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)

Respiratory infection with Pneumocystis carinii (PC) is the most frequent serious opportunistic infection in the clinical setting of acquired immunodeficiency syndrome (AIDS). The factors responsible for the predisposition of human immunodeficiency virus (HIV)-infected patients for PC infection are not fully understood. We postulated that changes in the alveolar lining material (ALM) could play a role in the pathogenesis of PC infection in AIDS. We have compared constituents of ALM in bronchoalveolar lavage fluid from normal, nonsmoking volunteers with that of HIV-infected patients with pneumonia. Using an ELISA, we found that surfactant protein A (SP-A) was markedly elevated in the pneumonia patients. Mean SP-A values for the normal nonsmoking individuals (n = 21) were 1.50 +/- 0.25 micrograms/ml (mean +/- SEM). SP-A levels in the HIV-infected patients (n = 22) were significantly elevated (p less than 0.01) with a mean of 5.23 +/- 0.54 micrograms/ml. This increase was greatest in the patients with more clinically severe pneumonia. The increase in SP-A did not appear to be pathogen-specific as it was also observed in cases of non-PC pneumonia. We also found that total protein levels were nearly five times higher in the HIV-infected pneumonia patients. These studies indicate that the protein component of the ALM is markedly different from normal in cases of HIV-associated PC and non-PC infection. Further investigation is needed to determine the mechanism of these alterations and their role, if any, in AIDS-related pneumonia.
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PMID:Increased recovery of surfactant protein A in AIDS-related pneumonia. 202 16

To determine the clinical utility of airway carcinoembryonic antigen (CEA) concentrations to distinguish malignant from inflammatory airway disease in patients undergoing bronchoscopy, we determined CEA concentrations by enzyme immunoassay in bronchial washings recovered in 48 subjects, including 20 patients with central lung cancer, 18 patients with chronic bronchitis, and ten nonsmoking patients with a diagnosis of pneumonia or peripheral granuloma. Concentrations of CEA in bronchial washings were standardized by using the total protein concentration in recovered fluid (CEA/TP). Concentrations of CEA were significantly increased in bronchial washings recovered from both patients with chronic bronchitis and lung cancer compared with patients with pneumonia or granuloma (252 +/- 47 ng/mg and 199 +/- 64 ng/ml vs 62 +/- 11 ng/mg, SEM, p less than 0.005). Airway CEA concentrations in patients with chronic bronchitis were somewhat increased compared with concentrations recovered from a cancer-involved airway (252 +/- 47 ng/ml vs 199 +/- 64 ng/mg, SEM, p less than 0.05). Measurement of airway CEA concentrations is not useful in distinguishing malignant from inflammatory airway disease as airway concentrations of CEA may be markedly increased in patients with both conditions.
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PMID:Airway carcinoembryonic antigen concentrations in patients with central lung cancer or chronic bronchitis. 219 39

Positive end expiratory pressure (PEEP) is an accepted treatment for children with acute respiratory failure secondary to restrictive lung diseases. Using a simple technique based on open circuit nitrogen washout, we determined the functional residual capacity (FRC) in 25 ventilated children (age 3 wk-10 y) with acute respiratory failure secondary to restrictive lung disease (pulmonary edema, bilateral pneumonia). FRC measured at a physiologic level of PEEP (2-4 cm H2O) was 45.0 +/- 3.6% (mean +/- SEM; range 12-80%) lower than normal predicted values. At the PEEP level chosen clinically (4-10 cm H2O, mean = 6.0), the FRC was below normal predicted values for nonintubated children by a mean of 31.8% (range 0-73%) (p = 0.0001) and only seven patients (28%) had FRC within 20% below predicted normal values. FRC normalized at PEEP levels of 6-18 cm H2O (mean = 11.6), which was up to 200% above the clinically chosen PEEP level. In six children without lung disease who were ventilated at a PEEP level of 2-4 cm H2O, the FRC was within normal range in two, but significantly higher (by 45%) in the other four. We conclude that FRC in ventilated children with acute restrictive lung disease is significantly lower than normal and the clinically chosen PEEP fails to normalize the FRC in most of the cases.
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PMID:Functional residual capacity in ventilated infants and children. 225 67

The Extra Vascular Lung Water (EVLW) was measured using the thermal sodium double indicator dilution technique in 21 patients undergoing surgery for esophageal cancer. This measurement is an important parameter in the control of the respiratory function. In the 16 cases without pulmonary complications, the preoperative EVLW was 5.3 +/- 0.2 (mean +/- SEM) ml/kg and the immediate postoperative EVLW was 4.8 +/- 0.4 ml/kg. This change was significant (p less than 0.05), but within 24 hours the EVLW returned to almost the same levels as those recorded before surgery. In only 3 cases, the EVLW were elevated beyond 7.5 ml/kg, but these high EVLW levels did not continue for more than 12 hours. Of the 5 patients with pulmonary complications, only two experienced pulmonary edema. Their preoperative EVLW levels were normal, but the immediate postoperative EVLW levels were significantly elevated beyond 10 ml/kg. These elevated levels were observed before the PaO2, the portable chest roentgenograms and the other test results changed following surgery. The high EVLW levels beyond 7.5 ml/kg continued for 72 hours after surgery. We found no correlation between the EVLW and measureable hemodynamic parameters (Cardiac Index, Pulmonary Wedge Pressure, Colloid Osmotic Pressure-Pulmonary Wedge Pressure gradient) during the observation period. In the other cases with pulmonary complications (2 cases were pneumonia, one was atelectasis with pneumonia), the changes in the EVLW levels were the same as for the cases without pulmonary complications. These results indicate that the EVLW is the optimum parameter for the control of the respiratory function and early diagnosis of pulmonary edema after surgery for esophageal cancer.
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PMID:[The measurement of extra vascular lung water using a thermal-sodium double indicator dilution technique in patients undergoing surgery for esophageal cancer]. 228 95

The aim of the study was to determine whether a single oral dose of omeprazole 40 mg is effective in increasing the pH of gastric residue above 2.5 at the time of anaesthetic induction in adult patients scheduled for elective gynaecological surgery. The patients were allocated to receive either chlorazepate dipotassium 25 mg alone or omeprazole 40 mg and chlorazepate dipotassium 25 mg on the night before surgery. Gastric volume and pH were measured after induction of anaesthesia. Patients who received omeprazole had a higher mean pH than control patients (p less than 0.001). The pH was less than 3.5 in 50% of patients in the control group, but in only 4.5% of those who received omeprazole (p less than 0.01). Mean (SEM) volume of gastric fluid was 15.2 (2.7) ml in the control group and 9.2 (1.8) ml in the omeprazole group, but the results were not statistically significant. A single dose of 40 mg omeprazole significantly decreased the number of patients at risk of aspiration pneumonitis.
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PMID:Omeprazole for prophylaxis of acid aspiration in elective surgery. 203 23

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

Clinically healthy calves were divided into five groups. Group 1 served as control; Group 2 received levamisole (LEV), 3 mg/kg, s.c.; Group 3 was aerosolized with parainfluenza-3 virus (PI-3); Group 4 received LEV and PI-3 and Group 5 was inoculated with Pasteurella haemolytica. They were killed 6 days after virus exposure or 5-6 days after bacterial inoculation. Lung mast cells were prepared by enzymatic treatment. Mast cell histamine (HIST) release was assayed spectrofluorometrically. Total HIST (micrograms/g) in mast cells was as follows (means +/- SEM): control (5.30 +/- 0.26); LEV (5.27 +/- 0.31); PI-3 (6.37 +/- 0.65); LEV + PI-3 (6.21 +/- 0.51); P. haemolytica (7.06 +/- 0.85). Spontaneous HIST release was as follows (% total, means +/- SEM): control (10.38 +/- 1.09), LEV (11.95 +/- 2.13), PI-3v (73.57 +/- 11.97), PI-3v + LEV (19.50 +/- 3.03), and P. haemolytica (70.59 +/- 5.94). Calcium ionophore A23187 (5 X 10(-6) M)-induced release (% total, means +/- SEM) was: 51.53 +/- 3.05, 50.02 +/- 2.70, 83.91 +/- 4.09, 75.21 +/- 4.51 and 70.59 +/- 6.91 for control, LEV, PI-3, LEV + PI-3 and P. haemolytica groups, respectively. Both virus and bacteria increased HIST content of lung mast cells and enhanced ionophore-induced release. Levamisole significantly reduced spontaneous HIST release in virus-infected calves but had no effect on ionophore-induced release. Results suggest a significant role for HIST in pathogenesis of bovine microbial pneumonia and that LEV probably does not modulate non-immunologic release of HIST from bovine lungs.
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PMID:Parainfluenza-3 virus-induced enhancement of histamine release from calf lung mast cells--effect of levamisole. 246 73

Pneumocystis carinii pneumonia (PCP) is the most common cause of pneumonia in HIV antibody positive patients, but other pneumonias remain important, i.e. streptococcal and mycobacterial infections. A definitive diagnosis relies on obtaining samples from the lung either noninvasively (induced sputum), or invasively (bronchoalveolar lavage, transbronchial or open lung biopsy). We have used the noninvasive technique of nebulized 99mTc DTPA transfer, to assess patients with PCP (n = 30) and other lung infections (n = 20) to see whether this test will distinguish between the various infections. The presence of a biphasic, rapid transfer curve indicates severe extensive alveolar damage and is seen in PCP or legionella pneumonia. The mean transfer time (T50 +/- SEM) for patients with PCP (whether smokers or nonsmokers) was 2.1 +/- 0.2 min, and for two of the patients with legionella 3.2 min. In PCP effective treatment causes the transfer to slow (mean T50 22.7 +/- 3.3 min, n = 24) and become monoexponential. Other causes of these changes in transfer are discussed. The other pneumonias (streptococcal, mycobacterial, and staphylococcal) did not result in biphasic curves or very rapid times, their T50 values are indistinguishable from cigarette smokers. In this patient group the DTPA transfer is a useful noninvasive investigation with a very rapid, biphasic curve indicating a high probability of PCP.
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PMID:The place of lung 99mTc DTPA aerosol transfer in the investigation of lung infections in HIV positive patients. 269 35

Although chronic eosinophilic pneumonia is a well-known disorder, acute eosinophilic pneumonia has not been as well characterized. We describe the clinical features, results of bronchoalveolar lavage, and follow-up studies of four patients with acute eosinophilic pneumonia. The patients presented with an acute febrile illness, severe hypoxemia (partial pressure of arterial oxygen less than 60 mm Hg), diffuse pulmonary infiltrates, an increased number of eosinophils (mean +/- SEM, 42 +/- 4.8 percent) in bronchoalveolar-lavage fluid, and an absence of infection and previous atopic illness. The illness resolved rapidly after treatment with erythromycin and corticosteroids. The patients received doses of oral prednisone that were tapered over 10 days to 12 weeks, and none have relapsed since the steroids were discontinued. After a minimum follow-up period of five months, clinical evaluation, chest radiography, and pulmonary-function tests have shown no residual abnormalities attributable to the acute eosinophilic pneumonia. Follow-up bronchoalveolar lavage has demonstrated less than or equal to 1 percent eosinophils in all patients. We believe that we are describing an acute form of eosinophilic lung disease distinct from previously described syndromes. It can be diagnosed by bronchoalveolar lavage and seems to respond to treatment with corticosteroids.
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PMID:Acute eosinophilic pneumonia as a reversible cause of noninfectious respiratory failure. 230 15

A total of 77 consecutive patients submitted to mechanical ventilation (MV) for greater than 48 h in a respiratory ICU (RICU) were studied to investigate the incidence, etiology, and consequences of ventilator-associated pneumonia. Eighteen (23%) patients developed a bacterial pneumonia after 5.6 +/- 1.0 days (mean +/- SEM; range 2 to 17) of MV. Three additional cases were demonstrated at autopsy, raising the incidence to 27%. Overall, the mean duration of MV increased from 9.7 +/- 0.9 to 32.2 +/- 5.1 days (p less than .0001) when pneumonia developed. A longer period of hospital stay before RICU admission and the presence of chronic obstructive pulmonary disease were significant characteristics of patients with pneumonia when compared to patients without nosocomial pulmonary infection. One or more etiological agents were identified in 14 patients from the pneumonia group by means of a highly specific technique (protected brush catheter, transthoracic needle aspiration, pleural fluid, and/or blood cultures). The predominant pathogens isolated were Gram-negative bacilli (Acinetobacter sp. and Pseudomonas sp.). Half of the cases were polymicrobial. Compared to other series, our results may reflect with more accuracy the actual incidence of nosocomial pneumonia in mechanically ventilated patients, since we used highly accurate techniques along with autopsy findings which allowed us to confirm or discard the diagnosis of bacterial pneumonia.
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PMID:Incidence and etiology of pneumonia acquired during mechanical ventilation. 276 59


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