Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We administered teicoplanin as specific antibiotic therapy for nosocomial "ICU specific" infections with methicillin-resistant Staphylococcus aureus and epidermidis (MRSA-MRSE). The above mentioned drug has been given to 20 patients (15 newborns and 5 not-newborns) admitted into intensive care unit during the years 1988, 1989, 1990 with MRSA-MRSE localized and/or systemic infection, affected by severe disease (RDS, pulmonary edema, congenital cardiac disease, cystic fibrosis) undergoing invasive procedures which presented high nosocomial infective risk (tracheal intubation, mechanical ventilation, venous and arterial cannulation, total parenteral nutrition, etc.). Complete recovery from systemic or localized infection (sepsis, low respiratory tract infection, high respiratory tract infection) occurred in 19 out of 20 patients, with a rate of success of 95%. Teicoplanin treatment lasted from a minimum of nine days to a maximum of thirty days. The dose was 5-6 mg/kg/die in one administration for the first three days, then 4 mg/kg/die. The tolerability of teicoplanin has proven satisfactory, since we had no major side effects during treatment and follow up.
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PMID:[Teicoplanin therapy in neonatal and pediatric intensive therapy]. 138 7

The role of CT in the diagnosis of pediatric lung disease is still evolving, but certain indications are already well established. In immunocompromised or other high-risk children who have fevers or respiratory symptoms but normal or nonspecific chest radiographs, HRCT can detect and localize disease, thus allowing earlier therapy. It also has been shown that HRCT can assess the severity of disease in bronchiectasis and cystic fibrosis and that it may provide a more sensitive means of evaluating therapy in these conditions. Areas for research include the effects of infection on the developing lung, quantification of bronchopulmonary dysplasia, the prevalence of complications in asthma, and the use of HRCT in pulmonary edema of all types. As CT scan times decrease, the use of CT will expand to younger, sicker, and less cooperative children. Dynamic scanning probably will develop to provide a more accurate assessment of the focal and generalized air trapping that accompanies many common pediatric diseases.
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PMID:High-resolution computed tomography of pediatric pulmonary parenchymal disorders. 849 89

Cystic fibrosis (CF) is a disease characterized mainly by altered exocrine gland function that eventually produces irreversible dysfunction of the pancreas and lungs. The respiratory insufficiency that develops in CF patients in the advanced stages of disease can only be corrected at this time by lung or heart-lung transplantation. We describe our experience with 6 terminal phase CF patients who underwent sequential double lung transplantation (SDLT). Anesthesia was intravenous, with exhaustive hemodynamic and respiratory monitoring. During surgery the most frequently encountered hemodynamic complications were low minute volume, arterial hypotension and irregular heart rate. The main respiratory complications were hypoxemia, hypercapnia and pulmonary edema of the implanted lung, which developed in all cases to varying degrees related to the organ's state of preservation and duration of ischemia. Other complications were the need for extracorporeal circulation in 1 case, oliguria and blood loss requiring multiple transfusions. The most critical moments were at the time of clamping the pulmonary artery, the period after revascularization of the donated lung, and at the start of patient ventilation through the first implanted lung so that the second could be implanted. Although our series is small, it is of interest given the limited Spanish experience with lung transplantation in CF patients, and the good early results obtained, which are similar to those reported for other diseases.
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PMID:[Anesthetic complications in sequential bipulmonary transplantation in patients with cystic fibrosis. Apropos of 6 cases]. 884 34

Increased serum levels of mucin-associated antigen have been previously demonstrated in patients with cystic fibrosis (CF) and interstitial pneumonia, and in lung-transplant recipients. The present study assessed the serum airway mucin levels in patients with acute respiratory distress syndrome (ARDS). An enzyme-linked immunosorbent assay (ELISA) method with a human-airway-mucin-specific monoclonal antibody (17Q2) was used to measure serum mucin levels in normal subjects, chronic smokers, patients with chronic bronchitis and other pulmonary diseases, patients with acute cardiogenic lung edema, and patients with ARDS. The serum mucin levels measured 9.9 +/- 0.8 ng/ml (mean +/- SEM, n = 59) in normal subjects, 12.7 +/- 1.6 ng/ml (n = 29) in chronic smokers, 21.8 +/- 1.9 ng/ml (n = 28) in patients with chronic bronchitis and other pulmonary diseases, 9.0 +/- 3.1 ng/ml (n = 5) in patients with acute cardiogenic lung edema. The serum mucin level was 53.8 +/- 6.6 ng/ml (n = 13) in patients with ARDS (p < 0.05, as compared with the four other groups). Serial measurements of serum mucin levels were obtained in patients with ARDS. Statistical analysis showed an inverse correlation of serial measurements of serum mucin with static respiratory-system compliance (p = 0.021), an inverse correlation of sequential serum mucin levels and log(Pa(O2)/Fl(O2)) (p = 0.016), and a positive correlation of sequential serum mucin levels and lung injury score (LIS) (p = 0.019). Gel-filtration analysis showed that mucin-associated antigens in ARDS sera were polydispersed and smaller than the antigens in normal sera. This study indicates that an increasing amount of degraded mucin occurs in patients with ARDS.
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PMID:Elevated serum levels of mucin-associated antigen in patients with acute respiratory distress syndrome. 937 60

Noninvasive PPV has been employed for decades in patients with chronic respiratory failure. Increasing use in patients with acute respiratory failure is a more recent phenomenon, mainly because of advances in noninvasive interfaces and ventilator modes. Noninvasive PPV delivered by nasal or oronasal mask has been demonstrated to reduce the need for endotracheal intubation, decrease lengths of stay in the ICU and hospital, and possibly reduce mortality. In the acute care setting, evidence now demonstrates the efficacy of noninvasive PPV for acute exacerbations of COPD, pulmonary edema, pulmonary contusions, and acute respiratory failure in patients who decline or who are not believed to be candidates for intubation. No firm conclusions can yet be made regarding patients with respiratory failure due to other causes, but studies suggest that noninvasive PPV may also be of benefit in patients with postoperative respiratory insufficiency, chest wall disease, and cystic fibrosis. Several factors are vital to the success of this therapy, including careful patient selection, properly timed intervention, a comfortable, well-fitting interface, patient coaching and encouragement, and careful monitoring. Noninvasive ventilation should be used as a way to avoid endotracheal intubation rather than as an alternative. Accordingly, a trial of noninvasive ventilation should be instituted in the course of acute respiratory failure before respiratory arrest is imminent, to provide ventilatory assistance while the factors responsible for the respiratory failure are aggressively treated. Moreover, the authors favor conservative management with expeditious intubation in patients who have other conditions that place them at risk during use of noninvasive ventilation or in patients failing to respond to noninvasive PPV. Noninvasive PPV clearly represents an important addition to the techniques available to manage patients with acute respiratory failure; however, because most studies have been retrospective and uncontrolled, many issues remain unresolved. Further controlled studies are needed to confirm the safety and efficacy of noninvasive PPV, evaluate the most appropriate selection of patients and timing of intervention, define the best type of interface, and assess the costs of noninvasive PPV in comparison with conventional therapy.
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PMID:Noninvasive ventilation in acute respiratory failure. 939 Aug 83

The epithelial Na channel (ENaC) plays a critical role in the active reabsorption of alveolar fluid at the time of birth or during pulmonary edema. Although rat (r) ENaC is regulated by glucocorticoids during fetal development, there are no data regarding the influence of gender hormones on ENaC expression or function. We report higher levels of mRNAs encoding the alpha-rENaC subunit or the cystic fibrosis transmembrane conductance regulator (CFTR) in the lungs of nonpregnant adult female relative to adult male Wistar rats. Combined, but not separate, administration of progesterone and 17 beta-estradiol increased mRNA levels encoding alpha-rENaC, gamma-rENaC, and CFTR within 24 h. We also found a dose-dependent increase in rENaC functional activity (as assessed by the amiloride-sensitive short-circuit current across primary monolayer cultures of alveolar epithelial cells mounted in Ussing chambers) after a 5-day incubation of cells in medium containing progesterone and 17 beta-estradiol. These findings suggest a gender-dependent influence on the lung's ability to recover from pulmonary edema and on the degree of airway fluid hydration in cystic fibrosis.
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PMID:Female gender hormones regulate mRNA levels and function of the rat lung epithelial Na channel. 948 27

Pulmonary surfactant is a complex and highly surface active material composed of lipids and proteins which is found in the fluid lining the alveolar surface of the lungs. Surfactant prevents alveolar collapse at low lung volume, and preserves bronchiolar patency during normal and forced respiration (biophysical functions). In addition, it is involved in the protection of the lungs from injuries and infections caused by inhaled particles and micro-organisms (immunological, non-biophysical functions). Pulmonary surfactant can only be harvested by lavage procedures, which may disrupt its pre-existing biophysical and biochemical micro-organization. These limitations must always be considered when interpreting ex vivo studies of pulmonary surfactant. A pathophysiological role for surfactant was first appreciated in premature infants with respiratory distress syndrome and hyaline membrane disease, a condition which is nowadays routinely treated with exogenous surfactant replacement. Biochemical surfactant abnormalities of varying degrees have been described in obstructive lung diseases (asthma, bronchiolitis, chronic obstructive pulmonary disease, and following lung transplantation), infectious and suppurative lung diseases (cystic fibrosis, pneumonia, and human immunodeficiency virus), adult respiratory distress syndrome, pulmonary oedema, other diseases specific to infants (chronic lung disease of prematurity, and surfactant protein-B deficiency), interstitial lung diseases (sarcoidosis, idiopathic pulmonary fibrosis, and hypersensitivity pneumonitis), pulmonary alveolar proteinosis, following cardiopulmonary bypass, and in smokers. For some pulmonary conditions surfactant replacement therapy is on the horizon, but for the majority much more needs to be learnt about the pathophysiological role the observed surfactant abnormalities may have.
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PMID:Pulmonary surfactant in health and human lung diseases: state of the art. 1044 27

The lungs are a delicate interface between the atmosphere and our bodies across which oxygen diffuses from the air we breathe to the blood which carries oxygen to the cells and mitochondria. In healthy lungs at sea level where there is a surfeit of oxygen, this process occurs easily, whereas, in lungs with disease it becomes a task which may not be fully successful and hypoxemia may ensue or worsen. At high altitude where the barometric pressure (Pb) and thus the supply of oxygen is lower, the job of getting oxygen to the blood, even in the healthy lung is more difficult, and in the diseased lung it may be impossible. This presentation will review the lungs' responses to high altitude, with emphasis on the abnormal. Both acute and chronic responses of patients with pre-existing lung disease will be reviewed. Pulmonary diseases encountered at high altitude in previously healthy people, such as high altitude pulmonary edema and chronic mountain sickness will be touched on only as they pertain to other patients. Pre-existing lung disease (with and without hypoxemia at sea level) such as obstructive lung diseases (asthma, COPD, emphysema), and restrictive lung diseases (sarcoid, asbestosis, interstitial pulmonary fibrosis) will be discussed in terms of gas exchange, lung mechanics, and treatment at high altitude. Disorders of ventilatory control; e.g., obesity-hypoventilation syndrome and sleep apnea, may present formidable problems, and guidelines for their treatment will be discussed. Infectious lung diseases; e.g., pneumonia, cystic fibrosis, and pulmonary vascular disorders such as chronic mountain sickness, primary pulmonary hypertension, and congenital absence of the pulmonary artery are important disorders that require special attention because of the accentuated hypoxic pulmonary vascular response encountered at high altitude. The purpose therefore, is to provide the medical practitioner with the insight into prevention, recognition, and treatment of pulmonary problems encountered specifically at high altitude, as well as guidance on how best to advise patients with lung disease who want to fly in airplanes and/or ascend to high altitude for work or pleasure.
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PMID:Lung disease at high altitude. 1063 92

The epithelial sodium channel (ENaC) plays a key role in the regulation of fluid absorption in the kidney, lung, colon and exocrine glands, and in the regulation of blood pressure. Abnormal functioning of ENaC is associated with several human diseases, including pseudohypoaldosteronism type I, Liddle's syndrome, pulmonary edema, and cystic fibrosis. ENaC is regulated by several hormones, ions and accessory proteins. This review focuses on the regulation of ENaC by recently described accessory proteins, mainly Nedd4, syntaxin 1A, CFTR, sgk, K-Ras2A and Cap-1.
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PMID:Regulation of the epithelial sodium channel (ENaC) by accessory proteins. 1099 Mar 73

The active absorption of fluid from the airspaces of the lung is important for the resolution of clinical pulmonary edema. Although ENaC channels provide a major route for Na(+) absorption, the route of Cl(-) transport has been unclear. We applied a series of complementary approaches to define the role of Cl(-) transport in fluid clearance in the distal airspaces of the intact mouse lung, using wild-type and cystic fibrosis Delta F508 mice. Initial studies in wild-type mice showed marked inhibition of fluid clearance by Cl(-) channel inhibitors and Cl(-) ion substitution, providing evidence for a transcellular route for Cl(-) transport. In response to cAMP stimulation by isoproterenol, clearance was inhibited by the CFTR inhibitor glibenclamide in both wild-type mice and the normal human lung. Although isoproterenol markedly increased fluid absorption in wild-type mice, there was no effect in Delta F508 mice. Radioisotopic clearance studies done at 23 degrees C (to block active fluid absorption) showed approximately 20% clearance of (22)Na in 30 min both without and with isoproterenol. However, the clearance of (36)Cl was increased by 47% by isoproterenol in wild-type mice but was not changed in Delta F508 mice, providing independent evidence for involvement of CFTR in cAMP-stimulated Cl(-) transport. Further, CFTR played a major role in fluid clearance in a mouse model of acute volume-overload pulmonary edema. After infusion of saline (40% body weight), the lung wet-to-dry weight ratio increased by 28% in wild-type versus 64% in Delta F508 mice. These results provide direct evidence for a functionally important role for CFTR in the distal airspaces of the lung.
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PMID:Novel role for CFTR in fluid absorption from the distal airspaces of the lung. 1181 69


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