Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034067 (emphysema)
 11,506 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We experienced three cases of lower respiratory tract infections worsened after Rhinovirus infection. Case 1: A 42-year-old male with diffuse panbronchiolitis was admitted to our hospital with the complaint of dyspnea on November 21, 1988. Rhinovirus was isolated from nasal washing and P. aeruginosa was cultured from transtracheal aspiration (TTA). Case 2: A 67-year-old male, whose underlying disease was pulmonary asbestosis, was admitted to our hospital complaining of pyrexia on June 12, 1990. Rhinovirus was isolated from TTA and H. influenzae and others were cultured from TTA. Case 3: A 64-year-old male with pulmonary emphysema was admitted to our hospital with a complaint of dyspnea on August 11, 1989. On December 17, 1989 the patient developed rhinorrhea and complained of purulent sputum, pyrexia and dyspnea after five days. Rhinovirus was isolated from nasal washing and TTA and S. nonhaemolyticus and others were cultured from TTA. As indicated in this report, it is interesting to study the relationship between viral infection of the upper respiratory tract and bacterial infection of the lower respiratory tract.
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PMID:[Three cases of lower respiratory tract infection worsened after rhinovirus infection]. 133 Dec 64

The gross and microscopic pathology of phocine distemper is described. The most striking features were pulmonary congestion and emphysema associated with proliferation of type II pneumocytes, often forming syncytia. Secondary bacterial infection was common and associated with marked atrophy of lymphoid tissues and degenerative changes in the mucosa of the airways.
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PMID:The pathology of phocine distemper. 159 27

We measured serum levels of IgG subclasses in 100 healthy adult humans and 64 patients with respiratory infections by utilizing the enzyme linked immunosorbent assay (ELISA). The patients were composed of 18 patients with acute bacterial pneumonia and bacterial infection of 9 patients with pulmonary emphysema, 27 patients with chronic bronchitis and 10 patients with bronchiectasis. In healthy adults, serum levels of IgG1 subclass decreased in proportion of age increase. Serum levels of IgG2 rose after 30 years of age. Serum levels of IgG3 and IgG4 showed no remarkable changes by age. In patients with respiratory infectious disease, serum levels of IgG1, IgG2 and IgG4 decreased significantly but IgG3 increased significantly. We also measured serum levels of IgG subclasses in 10 patients with acute bacterial pneumonia and bacterial infection of 5 patients with pulmonary emphysema, 12 patients with chronic bronchitis and 4 patients with bronchiectasis at both infected and convalescent phases. The serum levels of IgG2 in patients with pneumonia and pulmonary emphysema at convalescent phase were significantly lower than those in the patients of infected phase. Other subclasses showed no significant change. We summarized that IgG2 was consumed at the infected phase by protecting against bacterial infections. IgG2 probably has an important role of protecting against bacterial respiratory infections among all IgG subclasses.
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PMID:[Serum levels of healthy adult humans and changes of IgG subclass levels between infected and convalescent phase in respiratory infections]. 188 Apr 47

We studied the pulmonary diseases which had developed as consequent deformities after healing of tuberculosis, which we called tuberculosis sequelae. Results are described as follows. 1. The frequency of tuberculosis sequelae was about 6% in the patients with pulmonary diseases admitted to our hospital. 2. 93 cases of them consisted of 4 groups, which were 39 of repeated bacterial infection of lower respiratory tract, 23 of pulmonary aspergilloma, 13 of atypical mycobacteriosis and 28 of chronic respiratory failure. 3. Patients with tuberculosis sequelae were distributed more in the younger age group than others with resembled pulmonary diseases. The men to women ratio was about 2:1. Patients with pulmonary aspergilloma were younger than those with atypical mycobacteriosis. 4. Death rate in tuberculosis sequelae was about 5% per year. 46% of patients with atypical mycobacteriosis and 44% with chronic respiratory failure died within 4 years. 5. In chest X-ray findings, fibrosis and shrinkage of the lung, compensatory pulmonary emphysema, deformity or dilatation of bronchi, bulla formation and residual tuberculous cavities were recognized in 40 to 65% of the cases. Severe pleural thickness or past thoracoplasty were frequently recognized in the patients with chronic respiratory failure. All the patients with pulmonary aspergilloma had one or more residual cavities. 6. The frequency of systemic complications was not more than in the control population matched by age. Comparatively, serum IgG and IgA were elevated and PHA-induced lymphocyte activation was not lowered in the patients with pulmonary aspergilloma and atypical mycobacteriosis. From these results, the main factor in the development of tuberculosis sequelae seemed to be local defects of the chest.
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PMID:[Tuberculosis sequelae: clinical aspects]. 207 59

Reactive oxygen metabolic products derived from an activated NADPH oxidase present in the cell membrane of PMNs and mononuclear phagocytic cells play a critical role in the host's defense against bacterial infection. Recent studies have also demonstrated the ability of these toxic products to initiate eukaryotic cell injury and promote the development of the acute inflammatory responses. Experimental studies suggest that neutrophil-derived oxygen metabolites contribute to the development of the tissue injury associated with a variety of disease states, including emphysema, myocardial infarction, adult respiratory distress syndrome, immune complex-mediated vasculitis, and rheumatoid arthritis. Future studies to define further the mechanisms by which reactive oxygen-derived metabolic products mediate tissue injury will provide insight into the development of new therapeutic strategies for the modulation of disease states that are mediated by the recruitment and activation of PMNs.
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PMID:Polymorphonuclear leukocyte-mediated cell and tissue injury: oxygen metabolites and their relations to human disease. 299 29

One lung from 109 unselected hospital and 43 unselected non-hospital necropsies was studied using postmortem radiography with histological verification. Signs of acute bacterial infection, including bronchiolitis or bronchopneumonia, were present in 42.2% of the hospital necropsies and infection was the immediate cause of death in 8.3%. There was only one case of incipient bronchopneumonia among the non-hospital necropsies. Emphysema was the most common other pulmonary lesion in both groups. Gram negative bacteria were found significantly more often in the bronchial mucus of lungs with any pulmonary lesion, particularly those with signs of bacterial infection, than in the bronchial mucus of morphologically normal lungs in both groups of patients. In addition, the frequency of infections was associated with length of stay in hospital. This may reflect the prevalence of Gram negative infections in hospitals.
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PMID:Postmortem radiographic, histological and bacteriological studies of terminal respiratory infections and other pulmonary lesions in hospital and non-hospital necropsies. 650 89

Pneumoparotitis is a rare cause of enlargement of the parotid gland; it is often misdiagnosed and therefore incorrectly treated. We report three pediatric cases of self-induced pneumoparotitis and detail the clinical presentation, pathogenesis, radiographic findings, and treatment options. We also review the literature on the subject. In children, inflammatory swelling of the parotid gland is usually due to acute viral or bacterial infection, juvenile recurrent parotitis, or allergic, autoimmune, or systemic disease. Infrequently, swelling may result from air being forced through Stensen's duct, resulting in pneumoparotitis. This may occur as a transient or recurrent phenomenon. Recurrent parotid insufflation is not entirely benign and may predispose to sialectasias, recurrent parotitis, and even subcutaneous emphysema.
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PMID:Self-induced pneumoparotitis. 748 76

Cystic fibrosis (CF) is an inherited disorder associated with severe inflammation and repeated bacterial infection and colonization in the lung. Airway epithelium is involved in defence against bacteria, but this system may be defective in CF. Pro-inflammatory cytokines can stimulate the expression of inducible nitric oxide synthase (iNOS), an enzyme generating nitric oxide, which functions as an important mediator in host defence mechanisms. To understand better the poor resistance to infections in the CF lung, the expression of the iNOS gene was investigated in explanted lungs from patients with cystic fibrosis (n = 13), bronchiectasis (n = 3), emphysema (n = 14), and in normal lungs (n = 8). In addition, bronchial epithelial cell lines were examined to study iNOS gene expression in vitro. Strong immunoreactivity for iNOS was seen in inflammatory cells and bronchial epithelium in all the diseased lungs, except for bronchial epithelium in CF. Quantitative analysis showed a significant reduction in the area of epithelium immunostained in CF [CF 6.8 +/- 1.6 (% +/- SEM); emphysema 18.2 +/- 2.8; normal 9.6 +/- 0.8, P < 0.01], regardless of steroid treatment. These results were supported by in situ hybridization of iNOS mRNA, which showed a pattern of gene expression in CF, emphysema, and normal lung which paralleled that of protein immunoreactivity. Stimulation with cytokines (IL-1 beta, TNF-alpha, and IFN-gamma) increased the expression of iNOS mRNA detected by reverse transcriptase-polymerase chain reaction (RT-PCR) in cultures of normal (16HBE14o-), but not CF (CFBE41o-, with delta F508 CFTR mutation) epithelial cells. Expression of iNOS in inflammatory cells suggests that the gene is normal in CF. Absence of iNOS from bronchial epithelium may be due to low expression of the gene resulting from abnormalities in the signalling system that normally causes induction, such as cytokine receptors, second messengers or transcription factors. The resulting deficiency of the nitric oxide defence system may be relevant to the susceptibility of CF patients to pulmonary bacterial colonization.
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PMID:Lack of inducible nitric oxide synthase in bronchial epithelium: a possible mechanism of susceptibility to infection in cystic fibrosis. 961 86

The frequency with which bacterial infection causes exacerbations of chronic obstructive pulmonary disease (COPD) may depend on the dominant pathology present; patients with chronic bronchitis are more susceptible to bacterial bronchial infections than those at the emphysema or asthma ends of the spectrum. However, impairment in respiratory function may be very important in governing the outcome of an exacerbation. Placebo-controlled trials have provided conflicting evidence of the efficacy of antibiotics in acute exacerbations. Overall, there is a significant benefit, particularly in certain patient groups, defined by symptoms and past history. Haemophilus influenzae, Streptococcus pneumoniae, and Moraxella catarrhalis are the species most commonly isolated during exacerbations, and the same species may colonize the bronchial mucosa when the patient is in a stable state. Evidence is accumulating that bacteria are an independent stimulus of mucus hypersecretion and bronchial inflammation, and that they interact with other stimuli such as viral infection, atmospheric pollution, and tobacco smoke. New approaches are being used to investigate the importance of bacterial infection in patients with COPD. There are several good reasons why new more potent antibiotics might be expected to be superior to older standard compounds in the management of patients with problematic COPD. However, future studies should aim to confirm that bacteriologic superiority translates into improved clinical outcomes, and seek to measure the level of benefit.
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PMID:Evidence of bacterial infection in acute exacerbations of chronic bronchitis. 1105 21

Neutrophils are sequestered in the newly transplanted lung after reperfusion or with infection, rejection, and chronic graft dysfunction. Because unopposed (free) neutrophil elastase (NE) released into bronchoalveolar secretions may injure the lung allograft and impair bacterial clearance, we assessed total neutrophil numbers, myeloperoxidase activity as an index of neutrophil influx and degranulation, alpha1-antiprotease (alpha1-AP) concentrations, and unopposed NE activity in bronchoalveolar secretions from lung transplant recipients. Unopposed NE activity was present in bronchoalveolar lavage fluid (BALF) from recipients transplanted for emphysema associated with alpha1-AP deficiency as well as recipients without such deficiency (171 of 2,137 BALF; 8%). Ten of 17 (59%) recipients with alpha1-AP deficiency who were followed for at least 1 yr after transplant with multiple surveillance and diagnostic bronchoscopies had at least one BALF containing unopposed NE, usually associated with the presence of > or = 10(5) colony forming units/ml BALF of aerobic bacteria. In contrast, 19 of 58 (33%) with emphysema not associated with alpha1-AP deficiency, 8 of 32 (25%) recipients with cystic fibrosis (CF), 6 of 16 (38%) with idiopathic pulmonary fibrosis (IPF), and 11 of 36 (31%) with other indications for transplant had unopposed NE in BALF. alpha1-AP levels were significantly elevated in the early posttransplant time period and could be augmented considerably in alpha1-AP-deficient recipients with episodes of infection or rejection. Our findings indicate that unopposed NE activity can be found in both alpha1-AP-deficient and alpha1-AP-sufficient recipients after transplantation, usually in association with endobronchial bacterial infection.
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PMID:Neutrophils, unopposed neutrophil elastase, and alpha1-antiprotease defenses following human lung transplantation. 1143 46


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