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

Asthma is a chronic inflammatory disease of the lower respiratory tract which is triggered by exposure to allergens or other airway irritants. This inflammation results in airway hyperresponsiveness, bronchial muscle spasm, mucous gland hypersecretion and mucosal edema, which combine to create symptoms such as cough, wheezing and respiratory distress. Because the inflammatory process is highly variable, asthma is a disorder with many possible presentations. It may therefore proceed for years without clinical recognition, and may challenge the most astute diagnostician. It is important for otolaryngologists to be able to suspect, diagnose and treat asthma. This is so because asthma is a common disease in the otolaryngologic patient population, both as one of the options in the differential diagnosis of respiratory complaints, and as a comorbid condition which may complicate the treatment of other medical or surgical problems. Furthermore, both the understanding of asthma's pathophysiology, and its optimum treatment methods have undergone radical changes during the past decade. This three-part discussion reviews our modern understanding of asthma, and proposes diagnosis and treatment guidelines which can assist otolaryngologists in effectively managing their asthmatic patients. Part one summarizes current information on the pathophysiology and increasing prevalence of asthma, its clinical variability, the assessment of asthma sensitivity, and methods for diagnosis of asthma. Parts two and three cover the strategy for asthma management, and the use of both adjunctive and anti-inflammatory therapies for asthma control.
 ...
PMID:Asthma: an important disease to otolaryngologists--Part I: Suspecting and diagnosing asthma. 871 22

Skin prick test (SPT) reactivity to common airborne allergens and its relationships to sex, age, smoking habits, and respiratory symptoms/diseases were evaluated in a general population sample (n = 2841, 8-75 years of age) living in the Po delta area (northern Italy). Subjects completed a standardized questionnaire and underwent prick tests (12 local allergens, a negative and a positive control) and determination of total serum IgE. Atopy was evaluated by measuring the maximal diameter for each allergen, after subtracting that of the negative control. Thirty-one percent of subjects showed a positive skin response at a 3-mm threshold. Pollens, Dermatophagoides pteronyssinus, and D. farinae caused the highest frequencies of reactions. Young people and those who had never smoked had higher prevalence rates of SPT reactivity. Asthma, asthma symptoms, and rhinitis were significantly associated with SPT reactivity in both sexes (cough only in females) and with the number of positive reactions. IgE values were also significantly associated with SPT reactivity. In conclusion, our findings indicate that almost one-third of the general population of an Italian rural area is skin test positive, emphasizing the importance of assessing atopy in respiratory epidemiologic surveys.
 ...
PMID:Skin prick test reactivity to common aeroallergens in relation to total IgE, respiratory symptoms, and smoking in a general population sample of northern Italy. 878 68

We report the case of a 55-year-old male who experienced cough, dyspnea, wheezing, and nasal congestion immediately upon exposure to FD&C Blue Dye No. 2 (Indigotine) at work. The patient had worked for 10 years mixing and grinding powdered synthetic red, yellow, and blue dyes for use in foods; symptoms had occurred for 2 years and only with exposure to Indigotine (C16H8N2Na2O8S2), a free flowing blue powder. Prick testing to Indigotine (20 mg/mL) was negative. ELISA failed to detect specific IgE, IgA, IgM, or IgG to Indigotine-HSA conjugates. Bronchial challenge was done according to the method of Pepys et al. beginning with 4 x 10(-4) lactose dilution of Indigotine powder. After 5 minutes of exposure to 4 gm Indigotine/100 gm lactose, the patient developed dyspnea and audible wheezing. At 20 minutes postexposure, there was a 20% decline in FEV1 from prechallenge baseline; no late phase response was observed. A second bronchial challenge with sodium sulfate, the major nondye product additive was negative. To our knowledge, this is the first documented case of occupational asthma due to FD&C Blue Dye No. 2. The pathogenesis is uncertain but does not appear to be IgE mediated.
Allergy Asthma Proc
PMID:Occupational asthma caused by FD&C blue dye no. 2. 881 38

Asthma is a chronic inflammatory disease of the airways that may affect individuals at any age, and can be especially challenging to diagnose and treat in the elderly. The hallmarks of asthma--bronchial hyperreactivity and reversible airflow obstruction--lead to symptoms of intermittent wheezing, dyspnoea and cough. Occasionally, atypical symptoms such as chest pain or tightness occur and may mimic other diseases more common in the elderly, such as ischaemic heart disease. It is therefore important to use objective measures such as spirometry or bronchoprovocation testing to make a diagnosis. In recent years, trends in the treatment of asthma have changed from reliance on shorter-acting bronchodilating drugs to long term preventative therapy with inhaled corticosteroids. In some elderly asthmatic patients, symptoms may be mild and intermittent, and treatment with an inhaled beta 2-adrenergic agent may be all that is required. Most, however, experience persistent symptoms, and pharmacological therapy should begin with daily inhaled corticosteroids and be increased in a stepwise fashion according to the patient's needs. In such patients, short-acting beta 2-agonists should be continued as needed for acute symptomatic relief. Longer-acting beta 2-agonists, oral theophylline and inhaled anticholinergic therapy may be useful. When symptoms are more severe and potentially life-threatening, oral corticosteroids should be given. Since elderly patients are more likely to develop complications of asthma therapy and more likely to manifest adverse interactions with other therapeutic agents, more intense monitoring of asthma treatment is required in dealing with this population.
 ...
PMID:Drug treatment of asthma in the elderly. 888 79

The purpose of this study was to assess the prevalence of sinusitis in a nonselected sample of children, and the relation of sinusitis to allergic rhinitis (AR), atopy, asthma, and cough in the same population sample. Of 1246 children enrolled at birth in the Tucson Children's Respiratory Study, 835 were studied at a mean age +/-SD of 8.6 +/- 0.7 years. Questionnaires asking about MD-Sinusitis, MD-AR, MD-Asthma, and cough were completed by parents. Skin tests for seven common aeroallergens in the Tucson area had been performed in 630 of the participating children at the mean age +/-SD of 6.3 +/- 0.9 years. Prevalence of MD-Sinusitis was 13.1%; 78% of subjects with MD-Sinusitis also had MD-AR. Detailed analysis of the relation between MD-Sinusitis and individual environmental allergens tested for showed that only a response to Bermuda grass pollen was significantly associated with MD-Sinusitis after controlling for MD-AR [adjusted odds ratio 2.3 (95% CI 1.2-4.3)]. Having MD-Sinusitis was also significantly associated with MD-Asthma and cough [odds ratios 3.0 (95% CI 1.8-5.2)] and 2.5 (95% CI 1.6-3.8), respectively]. However, logistic regression demonstrated that, after controlling for MD-AR and skin test reactivity, MD-Sinusitis was no longer significantly associated with MD-Asthma or cough. We conclude that MD-Sinusitis is a common condition in childhood. The main independent risk factors in our community for MD-Sinusitis were grass pollen and current MD-AR. MD-Sinusitis was not associated with MD-Asthma or with cough after controlling for skin test reactivity and for MD-AR.
 ...
PMID:The relation between physician-diagnosed sinusitis, asthma, and skin test reactivity to allergens in 8-year-old children. 889 51

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.
 ...
PMID:Airway inflammation and asthma. 889 97

Exercise-induced asthma is defined as an intermittent narrowing of the airways, demonstrated by a decrease in some measure of flow, that the patient experiences as wheezing, chest tightness, coughing, and difficulty breathing that is triggered by exercise. Exercise will trigger asthma in most individuals who have chronic asthma, as well as in some who do not otherwise have asthma. Definitive diagnosis requires demonstration of a drop in flow rate, typically > or = 13-15% for forced expiratory volume in one second (FEV1) and > or = 15-20% for peak expiratory flow rate (PEFR), after exercise, associated with symptoms. Prevalence data indicate that this disorder is very common in those who participate in recreational sports as well as in highly competitive athletes, with at least 12-15% of unselected athletes having positive exercise challenges. Treatment of exercise induced asthma involves use of nonpharmacological measures (such as the use of the refractory period after exercise and prewarming air) as well as use of medications (beta-agonists, cromolyn, and nedocromil). With treatment, those who suffer from exercise-induced asthma may be able to participate and compete at the highest levels of performance.
Allergy Asthma Proc
PMID:Exercise-induced asthma: a practical guide to definitions, diagnosis, prevalence, and treatment. 899 24

This study was conducted to examine (1) whether an appropriate sputum can be obtained by inducing with inhalation of hypertonic saline in patients with chronic nonproductive cough and (2) whether eosinophils can be detected in the induced sputum. Appropriate samples were obtained by the induction in 25 of 31 patients with bronchial asthma (BA), 12 of 17 patients with cough-variant asthma (CVA), 17 of 20 patients with bronchodilator-resistant cough associated with atopy (atopic cough, AC), and 23 of 25 healthy subjects. Eosinophils were detected in the successfully induced sputum in 100%, 66.6%, and 88.2% of the patients with BA, CVA, and AC, respectively. Detection of eosinophils in induced sputum may be the initial diagnostic procedure for nonproductive cough of allergic nature.
J Asthma 1997
PMID:Detection of eosinophils in hypertonic saline-induced sputum in patients with chronic nonproductive cough. 908 98

Asthma is a common chronic condition and there is evidence that its prevalence may be rising. The European Respiratory Health Survey (ECRHS) was planned to produce comparable data on asthma epidemiology in Europe. In Greece, in particular, a similar study has not been conducted previously and no epidemiological data are available on adult asthma prevalence. Furthermore, the role of air pollution in the pathogenesis of asthma is currently an issue of debate. Athens is a city with high air pollution, and a study of asthma epidemiology in this city may confirm or refute a possible link with the expression of asthma. A questionnaire developed by the ECRHS was sent to a random sample of 3533 households in Peristeri, an industrialized borough of Athens. Responses were received from 2774 households (response rate 78%). Of all the data on individual subjects, only those from 3325 adults aged 20-44 years were considered, according to the study protocol. The self-reported current prevalence of asthmatic attacks and asthma-like symptoms were as follows: asthma attack 2.4%, use of asthma medication 2.1%, awakening by shortness of breath 5.6%, awakening by cough 17.8%, wheezing 15.8% and nasal allergies 18.4%. It is concluded that the prevalence of asthma and related symptoms in this region of Athens is rather low, despite the high air-pollution levels in the city.
 ...
PMID:Prevalence of asthma and asthma-like symptoms in Athens, Greece. 912 16

Patients with alpha 1-antitrypsin (AAT) deficiency, like those with asthma and chronic obstructive pulmonary disease, usually present with dyspnea, wheeze, and cough. The similarity in presentation and unfamiliarity among clinicians with AAT deficiency account for much of the delay in diagnosis. Normally, AAT inhibits serine proteases, which cause alveolar destruction, and alters the function of cells that release mediators of inflammation. Diagnostic findings suggesting deficiency include irreversible airflow obstruction, a decreased diffusing capacity of the lung for carbon monoxide, bibasilar bullous disease on chest films, and a low serum level of AAT. Asthma is usually diagnosed on the basis of clinical findings and response to inhaled beta agonists. The presence of inflammation is believed to be necessary for development of clinically significant asthma. Inflammation added to a deficiency of antiprotease inhibitor activity significantly worsens bronchial hyperreactivity. This is only one mechanism by which AAT deficiency may potentiate allergic and bronchospastic responses. The prevalence of bronchial asthma in patients with AAT deficiency is unknown. Studies by the National Institutes of Health regarding the natural history of AAT deficiency and its response to therapy are under way. Perhaps more will be discovered about the relationship between the disorder and bronchial asthma.
 ...
PMID:Alpha 1-antitrypsin deficiency and asthma. The continuing search for the relationship. 912 9


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>