Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:6.2.1.7 (BAL)
1,977 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A 49-year-old man with high alcohol consumption was admitted with fever, cough and progressive dyspnea after a one week history of influenza-like symptoms. Chest X-ray film on admission showed diffuse peribronchial shadows and patchy infiltration in the right lower lung field. Chest X-ray film the following day and chest CT film on the 4th day of admission showed multiple nodular shadows and cavity formation. At bronchoscopy the bronchial surface was covered by white plaque, and Asp. fumigatus was subsequently cultured from BAL fluid. On the basis of suspected invasive pulmonary aspergillosis, anti-fungal agents were commenced. However, the shadows on chest X-ray increased, and the patient died on the 10th day of admission of respiratory failure and septic shock. Histological examination revealed bronchial wall invasion by hyphae of aspergillus and abscess formation in the pulmonary parenchyma. The precipitin antibody against aspergillus antigen was positive in reserved serum. Anti-Influenza A virus antibody (CF) was positive (X 256), and hemagglutination inhibition test of Influenza A (H3N2) was positive (X 2048) in serum on admission. The suppression of cellular immunity and destruction of the mucociliary system of airways induced by Influenza A infection was suspected to have predisposed to aspergillus superinfection.
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PMID:[A case of invasive broncho-pulmonary aspergillosis associated with influenza A (H3N2) infection]. 140 13

A smelter exposed to zinc fumes reported severe recurrent episodes of cough, dyspnea and fever. Bronchoalveolar lavage showed a marked increase in lymphocytes count with predominance of CD8 T-lymphocytes. Presence of zinc in alveolar macrophages was assessed by analytic transmission electron microscopy. This is the first case of recurrent bronchoalveolitis related to zinc exposure in which the clinical picture and BAL results indicate a probable hypersensitivity pneumonitis.
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PMID:Occupational hypersensitivity pneumonitis in a smelter exposed to zinc fumes. 154 Nov 64

A 40-year-old man who lived in a wooden house built 30 years ago presented with complaints of fever, dry cough and dyspnea. Chest X-ray findings showed interstitial shadows throughout bilateral lung fields. After admission, high-dose administration of 3000 mg of methylprednisolone was performed because of deterioration of chest X-ray shadows and symptoms. In a week, clinical data and symptoms improved. Findings of BAL fluid on admission revealed a relative increase of lymphocytes, neutrophils and mast cells, and pathological findings of transbronchial lung biopsy revealed non-caseous granulation and alveolitis. Precipitating antibodies and indirect fluorescent antibodies against Trichosporon cutaneum and Cryptococcus neoformans had positive reactions and T. cutaneum was isolated and identified from the patient's house. A diagnosis of summer-type hypersensitivity pneumonitis was made according to the criteria advocated by Ando et al. This seemed to be a rare case of summer-type hypersensitivity pneumonitis prolonged after isolation from his normal living environment, successfully treated by high-dose administration of steroid.
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PMID:[A case of severe summer-type hypersensitivity pneumonitis treated with high-dose administration of steroid]. 177 Jun 86

A case of a 34 year old female with clinical and histological confirmed eosinophilic granuloma causing osteolytic lesions of the mandible and skull and diabetes insipidus. Dyspnea, cough, exercise intolerance with ventilatory disturbances and radiological evidence of interstitial lung disease were believed to be in the course of eosinophilic granuloma. The patient refused lung biopsy and BAL. After starting therapy with corticosteroids all respiratory symptoms improved.
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PMID:[Interstitial lung disease in Langerhans-cell granulomatosis in a 34-year-old woman]. 184 9

A 43-year-old man was admitted to our hospital because of cough and dyspnea. His chest X-ray showed bilateral basal infiltrative shadows. The increased eosinophils in BAL suggested chronic eosinophilic pneumonia (CEP), whereas the TBLB specimens showed findings compatible with desquamative interstitial pneumonia (DIP). The open lung biopsy specimens showed typical findings of DIP with a peripheral zone, suggestive of CEP. These two diseases may be only phasal differences of reaction to the same extrinsic stimulation.
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PMID:[A case of desquamative interstitial pneumonia (DIP) suggesting a relationship to chronic eosinophilic pneumonia (CEP)]. 221 8

Fifteen asthmatic patients were prospectively selected. If they had more than 450 eosinophils in peripheral blood on admission to hospital treatment and if before BAL had been performed they were not treated by corticosteroids. No associated disease was found which could cause the increased number of eosinophils in peripheral blood except bronchial asthma. BAL was performed when the subjects tested had no dyspnea, usually 1-3 days after the hospital admission. In contrast to blood eosinophilia, increase of eosinophils number in BAL was found to correlate to impairment of clinically measured parameters such as: ventilation level of blood gases and duration of hospitalisation. On the contrary there was no correlation between the level of blood eosinophilia and gas disturbance and duration of hospitalisation. Eosinophilic proteins (MBP, ECP, EPX, EPO) are not the only that harmfully effect the lung cells in the asthmatic attack but the fact that their level in lavage fluid correlates to eosinophilia degree in BAL is evident so the correlation between the number of eosinophils in BAL and impairment of clinically measured parameters is clear.
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PMID:[Evidence of the harmful effects of eosinophils in bronchial asthma]. 221 19

Bronchiolitis obliterans organizing pneumonia (BOOP) is a pathologic finding common to various injuries to the lung of either definite or idiopathic etiology. Since the presentation of patients with idiopathic BOOP varies, we studied 16 patients with BOOP on pulmonary histology to define more distinct and homogeneous clinical and imaging profiles of idiopathic BOOP. We distinguished three groups of patients: group 1 (n = 4), with multiple patchy migratory pulmonary involvement of the pneumonia type. Their clinical course was subacute, with cough, fever, weight loss, mild dyspnea, and increased ESR. Chest x-ray film and CT scan showed multiple alveolar opacities. All patients completely recovered with corticosteroid therapy but relapsed when therapy was stopped too rapidly. Group 2 (n = 5) had solitary pulmonary involvement of the pneumonia type occurring in a similar clinical context. Since carcinoma was suspected, they underwent surgical excision of the pneumonic area and recovered without relapse. Group 3 patients (n = 7) presented with diffuse pulmonary involvement of the interstitial lung disease type. They had more progressive onset of more severe dyspnea, crackles heard over all lung surfaces, and interstitial opacities with or without alveolar opacities on chest imaging. Improvement with corticosteroid therapy was obtained in only three patients. In all three groups, lung function test results showed a restrictive pattern. The obstructive pattern characteristic of pure bronchiolitis obliterans was found in none. BAL showed a mixed pattern (increase of both lymphocytes and polymorphonuclear cells) in the patients of the first two groups. Thus, we distinguished three characteristic clinical and imaging profiles in patients with idiopathic BOOP: multiple patchy pneumonia, solitary pneumonia, and diffuse interstitial lung disease. These profiles are so different that they should be distinguished in clinical studies of idiopathic BOOP.
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PMID:Idiopathic bronchiolitis obliterans organizing pneumonia. Definition of characteristic clinical profiles in a series of 16 patients. 280 73

To this point we have attempted to summarize what we believe to be the most exciting new findings relative to sarcoidosis, along with providing data in support of those comments. We wish to conclude this brief review by sharing some anecdotal thoughts (no benefit of controlled clinical trials) concerning how the individual practitioner may apply this "research" information in caring for patients. In newly diagnosed patients with sarcoidosis, especially with widespread use of transbronchial lung biopsy, we would recommend BAL at that time because it can provide very valuable information with minimal increased morbidity or cost. BAL, in combination with SACE and possibly gallium scan (not required in all), along with the usual measures such as pulmonary function studies, chest roentgenograms (all of which are already commonly done) permit the clinician to make an accurate conclusion about disease activity in the lungs. Because there are no published therapeutic trials of corticosteroids in which the ultimate prognosis of pulmonary sarcoidosis has been improved, the decision to initiate therapy in these patients remains a clinical one and is commonly based upon practitioner experience rather than a particular laboratory test per se. Once that decision has been made, a decision to repeat any "research" studies would have to be individualized. Clearly serial SACE measures are relatively inexpensive and without morbidity. Moreover, despite their lack of "diagnostic value" serial measurements in known sarcoidosis have been shown to be very valuable in assessing disease activity and may therefore provide the clinician with a valuable aid to monitoring steroid treatment. A less common and much more perplexing circumstance occurs when evaluating patients with sarcoidosis established for several years present with evidence of progressive or chronic pulmonary involvement and dyspnea. In such individuals a measure of activity would be very helpful because the clinician would like to avoid steroids in persons with end stage and irreversible fibrosis and consider their use in those individuals in whom there is evidence of continued disease activity. In this instance, gallium scan, SACE and even BAL may all prove valuable. When we have found SACE elevated and gallium scan positive, we have assumed the disease to be active (even if the chest X-rays show stability).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Immunopathogenesis, immunology and assessment of activity of sarcoidosis. 632 25

A 51-year-old man developed fever, cough, and dyspnea 5 days after completing murine monoclonal anti-CD3 antibody (OKT3) treatment for acute cardiac allograft rejection. Samples of BAL fluid grew influenza A virus. Progressive pulmonary infiltrates, respiratory compromise, and hypoxia developed, and the patient ultimately required 5 days of mechanical ventilation. Treatment with amantadine hydrochloride and ribavirin was prescribed, and the patient was discharged after 19 days. Influenza A virus has not been an important pathogen in cardiac transplant recipients. However, this is the first reported case of influenza A pneumonitis complicating anti-T lymphocyte therapy for cardiac allograft rejection. In comparison with our patient, two previously reported cases of influenza A infection in cardiac transplant patients have been less severe. The virulence of our patient's, life-threatening infection appears to be secondary to impairment of T lymphocyte-mediated immunity by OKT3. The role of therapeutic and even prophylactic amantadine therapy in this clinical setting has yet to be determined.
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PMID:Influenza A pneumonitis following treatment of acute cardiac allograft rejection with murine monoclonal anti-CD3 antibody (OKT3). 758 60

A 70-year-old male was admitted because of cough and sputum. Chest X-ray showed bilateral interstitial shadows, and usual interstitial pneumonitis was diagnosed by TBLB and BAL. He was followed without medication. The dyspnea increased and the abnormal shadow spread on chest X-ray. Autoimmune hemolytic anemia was newly diagnosed because the RBC count was 195 x 10(4)/mm3, Hb was 8.6 g/dl, and direct Coombs test and warm antibody were positive. In this case, there appears to be a relationship between deterioration of interstitial pneumonia and the on-set of autoimmune hemolytic anemia.
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PMID:[A case of UIP with autoimmune hemolytic anemia]. 808 50


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