Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

An 18-year-old woman presented with coughing, fever, progressive dyspnea, and diffuse infiltrates on the chest X-ray film. Analysis of bronchoalveolar lavage fluid showed 73% eosinophils. Acute eosinophilic pneumonia was diagnosed. Methylprenisolone, 1 g per day was given for three days and her condition improved dramatically. No relapse was observed. Analysis of bronchoalveolar lavage fluid also showed lymphocytosis, abnormally high concentrations of ECP, GM-CSF, IL-5 and sICAM-1, and hypersegmentation of eosinophil nuclei. After steroid treatment almost all these findings returned to normal; only lymphocytosis remained. Precipitating antibodies against four kinds of fungi, including Trichoderma viridae, were noted in the serum, but the environmental provocation test was negative and those fungi were not detected in the environmental culture growth. Comparison of bronchoalveolar lavage findings obtained before and after steroid treatment can provide information on the mechanism of eosinophil accumulation in the lung. This case also draws attention to the relationship between acute and chronic eosinophilic pneumonia.
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PMID:[A case of acute eosinophilic pneumonia: bronchoalveolar lavage findings before and after steroid treatment]. 756

A 57-year-old woman was admitted because of dry cough and middle-grade fever. Chest rentogenogram showed a diffuse infiltrative shadow in the right middle and lower lung fields. The symptoms disappeared after treatment with minocycline, but a new dense shadow appeared in the right upper and middle lung fields. Eosinophilic pneumonia was diagnosed from the results of bronchoalveolar lavage and transbronchial lung biopsy. The symptoms were alleviated and the infiltrative shadow was effaced after treatment with predonisolone (40 mg/day). The results of a biopsy with human eosinophils suggested that the serum and bronchoalveolar lavage fluid contained IL-5 and GM-CSF.
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PMID:[A case of chronic eosinophilic pneumonia involving IL-5 and GM-CSF]. 760 43

Asthma is currently identified by the presence of characteristic symptoms of wheezing, chest tightness, dyspnea and cough, and by the presence of reversible airway narrowing and/or airway hyperresponsiveness to a variety of inhaled bronchoconstrictor stimuli. Airway inflammation appears to be central to the pathogenesis of all of these clinical manifestations of asthma. There are increased numbers of activated eosinophils and of mast cells in the airways of patients with asthma, even those with mild disease. The presence and survival of these inflammatory cells may be promoted by the presence of increased levels of proinflammatory cytokines, such as GM-CSF, interleukin(IL)-3 or IL-5 in asthmatic airways. These cells have the capacity to release potent bronchoconstrictor mediators such as the cysteinyl leukotrienes, which are responsible, in part at least, for airway narrowing in asthma and for allergen-g exercise- and aspirin-induced asthma. Other cells, such as a subset of T-lymphocytes (TH2), may also be important in maintaining the inflammatory cascade through the formation and release of cytokines. Airway structural changes caused by the persisting inflammation, such as airway epithelial damage, or altered smooth muscle function or volume, are likely to be important in the pathogenesis of stable long-standing airway hyperresponsiveness. Mediators released from the inflammatory cells may be responsible for these changes. Despite the great increase in knowledge about the importance of airway inflammation in the pathogenesis of asthma, the precise sequence of events that leads to the presence of persisting airway inflammatory cells, airway structural changes and airway hyperresponsiveness in asthma remains to be clarified.
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PMID:Airway inflammation and asthma. 889 97

The patient was a 59-year-old woman who complained of coughing, sputum production, and dyspnea. Abnormal moving shadows were found by chest radiography. There was prolonged eosinophilia in blood. Eosinophilia was also found in bronchoalveolar lavage fluid, and examination of a specimen obtained by transbronchial lung biopsy revealed eosinophil infiltration in alveolar septal walls, which led to a diagnosis of chronic eosinophilic pneumonia. Because of an attack of bronchial asthma and a high level of IL-5 in serum on admission, the patient was given suplatast tosilate. Symptoms were relieved, eosinophil counts in blood and in bronchoalveolar lavage fluid decreased, and the radiographic abnormality disappeared. The patient was not treated with steroids, and there has been no reccurrence to date, one year after discharge.
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PMID:[Successful treatment of chronic eosinophilic pneumonia with suplatast tosilate]. 923 34

Induced sputum examination has emerged as an important investigative tool in airway diseases. Sputum can be easily induced by ultrasonic nebulization of hypertonic saline. Inprovements in sputum processing have established that sputum provides reproducible measurements of cell counts and fluid phase mediators. Adults and children with stable asthma demonstrate an infiltrate of eosinophils. With an exacerbation of asthma the eosinophil infiltrate increases and the cells become activated in response to cytokines including interleukin-5. A neutrophil infiltrate may accompany some exacerbations. Exacerbations resolve under the influence of corticosteroid therapy. Eosinophils undergo apoptosis and are removed by macrophages. Eosinophilic bronchitis is an important component in up to 20% of patients with chronic cough. Sputum examination promises to be an important technique to facilitate the understanding and management of asthma and cough in adults and children.
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PMID:How to measure airway inflammation: induced sputum. 975 12

Cell-mediated immune (CMI) responses to Bordetella pertussis antigens (pertussis toxin [PT], pertactin [PRN], and filamentous hemagglutinin [FHA]) were assessed in 48-month-old recipients of acellular pertussis [aP] vaccines (either from Chiron-Biocine [aP-CB] or from SmithKline Beecham [aP-SB]) and compared to CMI responses to the same antigens at 7 months of age, i.e., 1 month after completion of the primary immunization cycle. None of the children enrolled in this study received any booster of pertussis vaccines or was affected by pertussis during the whole follow-up period. Overall, around 75% of 4-year-old children showed a CMI-positive response to at least one B. pertussis antigen, independently of the type of aP vaccine received, and the proportion of CMI responders were at least equal at 48 and 7 months of age. However, longitudinal examination of individual responses showed that from 20 (against PT) to 37% (against FHA) of CMI responders after primary immunization became negative at 48 months of age. This loss was more than compensated for by conversion to positive CMI responses, ranging from 36% against FHA to 69% against PRN, in other children who were CMI negative at 7 months of age. In 60 to 80% of these CMI converters, a lack of decline or even marked elevation of antibody (Ab) titers against B. pertussis antigens also occurred between 20 and 48 months of age. In particular, the frequency of seropositivity to PRN and FHA (but not to PT) was roughly three times higher in CMI converters than in nonconverters. The acquisition of CMI response to B. pertussis antigens in 48-month-old children was not associated with a greater frequency of coughing episodes lasting >/=7 days and was characterized by a prevalent type 1 cytokine profile, with high gamma interferon and low or no production of interleukin-5, reminiscent of cytokine patterns following immunization with whole-cell pertussis vaccine or natural infection. Our data imply that vaccination-induced systemic CMI may wane by 4 years of age but may be acquired or naturally boosted by symptomless or minor clinical infection by B. pertussis. This might explain, at least in part, the persistence of protection against typical pertussis in aP vaccine recipients despite a substantial waning of both Ab and CMI responses induced by the primary immunization.
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PMID:Cell-mediated immune responses in four-year-old children after primary immunization with acellular pertussis vaccines. 1041 75

Asthma and chronic obstructive pulmonary disease (COPD) are complex conditions with imprecise definitions, which make definitive morphological comparisons difficult. The airways in asthma are occluded by tenacious plugs of exudate and mucus, and there is fragility of airway surface epithelium, thickening of the reticular layer beneath the epithelial basal lamina (the last two not usually features of COPD), and bronchial vessel congestion and oedema. There is an increased inflammatory infiltrate comprising 'activated' lymphocytes and eosinophils with release of granular content in the latter, and enlargement of bronchial smooth muscle, particularly in medium-sized bronchi. CD4+ve lymphocytes predominate over CD8+ve cells and neutrophils are sparse. In contrast, three conditions contribute to COPD. In chronic bronchitis there is cough and mucous hypersecretion with enlargement of tracheobronchial submucosal glands and a disproportionate increase of mucous acini. CD8+ve lymphocytes predominate over CD4+ve cells and there are increased numbers of subepithelial macrophages and intra-epithelial neutrophils. Exacerbations of bronchitis are associated with a tissue eosinophilia, apparent absence of IL-5 protein but gene expression for IL-4 and IL-5 is present. In small or peripheral airways disease, there is inflammation of bronchioli and mucous metaplasia and hyperplasia, with increased intraluminal mucus, increased wall muscle, fibrosis, and airway stenoses (also referred to as chronic obstructive bronchiolitis). Respiratory bronchiolitis involving increased numbers of pigmented macrophages is a critically important early lesion. Increasingly severe peribronchiolitis includes infiltration of T lymphocytes in which the CD8+ subset again predominates. These inflammatory changes may predispose to the development of centrilobular emphysema and reduced FEV1 via the destruction of alveolar attachments. In emphysema there is abnormal, permanent enlargement of airspaces distal to the terminal bronchiolus (i.e. within the acinus) accompanied by destruction of alveolar walls and without obvious fibrosis. The severity of emphysema, rather than type, appears to be the most important determinant of chronic deterioration of airflow, and in this there may be significant loss of elastic recoil and microscopic emphysema prior to the observed macroscopic destruction of the acinus.
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PMID:Differences and similarities between chronic obstructive pulmonary disease and asthma. 1042 18

A 47-year-old woman was referred to our hospital because of cough and an abnormal shadow in the left lung field. The infiltrate reduced without therapy and another infiltrate appeared in the right lung field. Bronchiolitis obliterans organizing pneumonia was clinically suspected due to the absence of signs of eosinophilia in peripheral blood and bronchoalveolar lavage fluid (BALF). Open lung biopsy specimens disclosed alveolitis with mononuclear cell infiltration and organization within the air spaces of bronchioli and alveolar ducts. The observation of pronounced eosinophil infiltration in the alveolar spaces of some specimens yielded a diagnosis of eosinophilic pneumonia. After steroid therapy, the abnormal shadows disappeared. BALF lymphocyte surface marker analysis detected no decrease in the CD4/CD8 ratio; activated CD4 and CD8 lymphocytes were notably higher than the corresponding levels in peripheral blood. IL-5, IL-3, and GM-CSF values in BALF were not significantly elevated. This was a case of borderline eosinophilic pneumonia that was difficult to diagnose on the basis of clinical parameters alone.
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PMID:[Eosinophilic pneumonia without eosinophilia in BALF or peripheral blood and diagnosed by open lung biopsy]. 1058 89

A 76-year-old woman who had complained of cough and productive sputum since mid-January, 1999, was admitted to our hospital with fever and dyspnea on February 4, 1999. She had been treated with levofloxacin at an outpatient clinic. On admission, she had orthopnea, and auscultation revealed coarse crackles and wheeze in the bilateral lung fields. Chest x-ray and CT films showed non-segmental infiltration in bilateral lung fields. Laboratory data revealed eosinophilia in peripheral blood (= 24%) and sputum (= 10%), airflow limitation, hypoxemia (PaO2: 46 Torr), and increased airway responsiveness to methacholine (Dmin: 0.127 units). A bronchoalveolar lavage (BAL) fluid showed increased total cells and a 55% increase in eosinophils, and CD4/CD8 ratio was decreased to 0.8. In addition, IL-5 was increased in BAL fluid. Transbronchial lung biopsy specimens revealed infiltrations of eosinophils in the alveolar and interstitial compartments. Histological features of the bronchial biopsy specimens included increased eosinophils in the submucosa and goblet cell metaplasia. The woman was diagnosed with eosinophilic pneumonia complicated by bronchial asthma. She was given theophylline, pranlukast hydrate, and an inhaled beta 2 receptor agonist (procaterol hydrochloride), and pre-admission drugs including Levofloxacin were discontinued. Her symptoms were improved, peak expiratory flow rate and PaO2 increased, airway responsiveness to methacholine decreased (Dmin: 0.615 units), and radiographic abnormalities disappeared without steroid therapy. A leukocyte migration test for levofloxacin was weakly positive. An environmental provocation test in the patient's home gave negative results. A challenge test for levofloxacin was not performed due to a lack of informed consent. Based on these findings, we diagnosed this case as levofloxacin-induced lung injury manifesting as eosinophilic pneumonia complicated by bronchial asthma. Levofloxacin should be added to the list of agents that can produce eosinophilic pneumonia.
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PMID:[Levofloxacin-induced eosinophilic pneumonia complicated by bronchial asthma]. 1092 Dec 86

A chronic inflammatory disorder of the respiratory airways, asthma is characterized by bronchial airway inflammation resulting in increased mucus production and airway hyper-responsiveness. The resultant symptomatology includes episodes of wheezing, coughing, and shortness of breath. Asthma is a multifactorial disease process with genetic, allergic, environmental, infectious, emotional, and nutritional components. The underlying pathophysiology of asthma is airway inflammation. The underlying process driving and maintaining the asthmatic inflammatory process appears to be an abnormal or inadequately regulated CD4+ T-cell immune response. The T-helper 2 (Th2) subset produces cytokines including interleukin-4 (IL-4), IL-5, IL-6, IL-9, IL-10, and IL-13, which stimulate the growth, differentiation, and recruitment of mast cells, basophils, eosinophils, and B-cells, all of which are involved in humoral immunity, inflammation, and the allergic response. In asthma, this arm of the immune response is overactive, while Th1 activity, generally corresponding more to cell-mediated immunity, is dampened. It is not yet known why asthmatics have this out-of-balance immune activity, but genetics, viruses, fungi, heavy metals, nutrition, and pollution all can be contributors. A plant lipid preparation containing sterols and sterolins has been shown to dampen Th2 activity. Antioxidant nutrients, especially vitamins C and E, selenium, and zinc appear to be necessary in asthma treatment. Vitamins B6 and B12 also may be helpful. Omega-3 fatty acids from fish, the flavonoid quercetin, and botanicals Tylophora asthmatica, Boswellia serrata and Petasites hybridus address the inflammatory component. Physical modalities, including yoga, massage, biofeedback, acupuncture, and chiropractic can also be of help.
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PMID:The etiologies, pathophysiology, and alternative/complementary treatment of asthma. 1120 55


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