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)

Radioimmunoassay of 5alpha, 7alpha-dihydroxy-11-keto-tetra-norprosta-1,16-dioic acid, main urinary metabolite of prostaglandin F2alpha (PGF2alpha-MUM), was performed in patients with various respiratory diseases including diffuse interstitial fibrosing pneumonitis (DIFP, fibrosing alveolitis). Twenty-four hr excretion of PGF2alpha-MUM in patients with primary lung cancer, pulmonary fibrosis secondary to collagen diseases and stationary DIFP was normal. On the other hand, 24 hr excretion of PGF2alpha-MUM in patients with carcinomatous pleuritis was high and that in patients with aggravating DIFP was markedly high. There was no correlation between serum LDH levels and 24 hr excretion of PGF2alpha-MUM.
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PMID:Radioimmunoassay of main urinary metabolite of prostaglandin F2alpha in patients with diffuse interstitial fibrosing pneumonitis (DIFP) and other respiratory diseases. 76 Feb 64

Pericarditis may be the most common cardiac manifestation in RA patients and the incidence in autopsy cases is more than 30%. Pericardial effusion shows low sugar and complement level and high level of LDH and gamma-globulin. The administration of corticosteroids has been successfully used in the treatment of rheumatoid pericarditis. The pulmonary involvement in RA include pleuritis, nodules and interstitial lung disease. Interstitial lung disease in RA patients appears to run a continuum from mild pneumonitis to severe pulmonary fibrosis and occasionally it include bronchiolitis obliterans organizing pneumonia (BOOP) which is sensitive to corticosteroid therapy. Although open lung biopsy is the definitive procedure for proving the diagnosis of interstitial lung disease, open lung is now being complemented or replaced by transbronchial lung biopsy and bronchoalveolar lavage (BAL). Corticosteroids will be effective to BOOP definitely and in general usual interstitial pneumonia (UIP) is resistant to treatment. In addition to the primary pulmonary manifestations of RA, anti-rheumatic drug reactions in the lung may be associated.
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PMID:[Cardiac and pulmonary manifestations in rheumatoid arthritis]. 158 50

Among 238 patients with advanced inoperable non-small cell lung cancer (NSCLC), we evaluated the characteristics of three-year survivors and analyzed them to determine whether or not there were any specific pretreatment prognostic factors which could make it possible to discriminate this group the rest. All patients received chemotherapy according to the protocol for phase II or III trials at the National Cancer Center, Japan, between 1980 and 1987. Eighteen (8%) patients survived for over three years. Five of the 18 responded to initial therapy, seven received thoracic irradiation and five surgical resection after chemotherapy. No patient achieved a complete response by chemotherapy. Among five disease-free survivors, two received surgery after completion of chemotherapy. Their clinical stage was IIIA. Three patients received radiation therapy, but they could not be evaluated. Although some radiologically detectable shadows remained, these patients survived for more than three years with no active lesion, indicating the difficulty in diagnosing a complete response to treatment. Thirteen patients survived for more than three years with disease. Some unknown biological factors might influence survival in this group. Pulmonary fibrosis, as treatment toxicity, was observed in six of the 18. The pretreatment prognostic factors that discriminated three-year survivors from the rest were Eastern Cooperative Oncology Group performance status (PS) (P = 0.0015), clinical T factor (P = 0.0093), and serum LDH (P = 0.0317) by means of univariate analysis, and PS (P = 0.0134) and clinical T factor (P = 0.0117) by means of multivariate analysis with a logistic regression procedure.
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PMID:Analysis of three-year survivors among patients with advanced inoperable non-small cell lung cancer. 165 15

A 70-year-old man was admitted to our hospital because of fever and progressive dyspnea in December 1989. He was already diagnosed as having erythrocytosis secondary to pulmonary fibrosis 4 years previously and the values of his hematocrit (Ht) were maintained between 44.5 and 62.9% by repeated phlebotomy. Immediately after admission, severe diarrhea developed and the Ht value was 61.5%. Around 1:30 a.m. of the 3rd hospital day, he developed disturbance of consciousness. In addition, the serum levels of LDH, CPK, aldolase, and myoglobin of muscle origin increased markedly and the Ht value showed 78.5%. While the level of consciousness was gradually restored by 600 ml phlebotomy and 1,500 ml saline infusion, dysarthria and hemiplegia became evident. The Ht value early in the morning of the 3rd hospital day was reduced to 59.4%. Although cranial CT and MRI performed 74 days and 15 months, respectively, after the onset of the symptoms failed to reveal any abnormal shadow, he was clinically suspected to have cerebral infarction. These findings emphasize that abrupt increase in Ht or blood viscosity is a possible factor triggering cerebral infarction, and adequate control of Ht value is recommended for the prevention of such a condition in the aged.
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PMID:[Cerebral infarction and high serum levels of muscle-derived enzymes associated with abrupt increase in hematocrit in a patient with secondary erythrocytosis]. 175 34

Previous work in this laboratory has demonstrated increased secretion of fibroblast growth factor (MDGF) activity by alveolar macrophages obtained from mice with bleomycin-induced pulmonary fibrosis. The mechanism by which bleomycin promotes this increase in MDGF secretion is not clear, however. The purpose of this study was to determine the direct effects of bleomycin on alveolar macrophages. Normal rat alveolar macrophages obtained by lavage were cultured in the presence or absence of bleomycin; conditioned media from these cultures were dialyzed to remove bleomycin and then assayed in vitro for MDGF activity. Alveolar macrophages incubated with 0.01 microgram to 1 microgram/ml bleomycin for 18 hours secreted significantly more MDGF than macrophages incubated without bleomycin. Viability of macrophages as determined by exclusion of trypan blue and release of LDH was unaffected by any dose tested. Maximal MDGF production was seen with bleomycin doses of greater than or equal to 0.1 microgram/ml. When alveolar macrophages were incubated with 0.1 microgram/ml bleomycin for 0.5-18 hours, MDGF activity was detected as early as 1 hour, with peak responses found at 4-8 hours. Macrophages stimulated with bleomycin continued to produce significant amounts of MDGF even after bleomycin was removed and replaced with fresh (bleomycin-free) media. MDGF secretion by bleomycin-stimulated alveolar macrophages was inhibited by cycloheximide, and the 5-lipoxygenase inhibitors NDGA (nordihydroguairetic acid) and BW755c, indicating not only a requirement for protein synthesis but also for metabolites of the 5-lipoxygenase pathway of arachidonic acid metabolism for full expression of activity(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effects of bleomycin on alveolar macrophage growth factor secretion. 246 42

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

Radioimmunoassays of urinary 5 alpha-7 alpha-dihydroxyketotetranorprosta-1,16-dioic acid and its delta-lactone(main urinary metabolite of PGF, PGF-MUM) were performed for the patients with several pulmonary diseases. The quantities of PGE and PGF in plasma for the patients with pulmonary emphysema especially were also measured by radioimmunoassay. Following results were obtained. 1) Twenty-four hours secretions of PGF-MUM in normal subjects were 18.4 +/- 9.1 microgram/day (24.5 +/- 9.2 microgram/day in male, 12.2 +/- 2.6 microgram/day in female) on an average. The values of PGF-MUM in male were significantly higher than those in female (P less than 0.03). 2) Twenty-four hours secretions of PGF-MUM for the patients with pulmonary emphysema were significantly lower (P less than 0.01) than those in the normal controls (P less than 0.01), and the values of PGF-MUM were correlated significantly (r=0.451, P less than 0.05) with arterial oxygen partial pressure. 3) Twenty-four hours secretions of PGF-MUM in the patients with asthma bronchiale, chronic bronchitis, hypersensitivity pneumonitis, pulmonary fibrosis and lung cancer were not significantly different from those in the normal controls. But, higher values of PGF-MUM were contained in the pulmonary fibrosis group, and the values of PGF-MUM were correlated with the serum LDH levels (r= 0.652, P less than 0.01). 4) The plasma PGF quantities were 0.7 +/- 0.5 ng/ml and the plasma PGE quantities were 1.7 +/- 0.6 ng/ml in normal subjects on an average. 5) The plasma PGF and PGE quantities in the patients with pulmonary emphysema were not significantly different from those in the normal controls. 6) A significant inverse correlation was observed between the decrease changes of pulmonary arterial pressures and the changes of plasma PGE quantities after oxygen inhalation for the patients with pulmonary emphysema (r= -0.737, P 0.01).
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PMID:[The quantities of main urinary metabolite of PGF, plasma PGF and plasma PGE in pulmonary diseases]. 712 48

Pulmonary disease induced by chemotherapeutic drug or radiation is one of the major cause, of death in patients with lung cancer. Many of these patients die from interstitial lung disease despite discontinuation of the drug and addition of corticosteroid treatment. The clinical presentation is similar for all of the chemotherapeutic drugs. For the early detection of interstitial lung disease due to a chemotherapeutic drug, serial measurements of the CO diffusing capacity (DLco), serum LDH, and serum KL-6 are useful. The first step in treatment is withdrawal of the drugs, and pulse therapy by using methylprednisolone is used as a standard therapy for interstitial lung disease due to chemotherapeutic agents. Immunosuppressive agents, such as cyclophosphamide or azathioprine, might be used as second-line drugs in patients for whom drugs either failed or could not tolerate corticosteroid treatment. Thus the usefulness of this therapy is unknown, and it should be considered as a marginal therapy. To develop an investigational therapy for the chemotherapeutic drug-induced interstitial lung disease, we investigated the efficacy of a new specific neutrophil elastase inhibitor (ONO-5046.Na) in bleomycin-induced pulmonary fibrosis. The inhibitory effect of ONO-5046.Na was observed in bleomycin-induced pulmonary fibrosis in mice. This specific neutrophil elastase could be a investigational therapeutic agent for interstitial lung disease due to chemotherapeutic agents used against lung cancer.
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PMID:[Strategy of therapy for interstitial lung disease due to chemotherapeutic drugs or radiation]. 936 19

A high level of serum KL-6 is a known feature of active pulmonary fibrosis. Some researchers have suggested that KL-6 is produced and secreted by type II pneumocytes. The present study evaluated serum KL-6 levels in patients with summer-type hypersensitivity pneumonitis (summer-type HP) (n = 6, 7 episodes), Mycoplasma pneumoniae pneumonia (n = 16), Chlamydia psittaci pneumonia (n = 3), Chlamydia pneumoniae pneumonia (n = 9), and bacterial pneumonia (n = 12). In addition, transbronchial lung biopsy (TBLB) specimens were examined pathologically in order to identify the site of production and secretion of KL-6. In patients with summer-type HP, the serum KL-6 levels exceeded 500 U/ml (2.996 +/- 2.016 U/ml), but was below 500 U/ml (302 +/- 126 U/ml, p < 0.001) in the patients with other infectious pneumonias, with the exception of two. One of these two patients with a high serum KL-6 level had adult respiratory distress syndrome due to Mycoplasma pneumoniae. The other had organizing pneumonia due to Chlamydia pneumoniae. TBLB specimens showed proliferative type II pneumocytes in all summer-type HP cases. We believe that the high serum KL-6 levels were produced by type II pneumocytes, and may provide a useful indicating serum marker for HP. Although serum LDH, serum CRP and PaO2 are known as monitoring markers in summer-type HP, our findings demonstrated no manifest correlations among these markers. However, serum KL-6 levels showed a strong positive correlation with serum LDH levels and an inverse correlation with serum CRP levels. These results suggest that serum KL-6 may be a better marker of the degree of disease activity than serum LDH, CRP, or PaO2 in summer-type HP.
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PMID:[Evaluation of serum KL-6 levels in summer-type hypersensitivity pneumonitis]. 986 78

Cigarette smoke toxicants are well known for their debilitating effects on lungs. Cigarette smoke toxicities cause various respiratory disorders including pulmonary emphysema, chronic obstructive pulmonary disease (COPD), pulmonary fibrosis and cancer. Farnesol, an isoprenoid, is known to possess anti-inflammatory and chemopreventive properties. In this study we report the protective efficacy of farnesol against massive lung inflammation, oxidative stress and consequent injuries caused by cigarette smoke toxicants. Farnesol was administered by gavage (50 and 100 mg/kg b.wt. in corn oil) one time daily for 7 days. On day 7 lung injuries were induced by intratracheal instillation of aqueous cigarette smoke extract (CSE). LDH, total cell count, total protein, phospholipid content and MDA formation were measured in bronchoalveolar lavage fluid (BALF). In lung tissue H2O2 content, reduced glutathione (GSH), glutathione reductase (GR), glutathione peroxidase (GPx) and catalase activities were evaluated. Prophylactic treatment with farnesol significantly shows lung protection by lowering the levels of LDH, total cell count, total protein and MDA in BALF. Farnesol maintained the phospholipid content of BALF in a positive manner. In lung tissue it positively modulated the CSE altered activities of GR, GPx and catalase. There was a marked increase in GSH content and decrease in H2O2 content of lung tissue by farnesol administration. Histopathological findings correlate with cellular and biochemical parameters of the lungs and potentiate the protective role of farnesol against CSE induced lung inflammation and injuries. These results suggest a potent role of farnesol in protection of lung against cigarette smoke toxicants induced lung injuries.
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PMID:Farnesol ameliorates massive inflammation, oxidative stress and lung injury induced by intratracheal instillation of cigarette smoke extract in rats: an initial step in lung chemoprevention. 1879 22


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