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)

Inhalation of nicotine (0-64 mg/ml) and capsaicin (2 x 10(-6)-2.5 x 10(-4) M) in 24 healthy nonsmoking subjects produced a concentration-dependent cough response. Two subjects coughed to capsaicin but not to nicotine. The mean (95% confidence interval) nicotine concentrations causing two and five coughs were 5.5 (3.5-8.7) and 15.8 (10.0-25.1) mg/ml, respectively, and were reproducible over 3 different days. Capsaicin inhalation did not alter the response to nicotine and vice versa. Both agents increased respiratory resistance, but the response was more rapid to capsaicin. Inhalation of nicotine (0-8 mg/ml) over 5 min caused increases in heart rate and blood pressure and a decrease in skin temperature. Inhaled ipratropium bromide (0.50 mg) had an antitussive effect and also inhibited the nicotine-induced bronchoconstriction, indicating a vagally mediated effect. Sodium cromoglycate (0.20 mg) did not affect cough or airway resistance changes caused by nicotine. This study shows that inhaled nicotine produces a concentration-dependent cough and airway obstruction in healthy subjects, probably because of stimulation of afferent nerve endings in the bronchial mucosa and mediated through parasympathetic cholinergic pathways. Respiratory reflexes evoked by nicotine are similar to those produced by capsaicin, but it is unclear whether these reflexes are mediated by the same type of sensory nerves.
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PMID:Inhaled nicotine in humans: effect on the respiratory and cardiovascular systems. 792 66

Bronchoconstriction associated with exercise can occur in nearly all individuals with asthma and in 35-40% of those with allergic rhinitis/hay fever symptoms. This represents approximately 12-15% of the population. Exercise-induced asthma (EIA) is a clinical syndrome characterized by transient airflow obstruction typically 5-15 min after cessation of physical exertion. Symptoms may include chest tightness, breathlessness, coughing, and/or wheezing. Some individuals may experience delayed bronchoconstriction (late phase response) 6-10 h after completing exercise. Approximately 40-50% of those with asthma exhibit a "refractory period", i.e., diminished bronchoconstriction to exercise performed within 2 h. The pathophysiology of EIA is related to thermal events within the intrathoracic airways. Alterations in the temperature of the airways and/or osmolarity in the epithelial lining fluid cause release of mediators in the airways and the development of bronchoconstriction. Although EIA can be strongly suspected by an appropriate history, pulmonary function testing is necessary to make a specific diagnosis. Measurement of lung function is an important first diagnostic test. If there is no evidence of airflow obstruction at rest, then either bronchoprovocation testing or exercise challenge testing is indicated. Nonpharmacologic therapy includes "warm-up" exercise prior to training or competition to induce a "refractory period" and to prevent/reduce bronchoconstriction. An inhaled beta 2-adrenergic agonist, e.g., albuterol, is usually effective for preventing/treating EIA. Cromolyn sodium is an alternative class of medication that inhibits both the early and late phase responses. Other bronchodilator agents are available if combination therapy with an inhaled beta 2-adrenergic agonist and cromolyn sodium is not effective.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Exercise-induced asthma. 849 82

There are several theories on the cause of ACE inhibitor-induced cough, but the exact mechanism is not known. In many patients, if cough develops, the ACE inhibitor can be discontinued and a drug in another therapeutic class used in its place. However, in patients with CHF, diabetic nephropathy, and patients who have experienced a myocardial infarction, discontinuing the ACE inhibitor may not be in the best interest of the patient. In this patient population it would be reasonable to try cromolyn sodium to treat cough, while continuing the ACE inhibitor. Data are not available to support the efficacy of cromolyn sodium to treat cough in patients with diabetic nephropathy, but these patients clearly benefit from the use of an ACE inhibitor. Other factors not addressed in the case reports and the clinical trial such as patient adherence, cost, and quality of life should also play a role in the decision to use cromolyn sodium. Cromolyn sodium has been effective for the treatment of ACE inhibitor-induced cough in many case reports and has had mild success in one small clinical trial. Although none of the reports adequately assessed adverse effects, studies examining cromolyn for other indications have demonstrated a relatively benign adverse effect profile. It is difficult to recommend an exact dose to use because of the dosing variability in the case reports. The majority of the case reports and the one clinical trial used dosages similar to recommendations for bronchial asthma (i.e., 2 puffs [1.6 mg] 4 times daily via MDI or 20-mg capsules 4 times daily via breath-activated inhalation). At this time, the use of cromolyn sodium is a viable option, but more controlled studies are needed to fully elucidate its role in the treatment of ACE inhibitor-induced cough.
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PMID:Cromolyn sodium for ACE inhibitor-induced cough. 918 21

Exercise-induced bronchospasm, exercise-induced bronchoconstriction, and exercise-induced asthma (EIA) are all terms used to describe the phenomenon of transient airflow obstruction associated with physical exertion. It is a prominent finding in children and young adults because of their greater participation in vigorous activities. The symptoms shortness of breath, cough, chest tightness, and wheezing normally follow the brief period of bronchodilation present early in the course of exercise. Bronchospasm typically arises within 10 to 15 minutes of beginning exercise, peaks 8 to 15 minutes after the exertion is concluded, and resolves about 60 minutes later, but it also may appear during sustained exertion. EIA occurs in up to 90% of asthmatics and 40% of patients with allergic rhinitis; among athletes and in the general population its prevalence is between 6% and 13%. EIA frequently goes undiagnosed. Approximately 9% of individuals with EIA have no history of asthma or allergy. Fifty percent of children with asthma who gave a negative history for EIA had a positive response to exercise challenge.6 Among high school athletes, 12% of subjects not considered to be at risk by history or baseline spirometry tested positive. Before the 1984 Olympic games, of 597 members of the US team, 67 (11%) were found to have EIA. Remarkably, only 26 had been previously identified, emphasizing the importance of screening for EIA even in well-conditioned individuals who appear to be in excellent health. The severity of bronchospasm in EIA is related to the level of ventilation, to heat and water loss from the respiratory tree, and also to the rate of airway rewarming and rehydration after the challenge. Postexercise decrease in the peak expiratory flow rate of normal children may be as much as 15%; therefore, only a decrease in excess of 15% should be viewed as diagnostic. EIA is usually provoked by a workload sufficient to produce 80% of maximum oxygen consumption; however, in severe asthmatics even minimal exertion may be enough to produce symptoms. Patients with normal lung function at rest may have severe air flow limitation induced by exercise,10 and as many as 50% of patients who are well-controlled with inhaled corticosteroids still exhibit EIA. A challenge of sufficient magnitude will provoke EIA in all patients with asthma. PHARMACOLOGIC THERAPY: Exercise, unlike exposure to allergens, does not produce a long-term increase in airway reactivity. Accordingly, patients whose symptoms manifest only after strenuous activity may be treated prophylactically and do not require continuous therapy. Most asthma medications, even some unconventional ones such as heparin, furosemide, calcium channel blockers, and terfenadine, given before exercise, suppress EIA. McFadden accounts for the efficacy of these disparate classes of drugs by their potential effect on the bronchial vasculature that modulates the cooling and/or rewarming phases of the reaction. Short-acting -agonists provide protection in 80% to 95% of affected individuals with insignificant side effects and have been regarded for many years as first-line therapy. Two long-acting bronchodilators, salmeterol and formoterol, have been found effective in the prevention of EIA.18-21 A single 50-microg dose of salmeterol protects against EIA for 9 hours; its duration appears to wane in the course of daily therapy. Cromolyn sodium is highly effective in 70% to 87% of those diagnosed with EIA and has minimal side effects. Nedocromil sodium provides protection equal to that of cromolyn in children. Children commonly engage in unplanned physical activity and sometimes are not allowed to carry their own medication. Thus, a simple long-acting regimen given at home is likely to be more effective than short-acting drugs that must be administered in a timely manner. Although the 12-hour protection by salmeterol reported by Bronsky et al may not persist with continued use, the 9-hour duration of action is
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PMID:Keeping children with exercise-induced asthma active. 1046 21

Respiratory consequences of work in food processing industry were studied in 764 female workers exposed to organic dusts associated with the processing of green and roasted coffee, tea, spices, dried fruits, cocoa and flour. A group of 387 female workers not exposed to respiratory irritants served as controls for the prevalence of acute (during work shift) and chronic respiratory symptoms. A greater prevalence of all acute and chronic respiratory symptoms was consistently found among exposed workers than among control workers. The highest prevalence of chronic respiratory symptoms was recorded for chronic cough (40%), followed by acute symptoms of dry cough (58.7%). The difference in the prevalence of chronic respiratory symptoms between the exposed and control workers was in general significant (p < 0.01 or p < 0.05). Mean acute reductions of lung function over the work shift were recorded in all of the studied groups; the mean across-shift decrease as a percentage of preshift values was particularly marked in FEF25 (-26.7%), FEF50 (-21.6%), followed by FEV1 (-9.9%) and FVC (-3.7%). The preshift (baseline) values of ventilatory capacity were decreased in comparison to the predicted ones, and were lowest for FEF50 and FEF25. This finding indicated an effect of organic dust on small airways. Our analysis suggested that both dust exposure and smoking history contributed independently to these respiratory findings. Disodium cromoglycate (DSCG) significantly diminished across-shift reductions for FEF50 and FEF25 in a subgroup of the examined workers. Our data suggested the female workers employed in food processing industry to be at risk of developing both acute and chronic respiratory symptoms as well as ventilatory capacity impairment as the result of occupational exposures.
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PMID:Respiratory function in female workers occupationally exposed to organic dusts in food processing industries. 1137 83


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