old woman was admitted to our hospital with complaints of fever, cough and increasing dyspnea on October 2, 1985. Laboratory findings revealed high LDH, azothermia and slightly leukocytosis with low percentage of flower cells. CRP was strongly positive. Gas disturbance was markedly. Anti-ATLA antibody using indirect immunofluorescence method was X40 positive. Subsets of peripheral lymphocytes showed OKT 4 dominant. (OKT 3; 67.5%, OKT4; 60.6%, OKT8; 8.8%). A chest X-ray film revealed cardiomegaly and fine granular shadows in bilateral lower pulmonary fields. Diagnosis of interstitial pneumonitis was defined in transbronchial lung biopsy (TBLB) specimen. O2 therapy, steroid therapy added antibiotics were ineffective, respiratory failure and renal failure were progressive, she died by septic shock in 39th hospital days. In autopsy, no characteristic histological changes of ATL were found in lymph node, bone marrow, spleen, liver, kidney and lung. Sepsis was the cause was of death. Finally this case diagnosed smoldering ATL and pulmonary fibrosis due to bronchial ectasia with repeated pulmonary bacterial infections. The pulmonary complications of patients with ATL were discussed.
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PMID:[Smoldering adult T-cell leukemia complicating severe respiratory failure--an autopsy case report]. 288 12


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