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 47-year-old man had an episode of severe respiratory failure after acute intoxication with arsenic. Features of the initial clinical presentation included nausea, vomiting, and diarrhea, acute psychosis, diffuse skin rash, and marked pancytopenia. A peripheral neuropathy then developed which resulted in severe weakness of all muscles of the limbs, the shoulder and pelvis girdles, and the trunk. The neuropathy continued to progress despite treatment with dimercaprol (BAL in oil). Five weeks after the initial exposure, the patient was no longer able to maintain adquate ventilation and required mechanical ventilatory support. Improvement in the patient's neuromuscular status permitted successful weaning from the ventilator after one month of mechanical ventilation. Long-term follow-up revealed no further respiratory difficulty and slow improvement in the strength of the peripheral muscles.
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PMID:Acute respiratory failure following severe arsenic poisoning. 22 46

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 63-year-old man with pulmonary sarcoidosis, diagnosed by mediastinal lymph node biopsy in 1977, was admitted in Feb. 1987 because of shortness of breath and cough. Chest X-ray showed bilateral hilar lymphadenopathy and a tumor shadow in the right lung field. Histological examination of specimens biopsied from the right lung revealed small cell carcinoma (S.C.C.). Bronchoalveolar lavage was performed to evaluate the disease activity of sarcoidosis, and the total number of cells and T-lymphocytes; the ratio of CD4+ cells to CD8+ cells was not increased. He was treated with combination chemotherapy, however, he died of respiratory failure after 7 months. An autopsy was performed, and the lesions were examined histologically. The sarcoid lesion in a lymph node obtained at autopsy was not active, in contrast to that obtained by mediastinal lymph node biopsy. Lung cancer and sarcoidosis are both common diseases, but their coexistence in the same patient is not common, and autopsied cases are rare. In this case, an autopsy was performed, and BAL had been performed prior to his death. The relationship between the BAL findings and the histology of sarcoidosis was examined. Based on the results of autopsy and BAL, the sarcoidosis was inactive prior to death, but had been histologically active 10 years previously. Therefore, this is a very interesting case, since we can examine the relationship between the two diseases, and the progression of each disease. This case also provides an interesting example of differentiation of sarcoidosis from S.C.C. Metastatic invasion of the hilar lymph nodes without bronchial stenosis and changes secondary to stenosis may often occur in patients with small cell lung cancer. Such metastatic invasion closely resembles the bilateral hilar lymphadenopathy of sarcoidosis; therefore, in some cases, it may be extremely difficult to differentiate the two diseases.
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PMID:[A case of small cell lung cancer associated with pulmonary sarcoidosis]. 166 44

Severe respiratory failure is always associated with a defect in the surfactant system. Surfactant substitution in newborn infants with respiratory distress syndrome (RDS) has gained worldwide acceptance. In the present study, we have evaluated whether surfactant diagnostics are of use in choosing recipients of exogenous surfactant. In addition, we studied whether factors apparently unrelated to surfactant influence the degree of respiratory failure and surfactant responsiveness. In small preterm infants, the surfactant indices in amniotic fluid (L/S ratio and phosphatidylglycerol), within 3 days of birth, predicted the risk of RDS with a sensitivity of 90-100%, and a specificity of 50-85%. The surfactant indices, measured in BAL, predicted the risk of ARDS (which became evident 1 to 7 days later) with a sensitivity of 50-60% and a specificity of 59-65%. In small preterm infants with RDS, the amount of fluids given during the first day correlated positively with the degree of respiratory failure and negatively with the degree of surfactant responsiveness. According to an experimental study, in hydrostatic lung edema, exogenous surfactant is diluted by edema fluid and becomes sensitive to inhibitors of surfactant function. Beside dosage, quality, and time of administration, the management of patients largely dictates the responsiveness to exogenous surfactant.
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PMID:Lung surfactant in respiratory distress syndrome. 192 23

Pneumonitis has been reported to be a rare complication of low-dose MTX treatment. This paper describes a 62-year-old male patient in whom clinically successful low-dose treatment was applied. After six months of treatment, a gradually progressive pulmonary symptomatology developed and abruptly deteriorated. Radiological examination revealed interstitial and intra-alveolar densifications; functional analysis revealed partial respiratory failure. The histological finding of interstitial lymphocytic infiltration with giant cells and a chronic intra-alveolar pneumonia, with bacteriological detection of E. coli and Proteus vulg. in the BAL fluid, confirmed the suspected diagnosis of primary MTX-induced pneumonitis with secondary bacterial superinfection. In view of the fact that the literature does not seem to contain unequivocal definition, it is urgently recommended that unequivocal criteria be established.
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PMID:[Pneumonitis as a complication of low-dose methotrexate therapy in chronic polyarthritis]. 236 74

We describe the cases of two individuals with advanced AIDS who sought treatment for rapidly progressive respiratory failure due to T gondii pneumonia. The first patient responded to specific therapy after an early diagnosis but died 2 months later of bacterial sepsis. In the second case, the diagnosis was made at autopsy. This led to a meticulous retrospective review of the original slides of material obtained from BAL. T gondii tachyzoites not previously identified during the initial analysis of the slides were seen on both GIE and PAP stains. Neither of our severely immunocompromised patients had evidence of central nervous system involvement. Even though we cannot exclude dissemination to other organs, a progressive pneumonitis mimicking a classic P carinii infection was the primary presentation. Trophozoites were identified by BAL in both cases, underscoring the diagnostic potential of this minimally invasive procedure.
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PMID:Toxoplasma gondii pneumonia in patients with the acquired immunodeficiency syndrome: diagnosis by bronchoalveolar lavage. 820 79

ARDS includes a complex series of events leading to alveolar damage, high permeability pulmonary edema, and respiratory failure. The endogenous pulmonary surfactant system is crucial to maintaining normal lung function, and only recently has it been appreciated that alterations in the surfactant system significantly contributed to the pathophysiology of the lung injury of patients with ARDS. Through a combination of analyzing BAL samples from patients with ARDS and extensive animal studies, there have been significant insights into the variety of surfactant abnormalities that can occur in injured lungs. These include altered surfactant composition and pool sizes, abnormal surfactant metabolism, and inactivation of alveolar surfactant by serum proteins present within the airspace. Positive effects of exogenous surfactant administration on acute lung injury have been reported. There is now a prospective, randomized clinical trial evaluating the efficacy of aerosolized exogenous surfactant in patients with ARDS. This trial has demonstrated improvements in gas exchange and a trend toward decreased mortality in response to the surfactant. Despite these encouraging results, there are multiple factors requiring further investigation in the development of optimal surfactant treatment strategies for patients with ARDS. Such factors include the development of optimal surfactant delivery techniques, determining the ideal time for surfactant administration during the course of injury, and the development of optimal exogenous surfactant preparations that will be used to treat these patients. With further clinical trials and continued research efforts, exogenous surfactant administration should play a useful role in the future therapeutic approach to patients with ARDS.
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PMID:Surfactant and the adult respiratory distress syndrome. 842 Apr 22

Drug-induced eosinophilic lung disease commonly presents as a simple pulmonary eosinophilia-like syndrome consisting of transient pulmonary infiltrates, peripheral eosinophilia, and mild pulmonary symptoms that disappear promptly upon withdrawal of the offending medication. However, a more fulminant presentation most resembling acute eosinophilic pneumonia has been recently described. We present a patient with BAL-confirmed eosinophilic pneumonia (EP) and respiratory failure after a trazodone overdose. This is the first case of EP associated with trazodone and only the third drug-mediated EP reported to precipitate respiratory failure.
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PMID:Eosinophilic pneumonia and respiratory failure associated with a trazodone overdose. 852 Jul 92

In summary, orthomyxo- and paramyxoviruses cause clinically important infections in transplant patients. Patients often develop lower respiratory tract involvement and sometimes respiratory failure, which almost is uniformly fatal. Bone marrow transplant recipients appear to be at higher risk of severe disease than are solid-organ recipients, but well defined criteria to predict those patients who will be severely affected are not available. Factors associated with more severe disease include the type of viral pathogen, with pneumonia occurring more commonly with RSV and PIV infection, and the degree of immunosuppression of the patient, particularly the pre-engraftment phase in bone marrow transplant recipients. Because mortality is associated with development of pneumonia, prompt diagnosis and studies for concurrent infections are essential. Evaluation of fever and upper respiratory tract symptoms in patients in the peritransplant period should include sampling of nasopharyngeal and throat for virus isolation and antigen detection for respiratory viruses. If patients develop lower respiratory tract symptoms, early bronchoscopy with BAL is indicated. No specific antiviral therapy has proved effective in the treatment of established respiratory viral infections of transplant patients. Aerosolized ribavirin or, in the instance of influenza A virus infection, oral rimantadine might be considered as early therapy to prevent severe lower respiratory disease. Intravenous ribavirin, currently available on a compassionate use basis, might be considered for treating measles virus infection. In patients with lower tract disease due to RSV, the addition of immunoglobulin with high neutralizing antibody titers to RSV or intravenous ribavirin are additional considerations to forestall respiratory failure. Controlled studies of these interventions are needed in transplant patients before their use can be recommended routinely.
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PMID:Orthomyxoviral and paramyxoviral infections in transplant patients. 874 76

In patients with AIDS, isolation of cytomegalovirus (CMV) from respiratory secretions is common. It is often found with other pathogens, which has led to debate regarding its role as a primary pulmonary pathogen. A retrospective investigation of patients with AIDS and CMV as a sole pulmonary isolate was performed in an attempt to describe their clinical presentation and course. All patients admitted to the hospital with pneumonia and with BAL or transbronchial biopsy (TBB) specimen positive for CMV between 1991 and 1994 were identified through a review of inpatient records. Inclusion criteria included positive CMV cultures from BAL, cytomegalic inclusion bodies from BAL or TBB, and thorough documentation of the absence of other pulmonary pathogens. Nine patients met the inclusion criteria for CMV pneumonitis. Seven were male and two were female, ages 26 to 44 years, and all had a history of opportunistic infections. Typical clinical presentation was characterized by increased respiratory rate, hypoxemia, and diffuse interstitial infiltrates. The mean CD4 count was 29.6 (+/- 22) cells per cubic millimeter, mean lactate dehydrogenase level was 414 (+/- 301) IU/L, and in seven patients in whom CMV antigen was measured it was greater than 50 positive cells per 200,000 WBCs. Three untreated patients died of respiratory failure and three had autopsy confirmation of CMV pneumonia. Five patients were treated with anti-CMV therapy for at least 2 weeks, and all demonstrated improvement in symptoms, oxygen saturation, and chest radiograph. At 3 months follow-up, all five patients were asymptomatic with no pulmonary symptoms. At 6 months follow-up, three of the five patients remained asymptomatic; the other two died of other opportunistic infections. In at least these nine patients, CMV represented a primary pulmonary pathogen. Patients who were treated responded quickly and were able to be discharged home from the hospital with marked improvement in their symptoms. We recommend that clinicians consider this diagnosis in the proper setting and consider treatment with anti-CMV therapy.
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PMID:Cytomegalovirus as a primary pulmonary pathogen in AIDS. 931 35


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