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)

Measurement of the acute phase response in patients suffering from bronchiectasis, emphysema, bronchus carcinoma and various benign space-occupying lesions was undertaken, using sensitive immunoradiometric assays for C-reactive protein (CRP) and serum amyloid-A protein (SAA). In some patients with bronchiectasis, clinically judged to be in remission, the results show a major ongoing acute phase response. Such a response could predispose these patients to the development of reactive secondary amyloidosis. In bronchus carcinoma the application of these measurements to judge the extent of tumor growth is limited as infection-complicating obstruction is a more potent initiator of the acute phase response than the neoplastic process per se.
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PMID:Acute phase response in bronchiectasis and bronchus carcinoma. 400 76

Measurement of the acute phase response in patients suffering from bronchiectasis, emphysema, bronchus carcinoma and various benign space occupying lesions was undertaken, using sensitive immunoradiometric assays for C-reactive protein and serum amyloid-A protein. In some patients with bronchiectasis, clinically judged to be in remission, the results show a major ongoing acute phase response. Such a response could predispose these patients to the development of reactive secondary amyloidosis. In bronchus carcinoma, the application of these measurements to judge the extent of tumour growth is limited as infection complicating obstruction is a more potent initiator of the acute phase response than the neoplastic process per se.
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PMID:Acute phase response in bronchiectasis and bronchus carcinoma. 647 23

Pneumoperitoneum is most commonly caused by the perforation of a hollow viscus, in which case an emergency laparotomy is indicated. We report herein the case of a patient who presented with the signs and symptoms of peritonitis, but who was found to have idiopathic pneumoperitoneum which was successfully managed by conservative treatment. A 70-year-old man presented with epigastric pain, nausea, and a severely distended and tympanitic abdomen. Abdominal examination revealed diffuse tenderness with guarding, but no rebound tenderness. He was febrile with leukocytosis and high C-reactive protein. Chest X-ray and abdominal computed tomography demonstrated a massive pneumoperitoneum without pneumothorax, pneumomediastinum, pneumoretroperitoneum, or subcutaneous emphysema, and subsequent examinations failed to demonstrate perforation of a hollow viscus. Thus, a diagnosis of idiopathic pneumoperitoneum was made, and the patient was managed conservatively, which resulted in a successful outcome. This experience and a review of the literature suggest that idiopathic pneumoperitoneum is amenable to conservative management, even when the signs and symptoms of peritonitis are present.
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PMID:Conservative management of idiopathic pneumoperitoneum masquerading as peritonitis: report of a case. 764 Apr 58

In chronic obstructive pulmonary disease (COPD) which consists of emphysema and chronic bronchitis, alveolar tissue and/or bronchiolar walls are progressively destroyed. This suggests cell death by necrosis and/or apoptosis although no direct evidence of apoptosis has been reported. It was speculated that the apoptosis-related factors are associated with the progression of COPD. Fas/Apo-1 receptor (Fas), Fas ligand (Fas-L) and soluble Fas ligand (sFas-L) are inducers, while soluble Fas (sFas) is an inhibitor of apoptosis. In this study, plasma sFas and sFas-L were measured in 19 COPD patients receiving supplemental O2 (severe COPD) and 20 COPD patients not receiving supplemental O2 (mild/moderate COPD). Twenty-two age- and sex-matched healthy volunteers (healthy controls) and 20 patients receiving supplemental O2 and with level of hypoxaemia similar to severe COPD due to other pulmonary diseases (disease controls) were also examined. Plasma sFas-L was within normal limits in all groups. Plasma sFas levels were similar among healthy controls, disease controls, and mild/moderate COPD patients, but significantly increased in severe COPD (2.6 +/- 1.1, 2.6 +/- 0.2, 2.8 +/- 0.2 and 4.8 +/- 1.0 ng ml-1, respectively). Although PaO2 was lower in severe COPD than in mild/moderate COPD, and PaCO2 was higher in severe COPD than in mild/moderate COPD, they were close between severe COPD and disease controls. Tumour necrosis factor-alpha (TNF-alpha), interleukin 6 (IL-6) and C-reactive protein (CRP) were increased in patients with COPD, but were similar in both severe and mild/moderate COPD patients. We conclude that increased plasma sFas, which is independent of hypoxaemia, and increases in PaCO2, TNF-alpha, IL-6 and inflammation, may be associated with progression of COPD.
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PMID:An increase of soluble Fas, an inhibitor of apoptosis, associated with progression of COPD. 989 64

Patients with homozygous (PiZ) alpha(1)-antitrypsin (AAT) deficiency have not only low baseline serum AAT levels (approximately 10 to 15% normal) but also an attenuated acute phase response. They are susceptible to the development of premature emphysema but may also be particularly susceptible to lung damage during bacterial exacerbations when there will be a significant neutrophil influx. The purposes of the present study were to assess the inflammatory nature of acute bacterial exacerbations of chronic obstructive pulmonary disease (COPD) in subjects with AAT deficiency, to compare this with COPD patients without deficiency, and to monitor the inflammatory process and its resolution following appropriate antibacterial therapy. At the start of the exacerbation, patients with AAT deficiency had lower sputum AAT (p < 0.001) and secretory leukoprotease inhibitor (SLPI; p = 0.02) with higher elastase activity (p = 0.02) compared with COPD patients without deficiency. Both groups had a comparable acute phase response as assessed by C-reactive protein (CRP) but the AAT-deficient patients had a minimal rise in serum AAT (to < 6 microM). After treatment with antibiotics, in patients with AAT deficiency, there were significant changes in many sputum proteins including a rise in SLPI levels, and a reduction in myeloperoxidase (MPO) and elastase activity (p < 0. 005 for all measures); the sputum chemoattractants interleukin-8 (IL-8) and leukotriene B(4) (LTB(4)) fell (p < 0.01), and protein leak (sputum/serum albumin ratio) became lower (p < 0.01). The changes were rapid and within 3 d of the commencement of antibiotic therapy the biochemical markers had decreased significantly, but took a variable time thereafter to return to baseline values. In conclusion, patients with AAT deficiency had evidence of increased elastase activity at the start of the exacerbation when compared with nondeficient COPD patients which probably reflects a deficient antiproteinase screen (lower sputum AAT and SLPI). The increased bronchial inflammation at presentation resolved rapidly with 14 d of antibiotic therapy.
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PMID:Evidence for excessive bronchial inflammation during an acute exacerbation of chronic obstructive pulmonary disease in patients with alpha(1)-antitrypsin deficiency (PiZ). 1058 15

Moderate elevation of serum C-reactive protein (CRP) is a risk factor for cardiovascular disease among apparently healthy individuals, although factors that create this inflammatory response in the absence of systemic illness have not been clarified. This study aimed to: (1) evaluate associations among periodontal disease, established risk factors for elevated CRP, and CRP levels within the US population; and (2) determine whether total tooth loss is associated with reduced CRP. Data were obtained from the third National Health and Nutrition Examination Survey. A random sample of the US population was interviewed in their homes and examined at mobile examination centers. CRP was quantified from peripheral blood samples and analyzed as a continuous variable and as the prevalence of elevated CRP (> or = 10 mg/L). Some 12,949 people aged 18+ years who had periodontal examinations and an additional 1,817 edentulous people aged 18+ years were included in the analysis. Dentate people with extensive periodontal disease (> 10% of sites with periodontal pockets 4+ mm) had an increase of approximately one-third in mean CRP and a doubling in prevalence of elevated CRP compared with periodontally healthy people. Raised CRP levels among people with extensive periodontal disease persisted in multivariate analyses (P < 0.01), with established risk factors for elevated CRP (diabetes, arthritis, emphysema, smoking, and anti-inflammatory medications) and sociodemographic factors controlled for. However, CRP levels were similarly raised in edentulous people. Furthermore, the established risk factors for elevated CRP modified relationships between oral status and CRP levels. Periodontal disease and edentulism were associated with systemic inflammatory response in the US population, most notably among people who had no established risk factors for elevated CRP.
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PMID:Acute-phase inflammatory response to periodontal disease in the US population. 1069 Jun 60

One of the issues concerning harmonization in the development of pharmaceutical products, especially antimicrobials, is discrepancy in the indications to be studied clinically. In particular, it has been very much questioned whether the underlying disease in Western patients diagnosed with acute exacerbation of chronic bronchitis (AECB) is identical with chronic bronchitis in Japan. We assessed chest X-ray films from 105 AECB patients enrolled in a clinical study of SB265805 (a fluoroquinolone antibacterial agent under development) conducted in Europe, and then compared their clinical signs/symptoms and laboratory data with Japanese historical data. Five of the 105 patients did not meet the criteria of AECB; i.e., 2 of them were diagnosed with pneumonia, 1 with bronchiectasis, 1 with pneumoconiosis, and 1 with bronchiectasis plus pulmonary emphysema. In the remaining 100 patients, chest X-ray findings and laboratory test results were consistent with the concept of chronic bronchitis, although 23 of them had other cardiac or pulmonary diseases as well. There were significant imbalances in distribution between Western patients and Japanese historical data in terms of age, cough, WBC counts, and C-reactive protein (CRP) levels. Compared with Japanese historical data, Western patients were younger and had a more severe cough, although increases in WBC and CRP were less remarkable. For other variables, i.e., sex, fever, and volume of sputum, no significant difference was detected in distribution. Overall, there was no significant difference between the two groups in regard to disease severity, as assessed by fever, WBC, and CRP.
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PMID:Comparison of chest X-ray findings and other parameters in acute exacerbation of chronic bronchitis in Japan and the West. 1140 55

To elucidate the biological significance of selectin for idiopathic pulmonary fibrosis, we titrated the serum soluble E-selectin. From 31 cases of idiopathic pulmonary fibrosis patients without signs or symptoms of infection, the serum was obtained and the concentration was titrated by enzyme-linked immunosorbent assay. The serum soluble E-selectin titer was significantly higher than that of healthy controls. However, significant elevation was not observed in the sera from the patients with other pulmonary diseases, such as pulmonary emphysema, sarcoidosis, or bronchiectasis. In the patients with idiopathic pulmonary fibrosis, the number of white blood cells, C-reactive protein or lactate dehydrogenase activity did not show a significant relationship with the soluble E-selectin titer. About 16 out of the 31 idiopathic fibrosis patients, the serum surfactant apoprotein-A titer, which is a parameter of the disease activity of idiopathic pulmonary fibrosis, was also tested. The surfactant apoprotein-A titer was loosely correlated with the soluble E-selectin titer. These observations suggest that E-selectin may be relevant to the pathogenesis of idiopathic pulmonary fibrosis, and it may be a novel clinical parameter for idiopathic pulmonary fibrosis.
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PMID:Increased level of soluble E-selectin in the serum from patients with idiopathic pulmonary fibrosis. 1507 24

Smoking is the leading preventable cause of illness and premature death in Germany, claiming over 110,000 lives a year because it directly increases the risk of dying from heart disease, stroke, emphysema and a variety of cancers. The overwhelming majority of smokers begin tobacco use before they reach adulthood. Among those young people who smoke, the average age is now 13-14. In Germany, about 39% of male and 31% of female adults (age 18-60 years) continue to smoke, despite information about the unequivocally negative health consequences of smoking. The exact mechanisms of smoking-related vascular disease are not yet known. Smoking causes acute hemodynamic alterations such as increase in heart rate, systematic and coronary vascular resistance, myocardial contractility, and myocardial oxygen demand. These short-term effects could lower the ischemic threshold in smokers with coronary artery disease and contribute to the increased risk for acute cardiovascular events. Endothelial damage is thought to be an initiating event in atherosclerosis and early studies have demonstrated that long-term smoking has direct toxic effects with structural changes of human endothelial cells. Recent research has shown the importance of the functional role of the endothelium in regulating vascular tone, platelet-endothelial interactions, leukocyte adhesion and smooth muscle cell proliferation via synthesis and release of a variety of substances such as nitric oxide. There is strong evidence that smoking leads to endothelial dysfunction mainly by increased inactivation of nitric oxide by oxygen-derived free radicals. Smoking also increases oxidative modification of LDL and is associated with lower HDL plasma levels. Smoking induces a systemic inflammatory response with increased leukocyte count and elevation of the C-reactive protein level. Importantly, the prothrombotic effects of smoking have been repeatedly demonstrated to cause alterations in platelet function, imbalance of antithrombotic vs prothrombotic factors, and decrease of fibrinolytic activity. Given the enormous health hazard of tobacco use, complete abstinence from smoking should be achieved. Smoking cessation counselling should be given to healthy subjects and even more vigorously to patients with manifested disease. Every effort should be undertaken to prevent children and adolescents from starting to smoke. Brief tobacco dependence treatment is effective, and every smoker should be offered at least brief treatment at every office visit. More intensive treatment is more effective in producing long-term abstinence from tobacco. Nicotine replacement therapy (nicotine patches or gum), clinician-delivered social support, and skills training are the three most effective components of smoking cessation treatment. A framework for tobacco control measures is necessary to reduce tobacco consumption and exposure to tobacco smoke. Recommendations on specific tobacco control interventions are: 1. increase in tobacco taxes; 2. comprehensive tobacco advertising bans; 3. legislation prohibiting smoking in work and public places; 4. prohibiting the sales of tobacco products to persons under 18; 5. comprehensive disclosure of the physical, chemical and design characteristics of all tobacco products; 6. training of health professionals to promote smoking prevention and cessation interventions; and 7. development of a national network of smoking cessation treatment services.
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PMID:[Prevention of coronary heart disease: smoking]. 1625 91

Chronic obstructive pulmonary disease (COPD) is characterized by an abnormal persistent inflammatory response to cigarette smoke. This noxious insult leads to emphysema and airway remodeling, manifested by squamous and mucous metaplasia of the epithelium, smooth muscle hypertrophy, and airway wall fibrosis. These pathologic abnormalities interact synergistically to cause progressive airflow obstruction. Although it has been accepted that the spectrum of COPD is vast, the reasons for the development of different phenotypes from the same exposure to cigarette smoke have not been determined. Furthermore, it is becoming increasingly clear that airways disease and emphysema often coexist in many patients, even with a clear clinical phenotype of either emphysema or chronic bronchitis. Recent studies have focused on the nature of the inflammatory response to cigarette smoke, the inflammatory cell lines responsible for COPD pathogenesis, and new biomarkers for disease activity and progression. New cytokines are being discovered, and the complex interactions among them are being unraveled. The inflammatory biomarker that has received the most attention is C-reactive protein, but new ones that have caught our attention are interleukin (IL)-6, tumor necrosis factor-alpha, IL-8, and IL-10. Further research should focus on how these new concepts in lung inflammation interact to cause the various aspects of COPD pathology.
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PMID:New concepts in the pathobiology of chronic obstructive pulmonary disease. 1845 59


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