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)

A 45-year-old Japanese woman presented with a high fever, a nonproductive coughing, and severe dyspnea, and was admitted to another hospital. During the week prior to hospitalization, she had been given Shosaikoto for treatment of liver dysfunction of unknown etiology. Mycoplasma pneumonitis was initially suspected, so she was treated with antibiotics (clindamycin and minocycline) and received oxygen therapy. Pulmonary insufficiency worsened rapidly, and she was transferred to our hospital. On admission, a chest roentgenogram revealed bilateral alveolar infiltrates predominantly in the medial lung fields. Furosemide and high-dose methylprednisolone were immediately administered, but hypoxemia increased. When the PaO2 was 55.7 Torr while the patient breathed 100% oxygen, mechanical ventilation with positive end-expiratory pressure (PEEP) was started. Arterial blood-gas values improved dramatically, and the chest roentgenogram became clear. Our diagnosis of noncardiogenic pulmonary edema is based on the chest-roentgenographic findings, infiltration of inflammatory cells as seen in two lung-biopsy specimens and bronchoalveolar lavage fluid, the lack of findings of heart failure on physical examination and electrocardiography, and the good clinical response to PEEP. A positive lymphocyte stimulation test in response to Shosaikoto implicated this non-traditional herbal medicine as an etiologic factor in the non-cardiogenic pulmonary edema. Shosaikoto has been identified as the cause of interstitial pneumonia or eosinophilic pneumonia, but pulmonary edema associated with Shosaikoto has not been previously described. This case suggests that methylprednisolone treatment may be insufficient for Shosaikoto-induced pulmonary edema, and that mechanical ventilation with PEEP is very effective.
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PMID:[Pulmonary edema associated with the Chinese medicine shosaikoto]. 986 80

The rodenticide alpha-naphthylthiourea (ANTU) causes pulmonary edema and pleural effusion that leads to death via pulmonary insufficiency. Rats become resistant to the lethal effect of ANTU if they are first exposed to a small, nonlethal dose of ANTU. Young rats are also resistant to ANTU. The mechanism by which rats develop resistance by a prior, small dose exposure has yet to be determined. Growth factor induced-pulmonary hyperplasia has been demonstrated to attenuate ANTU-induced lung leak. We hypothesized that a small dose of ANTU protects against a large dose through pulmonary cell hyperplasia induced by the protective dose. Furthermore, we hypothesized that this hyperplasia is associated with altered transcription of growth factors. Male Sprague-Dawley rats (175-225 g) were treated with a low dose of ANTU (5 mg ANTU/kg; ANTU(L)) 24 h before challenge with a 100% lethal dose of ANTU (70 mg ANTU/kg; ANTU(H)) resulting in 100% protection against the lethal effect of ANTU(H). ANTU(L) protection against ANTU(H) lasted for 5 days, slowly phased out, all being lost by day 20. Injury was assessed by estimating pulmonary vascular permeability and through histopathological examination. ANTU(H) alone resulted in an increase in pulmonary edema leading to animal death. However, injury was prevented if the rats were first treated with ANTU(L). There was a stimulation of pulmonary cell hyperplasia in the lungs of ANTU(L) treated rats as measured by [3H]-thymidine and bromodeoxyuridine incorporation. Treatment with the antimitotic agent colchicine abolished ANTU(L)-induced resistance to ANTU(H). ANTU resistant rats were also resistant to the lethal effect of paraquat. Paraquat is not taken up by pneumocytes if they are undergoing hyperplasia. ANTU(L) administration resulted in an up regulation of gene transcription for keratinocyte growth factor, transforming growth factor-beta, keratinocyte growth factor receptor and epidermal growth factor receptor as determined through reverse transcription-polymerase chain reaction. A significant increase in transforming growth factor-alpha was not observed. These findings collectively suggest that ANTU(L)-induced pulmonary cell hyperplasia underlies resistance to ANTU(H). Furthermore, the stimulation of hyperplasia may be due to altered growth factor and growth factor receptor expressions.
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PMID:Stimulated pulmonary cell hyperplasia underlies resistance to alpha-naphthylthiourea. 1075 3

Central nervous system and cardiovascular toxicity are well-known side effects of bupivacaine. We report a case of bupivacaine-induced myocardial depression and cardiogenic pulmonary edema. A previously healthy woman developed soon after bupivacaine epidural injection of 5 mL 0.5% (25 mg) cardiogenic shock complicated with pulmonary edema. There were pronounced rales on auscultation with a butterfly sign on chest radiograph. A cardiac ultrasound showed reduced myocardial contractility, diffuse hypokinesia, left ventricular ejection fraction (LVEF) 25%, mitral and pulmonary insufficiency. Right heart catheterization showed increased pulmonary artery wedge pressure (34 mm Hg) and a pulmonary artery pressure of 48 over 33 mm Hg. These findings suggest myocardial depression owing to bupivacaine sodium channel blocking of myocardial nerve and tissue and subsequent reduction of myocardial contractility. The patient completely recovered with normalization of clinical, roentenographic, ultrasound, and hemodynamic findings and discharged 10 days later in good condition.
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PMID:Bupivacaine-induced myocardial depression and pulmonary edema: a case report. 1095 83

We described a patient who had developed negative-pressure pulmonary edema associated with severe transurethral resection syndrome. A relatively healthy, 67-yr-old man (171 cm and 77 kg) with hypertrophic prostate was scheduled for transurethral resection of the prostate under spinal anesthesia. The patient was sedated with continuous propofol infusion because of his anxiety and wish of being asleep. Fifty minutes after starting the operation, electrolyte analysis revealed a decrease in serum Na+ concentration (116 mEq.l-1), and 10 mg of furosemide and hypertonic saline were administered. Thirty minutes later, the arterial oxygen saturation dropped suddenly and arterial blood gas analysis suggested marked pulmonary insufficiency (PaO2: 64 mmHg and PaCO2: 59.4 mmHg). The patient's trachea was intubated and endotracheal release of pinkish foamy sputum was observed. Chest X-ray showed severe lung edema. Massive absorption of the irrigation fluid might have decreased the electrolyte concentration (Na+: 101.0 mEq.l-1) and colloid oncotic pressure. No evidence of cardiac failure was observed immediately after the incidence of pulmonary edema with pulmonary catheter monitoring. The patient's airway was almost intact under spontaneous breathing, but augmented negative-pressure derived from intermittent snoring was considered to be sufficient to break hydrostatic balance of pulmonary capillary vessels and lead to severe pulmonary edema.
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PMID:[Negative-pressure pulmonary edema associated with transurethral resection syndrome]. 1121 29

Acute respiratory distress syndrome (ARDS) - is a life-threatening acute clinical syndrome of pulmonary insufficiency with high mortality. The causes of the syndrome are of every description - from crustacean poisoning to cardiopulmonary bypass. The rate of ARDS is not clear, because of diagnostical variety of ARDS and acute pulmonary dysfunction. The discussion on ARDS diagnostical criteria lasted for many years. The clinical criteria depend on how the essence of the disease is understood, on the size of lung infiltration, lung compliance and failure as well as degree of hypoxemia. The risk of ARDS increases with the increase of number of predisposing factors. The investigation data depend mainly on used datum-point for diagnostics of ARDS. It is obvious that non-cardiogenic light pulmonary edema is found very often, and serious lung lesions are rare enough. The aim of nowadays treatment is to cure the disease that causes the syndrome and to sustain vital functions. The early diagnostics of ARDS predisposing factors and minimization of their influence, the prevention, early diagnostics and timely treatment of complications are essential. In many cases ARDS caused by collateral factors is the constituent of multiple organ dysfunction syndrome. Anyway the ARDS predisposed by direct factors is often complicated by other organ (cardiovascular, renal, hepatic, hematogenous, central nervous system, gastrointestinal tract, etc.) dysfunction. In this case the treatment becomes more difficult and includes therapy correcting the function of other systems. In spite of intensive treatment, mortality of this syndrome still remains 50-90% according to the literature data. Though some authors state that recently the ARDS mortality decreased, but most of the authors did not notice any improvement during the last 20 years. The prognosis is determinated not only by pulmonary insufficiency itself (the cause of death in 5% of patients), but by the ARDS predisposing factor (the worst is sepsis and septic shock), multiple organ dysfunction syndrome, difficult physical state of the patient, sepsis as a cause or as a complication of ARDS, nosocomial pneumonia, progressive fibroproliferation in the lung. Considering the actuality of ARDS, the diagnostical criteria of ARDS, pathogenesis, clinical course and new treatment methods are reviewed in the publication.
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PMID:[Acute respiratory distress syndrome]. 1464 57

Administration of supplemental oxygen is frequently encountered in infants suffering from pulmonary insufficiency and in adults with acute respiratory distress syndrome. However, hyperoxia causes acute lung damage in experimental animals. In the present study, we investigated the roles of the Ah receptor (AHR) in the modulation of cytochrome P4501A (CYP1A) enzymes and in the development of lung injury by hyperoxia. Adult male wild-type [AHR (+/+)] mice and AHR-deficient animals [AHR (-/-)] were maintained in room air or exposed to hyperoxia (>95% oxygen) for 24 to 72 h, and pulmonary and hepatic expression of CYP1A and lung injury were studied. Hyperoxia caused significant increases in pulmonary and hepatic CYP1A1 activities (ethoxyresorufin O-deethylase) and mRNA levels in wild-type (C57BL/6J) AHR (+/+), but not AHR (-/-) mice, suggesting that AHR-dependent mechanisms contributed to CYP1A1 induction. On the other hand, hyperoxia augmented hepatic CYP1A2 expression in both wild-type and AHR (-/-) animals, suggesting that AHR-independent mechanisms contributed to the CYP1A2 regulation by hyperoxia. AHR (-/-) mice exposed to hyperoxia were more susceptible than wild-type mice to lung injury and inflammation, as indicated by significantly higher lung weight/body weight ratios, increased pulmonary edema, and enhanced neutrophil recruitment into the lungs. In conclusion, our results support the hypothesis that the hyperoxia induces CYP1A1, but not CYP1A2, expression in vivo by AHR-dependent mechanisms, a phenomenon that may mechanistically contribute to the beneficial effects of the AHR in hyperoxic lung injury.
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PMID:Disruption of the Ah receptor gene alters the susceptibility of mice to oxygen-mediated regulation of pulmonary and hepatic cytochromes P4501A expression and exacerbates hyperoxic lung injury. 1512 65

Smoke inhalation injuries are the leading cause of fatalities from burn injury. The major forms of inhalation injuries are carbon monoxide toxicity, injury to the upper airway, and pulmonary parenchymal damage. The compromised airway is protected by tracheal intubation, and respiratory failure is treated with assisted ventilation. Maintenance of good pulmonary hygiene, optomized fluid resuscitation, and routine invasive hemodynamic monitoring are the mainstays of therapy. The development of acute pulmonary insufficiency, pulmonary edema, or bronchopneumonia requires a comprehensive approach to all aspects of the illness. Acute pathophysiologic responses to inhalation injury are complex. Future therapies will target improved ventilatory strategies and the redundant host inflammatory response.
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PMID:Smoke inhalation injury. 1608 57

Although pulmonary arterial hypertension (PAH) is usually considered as a late complication in limited subsets of systemic sclerosis (SSc), PAH can also occur in diffuse SSc and in early SSc. The evaluation of the velocity of the tricuspid regurgitation on echocardiography is so far the most effective screening tool for pulmonary hypertension (PH) in SSc. Nevertheless, it is not measurable in about 20% of SSc patients ; In that case, pulmonary arterial pressure can be evaluated by using the velocity of a pulmonary insufficiency and indirect signs of PH should be analyzed: pulmonary ejection time, right heart cavities dilatation and aspect of the inferior vena cava. About 10% of SSc patients with a suspected of PAH on echocardiography have post-capillary PH at right heart catheterization mainly due to left ventricular diastolic dysfunction. In some SSc patients, PAH and post-capillary PH due to left ventricular diastolic dysfunction may be associated. This can be suspected in case of post-capillary PH with a transpulmonary gradient > 12 mmHg. Lung fibrosis is another cause of PH in SSc. The distinction between PH associated to lung fibrosis from PAH is sometimes difficult, particularly in patients with a FVC between 60 and 70% of expected. Pulmonary veno-occlusive disease is a possible cause of precapillary PH in SSc. The diagnosis of pulmonary veno-occlusive disease should be discussed in each case of PAH associated ScS due to the high risk of lung edema at the introduction of specific PAH drugs.
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PMID:[Systemic sclerosis associated pulmonary arterial hypertension: the pitfalls]. 2153 80

Naturally preserved and embalmed bodies from archeological contexts represent a powerful source of information for forensic investigators. They allow one to ascertain pathology, cause of death, to enhance diagnostic methodology, and to improve the analysis of altered remains. We investigated the complete head and lung remnants of a 3,500-year-old Egyptian dignitary by radiological, microscopic, and genetic approaches. The individual, a middle-aged male, suffered from severe periodontitis, mild atherosclerosis, and experienced cardiogenic pulmonary insufficiency with recurrent mini-bleeds and pulmonary edema. Histology and ancient DNA analyses excluded the presence of Mycobacterium tuberculosis or of any other pathogenic species. Based on our collection of evidence, we propose that acute decompensation complicating chronic cardiac insufficiency was the likely cause of death. The underlying causes for this failure remain unknown although chronic hypertension appears to be the most likely candidate. Our finding represents the earliest reported case of chronic heart failure in ancient mummies.
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PMID:Forensic Analysis Reveals Acute Decompensation of Chronic Heart Failure in a 3500-Year-Old Egyptian Dignitary. 2736 79


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