Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An imbalance of proteolytic enzymes and protease inhibitors may contribute to the development of bronchopulmonary dysplasia. We studied secretory leukocyte protease inhibitor (not previously addressed), and alpha 1-antitrypsin, alpha 1-antichymotrypsin, alpha 2-macroglobulin and elastase. Albumin was used as an internal reference. Infants with pneumonia had higher concentrations of secretory leukocyte protease inhibitor (p = 0.02) and elastase (p = 0.04) in bronchoalveolar lavage fluid than those with respiratory distress syndrome; those who also developed bronchopulmonary dysplasia had intermediate values. A decreased concentration of alpha 1-antitrypsin was found in the second and third postnatal weeks (p = 0.002). Further detailed studies of the balance between proteases and protease inhibitors and of the importance of pulmonary infections in the pathogenesis of bronchopulmonary dysplasia are suggested. Secretory leukocyte protease inhibitor is important both as an elastase inhibitor of bronchial mucus and as a marker of infection in the bronchi.
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PMID:Protease inhibitors in bronchoalveolar lavage fluid from neonates with special reference to secretory leukocyte protease inhibitor. 138 26

In spite of the development of various antibiotics, management of elderly patients with pneumonia remains an important problem. It is suggested that adult respiratory distress syndrome (ARDS) and disseminated intravascular coagulation (DIC) often occur in elderly patients with pneumonia. Although neutrophils are suggested to be involved in the genesis of these conditions, details remain unknown. We demonstrated that a highly cytotoxic substance, 9,10-epoxy-12-octadecenoate, is biosynthesized from linoleate by human neutrophils, thus it was named leukotoxin. Leukotoxin was detected in lung lavages from patients with ARDS. In these lung lavages, increases in albumin concentration and angiotensin converting enzyme (ACE) activity were also observed. Similar results were observed in lung lavages from rats after exposure to hyperoxia for 60 hours in an experimental model of ARDS. Intravenous administration of leukotoxin (100 mumol/kg) caused lung edema. Albumin concentration and ACE activity were increased in lung lavages of rats receiving leukotoxin. In contrast, these changes were not observed in rats administered with linoleate. Furthermore, administration of leukotoxin (100 mumol/kg) caused coagulation abnormality, i.e., increase in fibrin-fibrinogen degradation products, decrease in fibrinogen, and prolongation of activated partial thromboplastin time and prothrombin time. Administration of linoleate did not induce these changes. It is indicated that O2- was produced by respiratory burst enzyme located in neutrophil plasma membrane, and that hydroxyl radicals derived from O2- by Fenton reaction were responsible for leukotoxin synthesis. From our results, leukotoxin, a product of hydroxyl radicals and linoleate, might be responsible for the genesis of ARDS and DIC.
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PMID:[Leukotoxin and pulmonary injury]. 238 90

Bronchoalveolar lavage fluid (BALF) was analysed to obtain information on leakage of proteins from the blood into the respiratory lumen and on local synthesis. Albumin, ceruloplasmin and alpha-2-macroglobulin were measured in paired BALF and serum samples from patients with acute pneumonitis or asthma. Ceruloplasmin (CP) and alpha-2-macroglobulin (A2M) were measured by ELISAs thereby avoiding concentration of BALF. The quotients 10(3) ([protein]BALF)/(protein]serum), Qprotein, were calculated as well as the relative coefficients of excretion, RCE: Qprotein/Qalbumin. The QCP and QA2M increased parallel to Qalbumin in patients with pneumonitis and QCP increased parallel with Qalbumin in the asthma patients. This indicates that abnormal leakage of proteins from the blood rather than local synthesis cause the increased concentrations of these proteins in the BALF. Increased values for the RCE of CP and A2M were observed at normal Qalbumin. We therefore conclude that the determination of CP and A2M yields more detailed information on leakage of proteins from the blood into the airway compartment than that of albumin.
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PMID:ELISA of ceruloplasmin and alpha-2-macroglobulin in paired bronchoalveolar lavage fluid and serum samples. 244 79

Amiodarone (ADR), a new antiarrhythmic drug for life-threatening cardiac arrhythmias, causes pneumonitis or lung fibrosis in a sizeable minority of patients. The cause of lung damage is not known. We have shown that infusion of 10 mg amiodarone into the inflow circuit of ventilated and perfused rabbit lungs causes immediate increase in pulmonary artery pressure (mean +/- SEM) (from 13.6 +/- 1.2 to 40.6 +/- 9.5 mm Hg, p less than 0.01) and pulmonary edema with marked increase in the pulmonary generation of thromboxane and leukotrienes C4 and/or D4. Albumin (2 g%) in the perfusate prevents any increase in lung perfusion pressure or edema formation. When lung perfusion pressure increase is blocked with the combined cyclooxygenase and lipoxygenase inhibitor enolicam sodium (CG5391B, 35 microM in perfusate), significant lung edema still occurs after amiodarone, indicating that amiodarone causes increased alveolar-capillary membrane permeability. Addition of catalase (100 U/ml) or superoxide dismutase and catalase (100 U/ml each) to perfusate fails to protect from amiodarone lung injury. Immediate infusion of amiodarone (10 mg) into lungs ventilated with room air (ADR + RA) causes an increase in lung weight gain from baseline (delta W) of 5.7 +/- 1.5 g/min. Compared with ADR + RA, ventilation of lungs with 4% O2 (delta W = 0.7 +/- 0.3 g/min, p less than 0.05), pretreatment of rabbits for 3 days with butylated hydroxyanisole (BHA, 100 mg/kg/day i.p., delta W = 0.05 +/- 0.02 g/min, p less than 0.01), pretreatment of rabbits for 3 days with vitamin E (Vit E, 300 U/day orally, delta W = 0.6 +/- 0.2 g/min, p less than 0.05), or addition of N-acetylcysteine to the lung perfusate (NAC, 5 mM, delta W = 0.1 +/- 0.08 g/min, p less than 0.01) all protect from lung edema formation after amiodarone. Amiodarone (100 mg) also caused a marked increase in luminol-enhanced lung chemiluminescence, lung production of superoxide anion (O2-), and tissue levels of lung glutathione disulfide. These results suggest that amiodarone causes lung injury by an oxidant mechanism.
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PMID:Amiodarone causes acute oxidant lung injury in ventilated and perfused rabbit lungs. 245 31

The response of the lung was studied in CFLP mice after exposure of the whole thorax to X rays (250 kVp) or cyclotron neutrons (16 MeV deuterons on Be, mean energy 7.5 MeV). To measure blood volume and leakage of plasma proteins, 51Cr-labeled red blood cells and 125I-albumin were injected intravenously and 24 h later lungs were lavaged via the trachea. Radioactivities in lung tissue and lavage fluid were determined to estimate the accumulation of albumin in the interstitial and alveolar spaces indicating damage to blood vessels and alveolar epithelium respectively. Function of type II pneumonocytes was assessed by the amounts of surfactant (assayed as lipid phosphorous) released into the lavage fluid. During the first 6 weeks, lavage protein and surfactant were increased, the neutron relative biological effectiveness (RBE) being unity. During pneumonitis at 12-24 weeks, surfactant levels were normal, blood volume was decreased, and both interstitial and alveolar albumin were increased. Albumin levels then decreased. At late times after exposure (42-64 weeks) alveolar albumin returned to normal but interstitial albumin was still slightly elevated. Values of RBE for changes in blood volume and interstitial and alveolar albumin at 15 weeks and for changes in blood volume and interstitial albumin at 46 weeks were 1.4, comparable with that for animal survival at 180 days. The results indicate that surfactant production is not critical for animal survival. They suggest that changes in blood vessels and alveolar epithelium occur during acute pneumonitis; epithelial repair follows but some vascular damage may persist. The time course of the changes in albumin levels did not correlate with increases in collagen biosynthesis which have been observed as early as 1 month after exposure and persist for up to 1 year. Furthermore, a dose which had no effect on leakage caused a marked increase in collagen biosynthesis. Thus the present results do not support a causal relationship between exudation of vascular protein during pneumonitis and the later development of fibrosis.
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PMID:Vascular and epithelial damage in the lung of the mouse after X rays or neutrons. 291 6

Bronchoalveolar lavage (BAL) is a new diagnostic tool which could be applied repeatedly to investigate the nature of lesion in pulmonary diseases. To evaluate the clinical significance of the difference in immunoglobulin content for the differential diagnosis between benign and malignant pulmonary diseases, we performed bronchoalveolar lavage for 64 patients. They included 12 patients with bronchogenic carcinoma, 12 patients with pulmonary tuberculosis, 20 patients with benign non-specific bronchopulmonary diseases (these including 6 patients with pneumoconiosis, 6 patients with bronchietasis, 2 patients with paraquate intoxication, 6 patients with pneumonia) and 20 healthy persons as of the control group. We analyzed the following items: (1) cell count (2) differential count (3) protein content (4) immunoglobulin content. The results showed that there were increase in PMN cells in paraquate intoxication, pnuenmonia and bronchiectasis. While there was lymphocytosis in pulmonary tuberculosis. In comparison with the control group, there was elevation of statistical significance in the IgA/Albumin ratio in bronchogenic carcinoma and pulmonary tuberculosis. Although the IgG/Albumin ratio would be elevated with statistical significance among a variety of pulmonary diseases, it was particularly high in pulmonary tuberculosis. In contrast, the IgA/IgG ratio was significantly increased only in bronchogenic carcinoma. In conclusion, there were differences in the cell number, differential cell count, protein content and immunoglobulin content among various pulmonary diseases. It may be useful in making differential diagnosis between benign and malignant pulmonary disease and the prediction of prognosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A preliminary study for cellular, albumin and immunoglobulin components of bronchoalveolar lavage fluid in normal control, pulmonary T.B. and malignant lung diseases]. 319 60

A case is reported in whom the triad generalized lymphedema, nail dystrophy, and pleural effusion was associated to protein-losing enteropathy. This combination, not previously described, was also characterized by exacerbations of pleural effusion with recurrent episodes of broncho-pneumonia. Albumin turnover study showed depletion of the total body pool, decreased catabolic rate, and elevated albumin removal through the gastrointestinal tract. During bronchopneumonia, increased capillary permeability due to pleural involvement may worsen the basic deficit of pleural lymphatic drainage.
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PMID:Pleural effusion and recurrent broncho-pneumonia with lymphedema, yellow nails and protein-losing enteropathy. 397 79

An animal model of Legionella pneumophila pneumonia was developed to study aerosol infection, pathogenesis, and pulmonary host defense mechanisms. Guinea pigs were exposed in an inhalation facility that limited the aerosol of L pneumophila to the snout. Bronchoalveolar lavage was used to sample airspace cells, secretions, and bacteria during developing infection in 79 exposed animals and 13 uninfected controls. An influx of polymorphonuclear neutrophils followed exponential bacterial growth during the initial three days of infection and coincided with limitation of the increase in bacteria recovered. A macrophage influx occurred at three to five days. Bacteria were eliminated from the lung by 11 days after exposure. Albumin in lavage fluid peaked at two days. Most viable L pneumophila organisms were associated with alveolar macrophages, whereas most of the bacteria associated with polymorphonuclear neutrophils were nonviable. Recruited, and possibly immune, defenses appear to be required for successful resolution of legionella pneumonia.
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PMID:The kinetics of early inflammatory events during experimental pneumonia due to Legionella pneumophila in guinea pigs. 663 Oct 74

Fundoplication remains a common operation in the brain-damaged pediatric patient, but recent reports suggest a poor outcome in these patients. The factors that might be associated with complications or recurrence after fundoplication have not been extensively examined. Fifty-six brain-damaged children, aged 6 months to 12 years, with documented gastroesophageal (GE) reflux underwent preoperative nutritional evaluations (percentage of ideal weight, albumin, nutrition risk index [NRI]) and documentation of medications (dexamethasone for bronchopulmonary dysplasia) before standard Nissen fundoplication. Hospital stay, intensive care unit (ICU) stay, and time on ventilator, as well as major postoperative complications (wound infection/dehiscence, pneumonia) were prospectively analyzed. Survival and recurrence rates 1 to 3 years postoperatively were also assessed. Eighty-two percent of patients were < 90% ideal weight, and 50% had NRI < 90 (normal = 100) and 29% had albumin < 3.5 g/dL. Albumin < 3.5 was significantly (P < .01) associated with prolonged hospitalization (26.8 + 2.2 versus 15.1 + 1.1 days) and ICU stay (13.8 + 1.0 versus 4.4 + .5 days) and time on ventilator (8.0 + 1.0 versus 1.8 + .4 days). NRI < 90 showed similar significant differences (P < .01). Ideal body weight < 90% was not significant. Major complications developed in 54% of patients; only two or more preoperative nutritional deficiencies, or a nutritional deficiency plus dexamethasone were significantly associated (P < .01). Recurrence occurred in 21% of patients and was significantly correlated with preoperative dexamethasone alone (P < .01), and especially when dexamethasone plus a nutritional deficit were present (low albumin, P < .001; low NRI, P < .005).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A prospective analysis of factors influencing outcome after fundoplication. 747 33

A study has been made of the influence of the nutritional situation on post-operative infections in a sample of 217 patients. A nutritional evaluation file was prepared for each of them, based on anthropometric and analytical tests and delayed hypersensitivity skin tests (PCHR) during the first 24 hours of hospital admission. The criteria whereby a post-operative infection was considered to be present were surgical wound infection, intra-abdominal infection, pneumonia and post-operative fever of 38.5 degrees C or more without a demonstrable septic focus. They were also evaluated quantitatively using Elebeute and Stoner's sepsis index. In the study of the anthropometric parameters, the relation was noted between the body mass index (BMI) and usual weight Percentage (HW%), and septic risk areas (RA) were defined, as a new anthropometric data. A total of 33 patients (15.2%) showed some type of post-surgical infection, manifested in this group by an alteration of the nutritional state revealed by a lower BMI, increased weight loss, a lower albumin rate than in the control group. The septic prognostic value of the RAS is confirmed: no relation was found between septic complications and the PCHR. Finally a multiple regression procedure was prepared between the Elebeute and Stoner sepsis index and all the nutritional parameters studied, to give the following nutritional sepsis risk prognosis index (RSN): NSR = 14,265 - 1,764 x Albumin - 1,427 x Risk Area.
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PMID:[The prediction of postoperative septic complications via nutritional parameters. I. The prognostic formulation]. 801 94


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