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)

Sucralfate is an effective agent in reducing the incidence of upper GI tract (UGIT) stress bleeding and nosocomial pneumonia in critically ill patients. Many of these patients are not intubated and are at increased risk for aspiration of large volumes of UGIT contents containing sucralfate. The effects of aspirated sucralfate are unknown. To investigate this, large-volume aspiration (2 ml/kg) was simulated in freshly tracheostomized rats (n = 6, all experimental groups) using normal saline, particulate antacid, and sucralfate adjusted to pH 3.6 and 5.0. Four hours after aspiration, the rats were killed and their lungs were formalin-fixed. Significant increases in lung inflammation were seen by light microscopy in all experimental groups at pH 3.6. Antacid aspirated at pH 5.0 induced significant increases in airway as well as parenchymal inflammation. At pH 3.6, the antacid aspiration led to significant increases in lung edema and hemorrhage. Sucralfate aspiration produced significant increases in pulmonary hemorrhage at pH 5.0. Our microscopic findings are consistent with the acute pulmonary histopathologic changes known to occur after large-volume aspiration of particulate materials, including antacids. Additionally, we show that large-volume aspiration of sucralfate produced significant acute pneumonitis, including pulmonary hemorrhage. In view of the proven usefulness of sucralfate, further investigations are indicated to evaluate these experimental findings before extrapolating to critically ill patients.
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PMID:Acute histologic effects of simulated large-volume aspiration of sucralfate into the lungs of rats. 204 91

A 22 year-old man was brought to our hospital about twenty-three minutes following a high-speed motorbicycle accident in which he had blunt chest trauma. He was in severe respiratory distress with marked dyspnea and restless with extensive subcutaneous emphysema involving anterior chest wall, cervical and bilateral inguinal regions. A chest X-ray revealed bilateral pneumothorax involving mediastinal emphysema and also fracture of right submandibular and clavicula. In spite of orotracheal intubation and insertion of bilateral chest tube, continuous air leak and pneumothorax did not improve. Bronchoscopy revealed the disruption of mucosa of the right main bronchus at the bifurcation. Emergency right thoracotomy was performed and there was the complete disruption of the right main bronchus. Anastomosis of the right main bronchus with circumferential resection was undertaken on May 30, 1987 about two hours after trauma. About three months after reconstruction, bronchoscopic examination revealed stomal stenosis with deformation of tracheobronchial cartilage and granulation. The stenosis showed severe irregularity by deformed cartilage and thickened scar, so widening by Nd-YAG laser vaporization was inadequate in effect. Seven months after first reconstruction, we performed re-reconstructive operation, right upper sleeve lobectomy with partial resection of carcina and right wall of trachea for scar with severe deformation of cartilage. Following the operation, the patient suffered from sepsis with pneumonitis accompanied by lung edema. This complication was treated successfully. We considered that acute pneumonitis was caused by reventilation with increase of perfusion after tracheobronchial reconstruction. Consequently, we thought it important to treat such patients with long term IPPB postoperatively with adequate medication for respiratory system.
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PMID:[Successful re-reconstruction for complete disruption of the right main bronchus by blunt chest trauma]. 232 99

Topical beta-adrenergic blocking agents are commonly used to treat glaucoma. Exacerbations of asthma and bronchospasm caused by topical beta-adrenergic ophthalmic preparations are well known. We describe a 67-year-old woman who had aspiration pneumonitis characterized by a nodular infiltrate in the right middle lobe of the lung and nocturnal coughing after beginning topical application of an ointment (Lacri-Lube) for treatment of xerophthalmia. Bronchial washing demonstrated lipid-laden pulmonary alveolar macrophages. After the use of Lacri-Lube was discontinued, her cough and the chest roentgenographic abnormality totally disappeared. We postulate that the topical ophthalmic preparation, which contains mineral oil and petrolatum, drained into the nasopharynx, trachea, and bronchial tree through the nasolacrimal duct and caused lipoid pneumonitis from aspiration of the oil contents. To our knowledge, this is the first report of pulmonary complications caused by Lacri-Lube. We briefly review the pulmonary complications, including pulmonary edema, apnea from paralysis of respiratory muscles, bronchospasm from non-beta-adrenergic blocking drugs, and electrolyte abnormalities, attributable to topically and systemically administered ophthalmic medications.
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PMID:Pulmonary complications from ophthalmic preparations. 237 76

Platelet-activating factor (PAF) has been reported to play a role in the inflammatory reaction, but the mechanism of PAF in humans is still unclear. We examined the presence of PAF in pleural fluids from 23 patients with pleural effusion and in all cases detected PAF associated with eosinophil and/or neutrophil infiltrations. The amounts of PAF in pleural fluids were, respectively, 340, 50 to 170, and 1,250 to 2,130 fmol/ml for a patient with eosinophilic pneumonia, those with pneumothorax (n = 9), and empyema (n = 3). In contrast, patients with tuberculous pleuritis (n = 2), lung edema (n = 3), or malignant disease (n = 5) had no detectable amounts of pleural fluid PAF (less than or equal to 10 fmol/ml). The amount of PAF showed a close correlation with the numbers of eosinophils and neutrophils in the pleural fluids. Furthermore, PAF was mostly detected in the cellular fractions, and the molecular species of PAF from the patients with empyema were almost consistent with those of PAF generated by human blood neutrophils. These results indicate that neutrophils and, presumably, eosinophils were the cellular source of PAF in the pleural fluids in the pathologic state of inflammation.
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PMID:The presence of platelet-activating factor associated with eosinophil and/or neutrophil accumulations in the pleural fluids. 235 88

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

In this review, some common food plants and their toxic or otherwise bioactive components and mycotoxin contaminants have been considered. Crucifers contain naturally occurring components that are goitrogenic, resulting from the combined action of allyl isothiocyanate, goitrin, and thiocyanate. Although crucifers may provide some protection from cancer when taken prior to a carcinogen, when taken after a carcinogen they act as promoters of carcinogenesis. The acid-condensed mixture of indole-3-carbinol (a component of crucifers) binds to the TCDD receptor and causes responses similar to those of TCDD. Herbs contain many biologically active components, with more than 20% of the commercially prepared human drugs coming from these plants. Onion and garlic juices can help to prevent the rise of serum cholesterol. Most herbs used in treatments may have many natural constituents that act oppositely from their intended use. Some herbs like Bishop's week seed contain carcinogens, and many contain pyrrolizidine alkaloids that can cause cirrhosis of the liver. The general phytoalexin response in plants (including potatoes, tomatoes, peppers, eggplant, celery, and sweet potatoes) induced by external stimuli can increase the concentrations of toxic chemical constituents in those plants. In potatoes, two major indigenous compounds are alpha-solanine and alpha-chaconine, which are human plasma cholinesterase inhibitors and teratogens in animals. Because of its toxicity, the potato variety Lenape was withdrawn from the market. Celery, parsley, and parsnips contain the linear furanocoumarin phytoalexins psoralen, bergapten, and xanthotoxin that can cause photosensitization and also are photomutagenic and photocarcinogenic. Celery field workers and handlers continually have photosensitization problems as a result of these indigenous celery furanocoumarins. A new celery cultivar (a result of plant breeding to produce a more pest-resistant variety) was responsible for significant incidences of phytophotodermatitis of grocery employees. Since there is no regulatory agency or body designated to oversee potential toxicological issues associated with naturally occurring toxicants, photodermatitis continues to occur from celery exposure. Sweet potatoes contain phytoalexins that can cause lung edema and are hepatotoxic to mice. At least one of these, 4-ipomeanol, can cause extensive lung clara cell necrosis and can increase the severity of pneumonia in mice. Some phytoalexins in sweet potatoes are hepatotoxic and nephrotoxic to mice. The common mushroom Agaricus bisporus contains benzyl alcohol as its most abundant volatile, and A. bisporus and Gyromitra esculenta both contain hydrazine analogues. Mycotoxins are found in corn, cottonseed, fruits, grains, grain sorghums, and nuts (especially peanuts); therefore, they also occur in apple juice, bread, peanut butter, and other products made from contaminated starting materials.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Natural pesticides and bioactive components in foods. 240 25

With few exceptions, pulmonary complications in the immunocompromised host will proceed to death unless the clinician intercedes. The differential diagnosis of diffuse pulmonary disease in this setting includes (1) infection, most commonly from opportunistic organisms; (2) recurrence or extension of the basic underlying disease process to involve the lungs; (3) adverse pulmonary reaction to drugs; (4) a new, unrelated disease process such as cardiac pulmonary edema or pulmonary emboli; and (5) any combination of these categories. Up to a third of these patients have two or more complications, such as pneumonitis from two different opportunistic organisms or an opportunistic infection and a drug-induced pulmonary complication. An understanding of the host defense that is compromised enables the clinician to narrow the differential diagnosis. The most common types of impairment of defense mechanisms are reductions in the number of granulocytes, B-lymphocytes, or T-lymphocytes, and not uncommonly, two or all three of these types of cells are involved. Impairment of each of these cell types is associated with an increased frequency of infection by a particular group of organisms. Consequently, the clinician can be somewhat selective if empiric therapy is being considered. In the immunocompromised patient, most pulmonary complications, including drug-induced pulmonary disease and pulmonary emboli, are associated with fever that mimics an infection. Up to 25% of the pulmonary complications in these patients are noninfectious.
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PMID:Pulmonary disease in the immunocompromised host. 1. 240 12

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

Eleven cases of idiopathic chronic eosinophilic pneumonia were studied. Ten of the patients were followed up for more than 3 years and the last one for 15 years. The female predominance observed, the mean age of 51 years, the late manifestations of asthma-like symptoms preceding the systemic signs by 8 1/2 months on average and the scarcity of extra-pulmonary manifestations characterized the clinical data. The most frequent radiological signs were non-systematized, bilateral alveolar opacities in the axillary and apical regions, sometimes migratory and giving in 9 cases a mirror image of pulmonary oedema. Beside this major inflammatory syndrome, blood eosinophilia was present in 10 patients with 4,500 eosinophils on average per cubic millimetre. Eosinophils were also present in the bronchoalveolar lavage fluid of those who underwent this examination. Both clinical and radiological signs responded to corticosteroids in all cases, with return to normal chest radiography within less than 10 days. Subsequently, the possibility of radiological relapse in the same or other territories, together with the development of a steroid-dependent intrinsic asthma accounted for the fact that after a follow-up of about 3 years corticosteroid therapy could not be discontinued in any of our patients.
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PMID:[Chronic idiopathic eosinophilic pneumopathy. Carrington's disease]. 253 58

The microbiological etiology of pneumonia in 34 renal transplant patients with clinical and X-ray evidence of pulmonary parenchymal disease was studied. Fiberoptic bronchoscopy with bronchoalveolar lavage (BAL), transbronchial lung biopsy (TBB) and brushing was performed on 18 patients. Laboratory evaluation included histological and cytological methods, cultures for bacteria, fungus and virus and immunofluorescence techniques for the detection of Pneumocystis carinii, cytomegalovirus (CMV) and legionella. Serum samples were obtained concomitantly for antibody studies. CMV, the most common etiology, was considered to be the cause of disease in 18/34 patients. All but one of these patients had positive CMV isolates in culture on leucocytes. Pulmonary edema was found in 7 patients, bacterial pneumonia in 11 patients, P. carinii in 4 patients and Candida albicans in 1 patient. Multifactorial etiology was found in 12/34 cases. The overall mortality was 32%. Bronchoscopy gave correct diagnosis in 13/14 patients with infectious pulmonary diseases (93%). Bronchoscopy procedures were well tolerated and should be considered in transplant patients with evidence of pulmonary parenchymal disease.
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PMID:Cytomegalovirus the predominant cause of pneumonia in renal transplant patients. A two-year study of pneumonia in renal transplant recipients with evaluation of fiberoptic bronchoscopy. 254 42


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