Spontaneous rupture of a true splenic cyst diagnosed by laparoscopy.
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Adult↗
Biomedical subjects
G Nakos
Publications and source records attributed to G Nakos.
Anti-phospholipid antibodies in serum from patients with Guillain-Barré syndrome.
OBJECTIVE: The Guillain-Barré syndrome (GBS) is an acute inflammatory polyneuropathy related to autoimmunity. However, no conclusive etiological concept has yet been found. We examined the variation in autoantibodies to lipids in serum of GBS patients in response to the course of the disease but investigated titer modifications during treatment with gamma-globulin. DESIGN AND SETTING: Prospective clinical study in a 14-bed general ICU. PATIENTS: Nine patients with GBS and nine controls were included in the study. MEASUREMENTS AND RESULTS: Four blood samples were obtained before and after treatment. Serum samples, diluted 1:60, were tested by enzyme-linked immunosorbent assay for IgM, IgA, and IgG antibodies to phosphatidylcholine, phosphatidylinositol, cardiolipin, phosphatidic acid, phosphatidylserine, phosphatidylglycerol, phosphatidylethanolamine, sphingomyelin, and gangliosides. Anti-phospholipid antibodies of the IgM, IgA, and IgG families were detected in all GBS patients but in none of the controls. Phosphatidylinositol, cardiolipin, phosphatidylcholine, and phosphatidic acid were the main antigens. All patients developed anti-phosphatidylinositol antibodies of the IgM family and anti-cardiolipin antibodies of the IgA and IgG families. A decrease in the level of anti-phospholipid autoantibodies was observed after 1 day of treatment with gamma-globulin. Two days after ending gamma-globulin administration the IgG antibodies increased again. CONCLUSIONS: Our findings suggest that in GBS there is an extensive immune reaction, which is altered after gamma-globulin treatment. Anti-cardiolipin and anti-phosphatidylinositol antibodies could be useful markers for the response to treatment.
Adult↗
Mechanically ventilated lung and response to pseudomonas aeruginosa.
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Animals↗
Amiodarone-induced acute lung toxicity in an ICU setting.
Amiodarone is a highly effective antiarrhythmic drug, albeit notorious for its serious pulmonary toxicity. The incidence of amiodarone-induced pulmonary toxicity (APT) appears to be 1% per year (1). We report a case of very acute APT in a man suffering from postoperative atrial fibrillation.
Aged↗
Platelet-activating factor acetylhydrolase and acute respiratory distress syndrome: unanswered questions.
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1-Alkyl-2-acetylglycerophosphocholine Esterase↗
Ventilator-associated pneumonia and atelectasis: evaluation through bronchoalveolar lavage fluid analysis.
OBJECTIVE: Surfactant offers protection against alveolar collapse and contributes to the local defense mechanism, but it is unclear if surfactant alterations have a role in the development of atelectasis or ventilator-associated pneumonia (VAP). The present study was undertaken to monitor surfactant, as well as biochemical BAL fluid alterations, during the course of VAP and atelectasis in mechanically ventilated patients without primary cardiopulmonary disease, to elucidate the pathogenesis and to differentiate these two entities. DESIGN. Prospective controlled study. SETTING: 14-bed general ICU of a 750-bed University Hospital. PATIENTS: Sixty-one ventilated patients, without primary cardiopulmonary disease-normal initial chest X-ray, satisfactory oxygenation (PaO(2)/FiO(2)>300 mmHg), and expected time of ventilation exceeding 2 weeks-were initially enrolled. Twelve of them developed VAP and eight lobar or segmental atelectasis during the 2-week study period. INTERVENTIONS: An initial BAL was performed in all patients within 48 h from admission. Patients who developed VAP or atelectasis were subjected to a second and third BAL during and after the resolution of VAP or atelectasis, respectively. MEASUREMENTS AND RESULTS: VAP and atelectasis resulted in a significant increase of total protein and markers of inflammation, such as PAF and neutrophils, which partially remitted after their resolution. Large surfactant aggregates, which contribute to surface tension decrease, were significantly reduced during both entities and remained low even after their resolution. CONCLUSIONS: BAL alterations during VAP and atelectasis suggest increased alveolar-capillary permeability, severe surfactant abnormalities, and signs of local inflammatory reaction. These alterations are associated with the observed deteriorated gas exchange and lung mechanics and could predispose to further lung injury in ventilated patients.
Analysis of Variance↗
Bronchoalveolar lavage alterations during prolonged ventilation of patients without acute lung injury.
Mechanical ventilation deteriorates previously injured lung, but little is known about its effect on healthy human lung. This work was designed to assess the effect of prolonged mechanical ventilation on bronchoalveolar lavage (BAL) fluid composition of patients without acute lung injury. Twenty-two ventilated patients (tidal volume 8-10 mL x kg(-1), positive end-expiratory pressure 3-5 cmH2O) without lung injury, who did not develop any complication from the respiratory system during the 2-week study period, were studied. They were subjected to three consecutive BALs, the first during 36 h from intubation, the second at the end of the first week of mechanical ventilation and the third at the end of the second week of mechanical ventilation. Total BAL protein increased during mechanical ventilation (148 +/- 62, 381 +/- 288, 353 +/- 215 microg x mL(-1) BAL for the first, second and third BAL, respectively). In contrast, BAL phospholipids decreased (2.7 +/- 1.1, 1.4 +/- 0.6, 1.2 +/- 0.7 microg x mL(-1) BAL, respectively). Large surfactant aggregates were reduced and inflammatory markers, such as platelet activating factor (PAF), PAF-acetylhydrolase and neutrophils, significantly increased after 1 week, but partially remitted after 2 weeks of mechanical ventilation. In summary, this study demonstrates that prolonged mechanical ventilation even of patients without acute lung injury is associated with the presence of inflammatory markers and surfactant alterations.
Adolescent↗
Effects of bulk precipitation pH and growth period on cation enrichment in precipitation beneath the canopy of a beech (Fagus moesiaca) forest stand.
The effects of bulk precipitation pH and growth period (growing and dormant) on cation enrichment beneath foliage were examined in a beech (Fagus moesiaca) forest stand during a 48-month period. The bulk precipitation pH values ranged from 4.2 to 7.2. The lowest values were observed in winter due to fossil fuel combustion in a nearby big city. The ratio of monthly ion fluxes of throughfall plus stemflow over monthly ion fluxes of bulk precipitation was chosen as an index of cation enrichment and, therefore, as the dependent variable. Bulk precipitation pH and growth period were chosen as independent factors. Precipitation interception (%) by tree canopies was also taken into account. It was found that the pH factor was significant only for H+ ion enrichment suggesting neutralization of H+ ions in the beech canopy, whereas Mg2+ and K+ enrichment were greater in the growing period, probably as a result of leaching. Crown interception was negatively significant for NH4+-N enrichment.
Acid Rain↗
The characteristics of bronchoalveolar lavage from a patient with antiphospholipid syndrome who developed acute respiratory distress syndrome.
The purpose of this study was to investigate the biochemical characteristics as well as the occurrence and specificity of antiphospholipid antibodies in the bronchoalveolar lavage (BAL) fluid from a patient with both antiphospholipid antibodies syndrome (APS) and acute respiratory distress syndrome (ARDS). Proteins, lipids, cells and autoantibodies were determined. Immunoglobulins were purified with affinity chromatography. Autoantibody identification was assessed with enzyme-linked immunosorbent assay (ELISA) and with electrophoresis, followed by immunoblotting and revelation with antihuman IgG-peroxidase conjugate. Antiphospholipid antibodies were found to be present in the BAL fluid as well as in the serum from a patient with APS. Specifically, antiphosphatidylserine and antiphosphatidic acid IgG antibodies in the BAL fluid and antiphosphatidylcholine and anticardiolipin IgG antibodies in the serum were detected at high levels. BAL fluid protein and the percentage of neutrophils were found to be increased. A quantitative as well as qualitative deficiency of surfactant phospholipids was also observed. Antibodies directed against surfactant phospholipids could cause surfactant abnormalities and an inflammatory reaction. These disorders may be one of the causes of the ARDS or a factor in the perpetuation of the inflammation.
Adult↗
Autoantibodies to lipids in bronchoalveolar lavage fluid of patients with acute respiratory distress syndrome.
OBJECTIVE: To investigate the presence of autoantibodies to lipids in the bronchoalveolar lavage (BAL) fluid from adult patients with acute respiratory distress syndrome (ARDS). DESIGN: Analysis of immunoglobulin G (IgG) in BAL fluid by electrophoresis followed by immunoblotting and characterization of immunoglobulins as antilipid autoantibodies. SETTING: Intensive care unit of a university hospital and two research university laboratories. SUBJECTS: Twenty-seven mechanically ventilated patients in total, including nine patients with ARDS and two control groups. INTERVENTIONS: Patients were ventilated with a mechanical ventilation mode. Six aliquots of 20-mL sterile normal saline at 37 degrees C were infused through the working channel of the bronchoscope. MEASUREMENTS: Total protein, detection of IgG by electrophoresis followed by immunoblotting, and characterization of IgG by enzyme-linked immunosorbent assay using different lipids as target antigens. MAIN RESULTS: Antiphospholipid autoantibodies are present in BAL fluid of ARDS patients. Among the phospholipids tested, phosphatidic acid and phosphatidylserine gave the most significant activity. The IgG fraction, purified from BAL fluids by affinity chromatography, gave the same pattern of binding as that of the BAL fluid. CONCLUSION: The presence of antiphospholipid autoantibodies in BAL fluid suggests involvement of autoimmune mechanisms in the pathogenesis of ARDS.
Adult↗
Effect of the prone position on patients with hydrostatic pulmonary edema compared with patients with acute respiratory distress syndrome and pulmonary fibrosis.
This study examined the effect of the prone position on mechanically ventilated patients with hydrostatic pulmonary edema (HPE). Eight patients with acute HPE and mechanically ventilated in the prone position (Group 1) were studied. Six patients with acute HPE and mechanically ventilated in the supine position (Group 2), 20 patients with ARDS (Group 3), and 5 patients with pulmonary fibrosis (PF) (Group 4) served as control patients. Patients with HPE, who after being mechanically ventilated for at least 6 h needed an FI(O(2)) >/= 0.6 to achieve an Sa(O(2)) of approximately 90%, and did not respond to recruitment maneuvers, were turned to the prone position. Parameters of oxygenation, lung mechanics, and hemodynamics were determined in both the supine and prone positions. All patients with HPE exhibited improvement of oxygenation when they were placed in the prone position. The Pa(O(2))/FI(O(2)) ratio increased from 72 +/- 16 in the supine position to 208 +/- 61 after 6 h in the prone position (p < 0.001); the rise in Pa(O(2)) was persistent, without detrimental effect on hemodynamics. Fifteen of 20 patients with ARDS (75%) improved oxygenation when in the prone position. The Pa(O(2))/FI(O(2)) ratio increased from 83 +/- 14 in the supine position to 189 +/- 34 after 6 h in the prone position (p < 0.001). In contrast, 5 of 20 patients with ARDS (25%) and none of the patients with PF responded favorably to prone positioning. Patients with HPE and early ARDS responded better to prone positioning than did patients with late ARDS and PF. Patients with HPE and ventilated in the supine position had a lower Pa(O(2))/FI(O(2)) ratio and the duration of mechanical ventilation was longer compared with that of patients in the prone position. Our results show that the prone position may be a useful maneuver in treating patients with severe hypoxemia due to pulmonary edema. The presence of pulmonary edema, as in early ARDS and HPE predicts a beneficial effect of the prone position on gas exchange. In contrast, the presence of fibrosis, as in late ARDS and pulmonary fibrosis, predisposes to nonresponsiveness to prone positioning.
Adolescent↗
Cisapride decreases gastric content aspiration in mechanically ventilated patients.
OBJECTIVE: To determine the effect of the prokinetic agent cisapride in the prevention of aspiration of gastric contents. DESIGN: A prospective randomized two-period crossover study. SETTING: Fourteen-bed polyvalent intensive care unit in a University Hospital. PATIENTS: Eighteen intubated, mechanically ventilated patients who were seated in a semirecumbent position were studied. METHOD: Tc-99 m sulfur colloid (80 megabecquerels) was administered via nasogastric tube on 2 consecutive days. Patients randomly received cisapride (10 mg, via nasogastric tube) one day and a placebo the other. Bronchial secretions were obtained before and for 5 consecutive h after Tc-99 m administration. The radioactivity was measured in a standard amount (1ml) of bronchial fluid using a gamma counter and expressed as counts per min (cpm) after correction for decay. RESULTS: Sixteen out of 18 (88%) patients had increased radioactivity in bronchial secretions. The radioactivity increased over time both with and without cisapride, although it was lower in patients receiving cisapride than in those receiving a placebo. The cumulative bronchial secretion radioactivity obtained when patients received cisapride was significantly lower than when patients received a placebo: 7540 +/- 5330 and 21965 +/- 16080 cpm, respectively (P <0.05). CONCLUSION: Our results suggest that aspiration of gastric contents exists even in patients who are kept in a semirecumbent position. Moreover, cisapride decreases the amount of gastric contents aspiration in intubated and mechanically ventilated patients and may play a role in the prevention of ventilator associated pneumonia. Cisapride, even with the patient in the semirecumbent position, did not completely prevent gastric content aspiration.
Journal Article↗
The effect of hyperoxaemia on erythropoietin secretion in anaemic patients.
Erythropoietin (EPO) controls red cell production. Hypoxaemia, reduced blood oxygen-carrying capacity and increased affinity of haemoglobin (Hb) for oxygen are the primary stimuli for EPO secretion. The effect of hyperoxaemia (arterial oxygen tension (Pa,O2) > 13.3 kPa) on EPO secretion has not been thoroughly studied and is not fully understood. The primary purpose of this study was to evaluate EPO production in patients with acute respiratory failure as well as to determine the effect of hyperoxaemia on EPO secretion in patients with and without anaemia. A prospective clinical study was carried out in a 14-bed general (medical and surgical) intensive care unit in a university hospital. Twenty-one patients with acute or acute on chronic respiratory failure, requiring mechanical ventilation, were included in this study. The patients were divided into two groups; group I comprised patients who developed anaemia, and group II patients who did not. EPO levels and haematological parameters were measured in venous blood under three oxygenation conditions: hypoxaemia, hyperoxaemia and normoxaemia. All patients exhibited high EPO levels during hypoxaemia (mean value 108.7 +/- 27 mU.mL-1 (+/- SD)). During hyperoxaemia, EPO levels decreased in both groups (mean value 21.6 +/- 15.2 mU.mL-1 in group I, 36.8 +/- 19 mU.mL-1 in group II). During normoxaemia, EPO levels increased again in group I patients, but in group II patients EPO production remained stable. In conclusion, hyperoxaemia inhibits erythropoietin secretion in spite of anaemia and low arterial oxygen tension. Hyperoxaemia may be a contributing factor to anaemia in intensive care unit patients under oxygen therapy.
Adult↗
Differential determination of phospholipase A(2) and PAF-acetylhydrolase in biological fluids using fluorescent substrates.
The purpose of the present study was the development and evaluation of a fluorimetric method for the screening and differential determination of phospholipase A(2) and PAF-acetylhydrolase in bronchoalveolar lavage (BAL) fluid and serum. Phospholipase A(2) was determined using C(12)-NBD-PC in the presence of Ca(2+), from the slope of the fluorescence enhancement due to the formation of C(12)-NBD-fatty acid. PAF-acetylhydrolase was determined using C(6)-NBD-PC, from the slope of the curve due to C(6)-NBD-fatty acid formation in the absence of Ca(2+). The results were confirmed after TLC analysis. The method's selectivity was evaluated by comparing to radiometric measurements. Light scattering did not interfere and inner filter effects was not observed under our experimental conditions. The effects of pH, temperature, and Ca(2+) were investigated. Protein caused an increase in the background fluorescence of both NBD-PCs. The standard curves of both NBD-fatty acids exhibited the same slope. Linearity extended at least up to 4. 5 nmoles per ml of reaction mixture at the normal pH 7.4. The fluorescence of the NBD-fatty acids remained stable for increasing concentrations of BAL fluid and serum and for BSA up to 100 microg/ml of reaction mixture. Porcine pancreatic PLase A(2) showed preference for C(12)-NBD-PC in the presence of Ca(2+), while without Ca(2+), serum PAF-AcH hydrolyzed only C(6)-NBD-PC. The method is highly sensitive, accurate, and reproducible and can be applied for the differential determination of phospholipase A(2) and PAF-acetylhydrolase activities in BAL fluid and serum.
1-Alkyl-2-acetylglycerophosphocholine Esterase↗
Bronchoalveolar lavage fluid characteristics of early intermediate and late phases of ARDS. Alterations in leukocytes, proteins, PAF and surfactant components.
OBJECTIVE: To determine the concentration of proteins and phospholipids, markers of inflammatory reaction such as platelet-activating factor (PAF), and cell alterations in bronchoalveolar lavage (BAL) fluid during the evolution of the acute respiratory distress syndrome (ARDS). DESIGN: Prospective controlled study. SETTING: 14-bed medical-surgical intensive care unit in a 750-bed university teaching hospital. PATIENTS: 19 mechanically ventilated patients, 9 patients with ARDS and 10 patients without cardiopulmonary disease (controls), were eligible for this study. INTERVENTIONS: BAL was performed during the early, intermediate, and late phases of ARDS. MEASUREMENTS AND RESULTS: Total phospholipids and individual phospholipid classes of the surfactant, proteins, PAF, and cells were measured. High levels of PAF, an increase in neutrophils and proteins, and quantitative as well as qualitative alterations in phospholipids in BAL fluid were observed in ARDS patients compared to the control group. PAF, proteins, and neutrophils were higher in early ARDS than in intermediate or late ARDS. The surfactant pool increased in the early phase and decreased in the intermediate or late phase of the syndrome. The qualitative alterations of surfactant consist of reduced phospholipid content in the surfactant structures with good surface properties; moreover, there was a considerable decrease in the percentage of phosphatidylcholine and phosphatidylglycerol, followed by an increase in phosphatidylethanolamine, phosphatidylserine, phosphatidylinositol, and sphingomyelin in all three phases of ARDS compared to the control group. Lysophosphatidylcholine was detectable only in late ARDS. CONCLUSION: Total surfactant phospholipids, surfactant components, and inflammatory markers such as PAF, cells, and proteins were affected in patients with ARDS. These factors, undergoing quantitative alterations during the course of ARDS, could have a significant role in the pathogenesis and evolution of ARDS.
Adolescent↗
Acute myelinolysis in the cervical spinal cord.
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Acute Disease↗
Bronchoalveolar lavage alterations in pulmonary embolism.
The objective of this study was to determine quantitative and qualitative surfactant alterations, proteins, and platelet activating factor (PAF) in bronchoalveolar lavage (BAL) fluid from patients with pulmonary thromboembolism (PTE) with respect to ventilated patients without PTE. Patients with PTE underwent BAL at the most affected lung area on the first and tenth days of PTE diagnosis. Total proteins and albumin, total lipids, individual phospholipid classes, PAF and PAF-acetylhydrolase (PAF-AcH) activity were determined in BAL fluid. Total proteins and albumin were found to be increased in both successive samples of patients with PTE when compared with the control group (p < 0.001 and p < 0.05, respectively). Total phospholipids, though, were elevated on the first day, but they decreased on the tenth day, in comparison with the control groups (p < 0.05). Alterations in the percentage of individual phospholipid classes were observed in both successive samples of BAL fluid when compared with those in the control subjects. PAF and PAF-AcH were detected in high levels on the first day (p < 0.001), which were reduced on the tenth day (p < 0.05). An inverse correlation between PAF levels and PaO2/FIO2 ratio was observed. Finally, the percentage of macrophages decreased and the percentage of neutrophils increased during the course of PTE. In conclusion, pulmonary embolism is associated with alterations in lung surfactant and inflammation in lung tissue, expressed by an increase in PAF and in neutrophils.
1-Alkyl-2-acetylglycerophosphocholine Esterase↗
Proteins and phospholipids in BAL from patients with hydrostatic pulmonary edema.
The purpose of the present study is twofold: to evaluate alterations in total phospholipid content and individual phospholipid classes of the surfactant, and to detect markers of inflammatory reaction in bronchoalveolar lavage (BAL) from patients with hydrostatic pulmonary edema (HPE). Mechanically ventilated patients with HPE (Group 1) were compared with mechanically ventilated patients without cardiopulmonary disease (Group 2), considered as the control group. Group 3, including patients with high-permeability pulmonary edema, was used for further comparison. BAL was obtained and immediately cooled at 4 degrees C. Total proteins, albumin, and platelet-activating factor--acetylhydrolase (PAF-AcH) were measured. Total lipids were extracted and analyzed after thin-layer chromatographic separation. PAF was determined with bioassay. Total BAL proteins and albumin were found significantly higher in patients with HPE compared with control, but were lower compared with adult respiratory distress syndrome (ARDS). PAF was elevated in patients with HPE and ARDS, whereas in the control group it was actually in nondetectable levels. PAF was significantly higher in ARDS than in HPE patients. BAL neutrophils concentration was higher in HPE compared with control, but lower compared with ARDS. There was an inverse correlation between PAF-AcH and PAF. Quantitative reduction of total BAL phospholipids (PL) and qualititative deficiency was observed in both patients with HPE and ARDS. The findings of this study suggest that there is evidence of inflammation in the airspaces of patients with HPE.
1-Alkyl-2-acetylglycerophosphocholine Esterase↗