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 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In 15 patients with cystic fibrosis 18 blood samples were investigated for signs of infection including full white blood count, c-reactive protein (CRP) and tumour-necrosis-factor alpha (TNF). Ten patients were hospitalized for pulmonary exacerbation, one for orthostatic collapse and one for equivalent of meconium ileus. The latter two as well as three out-patients with cystic fibrosis on routine-visits served as controls. Blood was taken on admission and at the time of the visit in our out-patient department, respectively. In three cases, blood was taken repeatedly during their stays in hospital. While leucocytosis (17.700 +/- 3.500) and elevated CRP-levels (6.4 +/- 7.3 mg/dl) pointed to an infectious cause of deterioration in the exacerbation-group, TNF-levels without exception were undetectable (less than 15 pg/ml). In the control group, leucocyte counts (10.700 +/- 3.600) and CRP-levels (1.2 +/- 1.1 mg/dl) showed minor pathologic results. TNF-levels were undetectable, too. While elevated TNF-levels measured quantitatively in patients with invasive bacterial infections, e.g. septicaemia due to Neisseria meningitidis, correlate well with prognosis of disease, in patients with cystic fibrosis such a relationship can't be found.
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PMID:[Tumor necrosis factor in the serum--a useful supplemental parameter in the diagnosis of infection in cystic fibrosis?]. 185 50

Direct electron microscopic examination of postmortem lung material from cystic fibrosis patients infected with Pseudomonas aeruginosa has shown that these bacterial cells form distinct fiber-enclosed microcolonies in the infected alveoli. Similar examination of bronchoscopy material from infected cystic fibrosis patients showed that the fibres of the enveloping matrix are definitely associated with the bacterial cells. The fibers of the extracellular matrix stain with ruthenium red and are therefore presumed to be polyanionic. When mucoid strains of P. aeruginosa were recovered from cystic fibrosis patients and grown in a suitable liquid medium, they were found to produce large microcolonies whose component cells were embedded in a very extensive matrix of polyanionic fibers that could be stabilized by reaction with antibodies to prevent collapse during the dehydration steps of preparation for electron microscopy. When these mucoid strains of P. aeruginosa were used to produce pulmonary infections of rats by the agar bead method, the infected alveoli contained large fiber-enclosed bacterial microcolonies. We conclude that the cells of P. aeruginosa that infect cystic fibrosis patients form microcolonies that are enveloped in a fibrous anionic matrix and that these microcolonies can be duplicated in in vitro cultures and in animal model systems.
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PMID:Production of mucoid microcolonies by Pseudomonas aeruginosa within infected lungs in cystic fibrosis. 677 62

In 24 patients with cystic fibrosis (6-20 years old), divided into two groups, we studied indices of airways obstruction before, 20-30 min and 2 h after chest physiotherapy. The physiotherapy lasted for 30 min and included expectoration of 2-10 ml of sputum. In one group of 14 patients, studies were made only 30 min after chest physiotherapy. No significant improvements of the ventilatory tests occurred. In fact, Vmax at 25% of VC deteriorated (P less than 0.05) in this group as a whole. In some patients also CV/VC increased, and N2 and CO2 alveolar slopes became steeper. Only Gaw/TGV improved in 20% of the patients by more than 10% of the control value. In the second group of 10 patients, ventilatory studies were repeated 3 times at one month intervals. They did not change significantly at 20 min and 2 h after chest physiotherapy. Gaw/TGV value improved by more than 10% in 20% of the patients. During chest physiotherapy, the patients were stimulated to cough. This might contribute to the immediate negative effects on ventilatory function by causing collapse of the central airways, as documented by cinebronchographic studies in 8 patients.
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PMID:Chest physiotherapy and airway obstruction in patients with cystic fibrosis - a negative report. 688 55

Allergic bronchopulmonary aspergillosis, known to be associated with cystic fibrosis in older patients, occurred in 7 young atopic children with cystic fibrosis. The diagnosis was suggested by the onset of, or the increase in, asthmatic symptoms accompanied by major chest x-ray changes ranging from total collapse of a lung or lobe to extensive but changing areas of consolidation. Each of the children had a blood eosinophilia, positive type I skin tests to Aspergillus fumigatus, and reversible airways obstruction. Most had a positive type III skin test and circulating precipitins to A. fumigatus, with raised IgE levels which contained specific antibodies to the fungus on radioallergosorbent (RAST) test. None had advanced suppurative chest disease of cystic fibrosis. None was given specific antifungal agents; two received systemic treatment with corticosteroids, the other received additional drugs for their asthma. Two developed total collapse of one lung, one child being only 2 years old. Five have had recurrences of pulmonary shadowing typical of allergic aspergillosis but are not showing significant progression of their cystic fibrosis lung disease. Our experience suggests that there should be an increased awareness of this condition, particularly its association with extensive pulmonary collapse or consolidation in children with cystic fibrosis who are atopic.
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PMID:Allergic bronchopulmonary aspergillosis complicating cystic fibrosis in childhood. 700 53

Historically, most methods for detecting linkage disequilibrium were designed for use with diallelic marker loci, for which the analysis is straightforward. With the advent of polymorphic markers with many alleles, the normal approach to their analysis has been either to extend the methodology for two-allele systems (leading to an increase in df and to a corresponding loss of power) or to select the allele believed to be associated and then collapse the other alleles, reducing, in a biased way, the locus to a diallelic system. I propose a likelihood-based approach to testing for linkage disequilibrium, an approach that becomes more conservative as the number of alleles increases, and as the number of markers considered jointly increases in a multipoint test for linkage disequilibrium, while maintaining high power. Properties of this method for detecting associations and fine mapping the location of disease traits are investigated. It is found to be, in general, more powerful than conventional methods, and it provides a tractable framework for the fine mapping of new disease loci. Application to the cystic fibrosis data of Kerem et al, is included to illustrate the method.
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PMID:A powerful likelihood method for the analysis of linkage disequilibrium between trait loci and one or more polymorphic marker loci. 788 34

Immediately after heart-lung transplantation for cystic fibrosis, a patient had development of a right lower lobe retrocardiac density that persisted on all postoperative chest radiographs. A computed tomographic examination of the thorax performed 3 weeks after surgery showed that there was partial collapse of the left lower lobe in the right hemithorax. The patient required a posterolateral thoracotomy for cure.
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PMID:Dextroposition of the left lower lobe after heart-lung transplantation. 840 32

The usefulness of thin-section computed tomography (CT) in the identification of the specific and clinically relevant pathologic changes in airway disease has been well documented. However, this approach has not been used for objective evaluation in patients with diffuse panbronchiolitis. Therefore attempts were made to use it in patients with diffuse panbronchiolitis. The study group included 12 men and 10 women, 17 to 69 years of age (mean, 47 years) with diffuse panbronchiolitis. All patients were evaluated by thin-section CT and pulmonary function testing. The CT score was calculated by a modified score criteria. The correlations between the CT score and the pulmonary function parameters were assessed by Pearson's linear regression analysis. Bronchiolar inflammation and airway-ectasia were present in all 22 patients. Periairway thickening was present in 17 patients. Pus plugging was present in 18 patients. Two patients had bullae formation, and 6 had air-trapping. Pulmonary collapse or consolidation was evident in 6 patients. The CT score demonstrated a significant negative correlation with FEV1% (r = -3.267, p = .0230), %VC (r = -4.658, p = .0018), and arterial blood oxygen concentration (r = -1.009, p = .0381). The thin-section CT findings in patients with diffuse panbronchiolitis closely resembled those in patients with cystic fibrosis, previously described. Furthermore, a CT scoring system is useful for objective evaluation of lung disease severity in patients with diffuse panbronchiolitis.
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PMID:Diffuse panbronchiolitis--a thin-section CT scoring system. 870 61

Following lung transplantation for end-stage cystic fibrosis, two male patients presented with shortness of breath, peripheral blood eosinophilia and segmental lung collapse. At bronchoscopy, each had bronchial mucous plugging containing Aspergillus fumigatus. This finding was associated with a systemic eosinophilia and skin test positivity to Aspergillus. Augmented steroid therapy resulted in the successful resolution of the symptoms. We believe that these are the first reported cases of allergic bronchopulmonary aspergillosis in lung allograft recipients.
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PMID:Allergic bronchopulmonary aspergillosis in lung allograft recipients. 883 50

Cystic fibrosis (CF) patients frequently experience recurring airway infections characterized by thick, viscous sputum. The consistency and nature of these purulent secretions may produce a significant barrier to the successful delivery of drugs and gene therapy vectors designed to treat CF. We have carried out a series of in vitro studies to determine the distribution of two macromolecular components typically present in purulent sputum, bacterial alginate and neutrophil-derived DNA. Sputum samples were obtained from hospitalized CF patients. DNA and alginate were disrupted, respectively, by the in vitro additions of human recombinant deoxyribonuclease I (rhDNase) or alginate lyase prepared from a mucoid strain of Pseudomonas aeruginosa. N-acetyl-L-cysteine (acetylcysteine) was similarly used to collapse the mucin matrix of these samples for comparison. Using a centrifugation-based rheological method known as the compaction assay, a greater maximal response was observed for rhDNase compared to alginate lyase treatment. A simultaneous addition of these enzymes to purulent sputum produced an additive compaction response. Electron microscopy was used to identify alginate and DNA components within the mucin matrix of sputa and to evaluate changes following treatment with high concentrations of alginate lyase or rhDNase. DNA was more widely distributed throughout purulent samples than alginate. Differences in the distribution of DNA and alginate may explain, at least in part, the larger compaction response to rhDNase versus alginate lyase treatment. An improved understanding of DNA and alginate distribution within purulent CF sputum may lead to improvements in drug and vector delivery to airway epithelial cells.
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PMID:Distribution of DNA and alginate in purulent cystic fibrosis sputum: implications to pulmonary targeting strategies. 901 Aug 13

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


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