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)

Chronic exposure to irritants such as tobacco smoke (TS) can induce spontaneous and enhanced irritant-induced coughing, especially in asthma. To determine if the mechanism of enhanced coughing involves activation of capsaicin-sensitive sensory receptors (C-fibers), we exposed both non-sensitized (NS) and ovalbumin-sensitized guinea pigs to TS (5 mg/L air, 30 min exposure, and 7 days/week). Similar groups were exposed to compressed air. After 90 days of exposure, we challenged the airways with capsaicin, bradykinin, histamine and methacholine. Capsaicin induced coughing as well as bronchoconstriction in guinea pigs exposed to TS. In ovalbumin (OA) guinea pigs coughing and bronchoconstriction were enhanced. Tachykinin receptor antagonists attenuated coughing to both capsaicin and acute TS challenge. Bradykinin also induced coughing and bronchoconstriction in guinea pigs exposed to TS. There was no statistical separation between the two TS groups however. Histamine and methacholine induced similar bronchoconstriction but fewer coughs in all four experimental groups. In conclusion, chronic TS exposure induced coughing to capsaicin and bradykinin challenge. The effect of capsaicin was further enhanced in OA guinea pigs. Enhanced coughing induced by TS exposure likely involves activation of capsaicin-sensitive sensory C-fibers and neuropeptide release with possible subsequent activation of rapidly-adapting receptors.
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PMID:Chronic tobacco smoke exposure increases cough to capsaicin in awake guinea pigs. 1134 40

Alcoholic drinks are capable of triggering a wide range of allergic and allergic-like responses, including rhinitis, itching, facial swelling, headache, cough and asthma. Limited epidemiological data suggests that many individuals are affected and that sensitivities occur to a variety of drinks, including wine, beer and spirits. In surveys of asthmatics, over 40% reported the triggering of allergic or allergic-like symptoms following alcoholic drink consumption and 30 - 35% reported worsening of their asthma. Sensitivity to ethanol itself can play a role in triggering adverse responses, particularly in Asians, which is due mainly to a reduced capacity to metabolize acetaldehyde. In Caucasians, specific non-alcohol components are the main cause of sensitivities to alcoholic drinks. Allergic sensitivities to specific components of beer, spirits and distilled liquors have been described. Wine is clearly the most commonly reported trigger for adverse responses. Sensitivities to wine appear to be due mainly to pharmacological intolerances to specific components, such as biogenic amines and the sulphite additives. Histamine in wine has been associated with the triggering of a wide spectrum of adverse symptoms, including sneezing, rhinitis, itching, flushing, headache and asthma. The sulphite additives in wine have been associated with triggering asthmatic responses. Clinical studies have confirmed sensitivities to the sulphites in wine in limited numbers of individuals, but the extent to which the sulphites contribute to wine sensitivity overall is not clear. The aetiology of wine-induced asthmatic responses may be complex and may involve several co-factors.
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PMID:Allergic and asthmatic reactions to alcoholic drinks. 1274 10

The hypothesis that respiratory reflexes, such as cough, reflect the net and often opposing effects of activation of multiple afferent nerve subpopulations throughout the airways was evaluated. Laryngeal and tracheal mucosal challenge with either citric acid or mechanical probing reliably evoked coughing in anesthetized guinea pigs. No other stimulus reliably evoked coughing in these animals, regardless of route of administration and despite some profound effects on respiration. Selectively activating vagal C-fibers arising from the nodose ganglia with either adenosine or 2-methyl-5-HT evoked only tachypnea. Selectively activating vagal afferents arising from the jugular ganglia induced respiratory slowing and apnea. Nasal afferent nerve activation by capsaicin, citric acid, hypertonic saline, or histamine evoked only respiratory slowing. Histamine, which activates intrapulmonary rapidly adapting receptors but not airway or lung C-fibers or tracheal bronchial cough receptors induced bronchospasm and tachypnea, but no coughing. The results indicate that the reflexes initiated by stimuli thought to be selective for some afferent nerve subtypes will likely depend on the net and potentially opposing effects of multiple afferent nerve subpopulations throughout the airways. The data also provide further evidence that the afferent nerves regulating cough in anesthetized guinea pigs are distinct from either C-fibers or intrapulmonary rapidly adapting receptors.
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PMID:Differential effects of airway afferent nerve subtypes on cough and respiration in anesthetized guinea pigs. 1876 68

Chronic cough is a major clinical problem. The causes of chronic cough can be categorized into eosinophilic and noneosinophilic disorders, the former being comprised of asthma, cough variant asthma (CVA), atopic cough (AC) and non-asthmatic eosinophilic bronchitis (NAEB). Cough is one of the major symptoms of asthma. Cough in asthma can be classified into three categories; 1) CVA: asthma presenting solely with coughing, 2) cough-predominant asthma: asthma predominantly presenting with coughing but also with dyspnea and/or wheezing, and 3) cough remaining after treatment with inhaled corticosteroid (ICS) and beta2-agonists in patients with classical asthma, despite control of other symptoms. There may be two subtypes in the last category; one is cough responsive to anti-mediator drugs such as leukotriene receptor antagonists and histamine H1 receptor antagonists, and the other is cough due to co-morbid conditions such as gastroesophageal reflux. CVA is one of the commonest causes of chronic isolated cough. It shares a number of pathophysiological features with classical asthma with wheezing such as atopy, airway hyperresponsiveness (AHR), eosinophilic airway inflammation and various features of airway remodeling. One third of adult patients may develop wheezing and progress to classical asthma. As established in classical asthma, ICS is considered the first-line treatment, which improves cough and may also reduce the risk of progression to classical asthma. AC proposed by Fujimura et al. presents with bronchodilator-resistant dry cough associated with an atopic constitution. It involves eosinophilic tracheobronchitis and cough hypersensitivity and responds to ICS treatment, while lacking in AHR and variable airflow obstruction. These features are shared by non-asthmatic eosinophilic bronchitis (NAEB). However, atopic cough does not involve bronchoalveolar eosinophilia, has no evidence of airway remodeling, and rarely progresses to classical asthma, unlike CVA and NAEB. Histamine H1 antagonists are effective in atopic cough, but their efficacy in NAEB is unknown. AHR of NAEB may improve with ICS within the normal range. Taken together, NAEB significantly overlaps with atopic cough, but might also include milder cases of CVA with very modest AHR. The similarity and difference of these related entities presenting with chronic cough and characterized by airway eosinophilia will be discussed.
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PMID:Eosinophilic airway disorders associated with chronic cough. 1912 5

Histamine H1 antagonists rarely cause drug-induced lung injury (DLI). A woman in her 60s, who had been taking antihistaminic levocetirizine for 2 months, presented with progressive cough and shortness of breath. A chest radiograph showed patchy infiltrations on both lower lung fields. Chest computed tomography findings were consistent with non-specific interstitial pneumonia. Serum markers associated with interstitial pneumonias were elevated. Room air arterial blood gas analysis revealed hypoxemia. Restrictive ventilatory impairment was noted with reduced diffusing capacity. Transbronchial lung biopsy specimens demonstrated unclassifiable alveolitis. Steroid pulse therapy was introduced for respiratory distress, but the initial response to treatment was poor. A drug lymphocyte stimulation test was positive for levocetirizine. The interstitial pneumonia improved following withdrawal of levocetirizine. Her illness has not recurred under steroid therapy and the discontinuation of levocetirizine. Antihistaminics may have a potential risk of DLI.
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PMID:Histamine H1 antagonist levocetirizine as a potential cause of lung injury. 2609 Jan 14

Picralima nitida is used traditionally for management of cough. This study, therefore, investigated the antitussive, expectorant, and analgesic properties of the ethanolic seed extract of Picralima nitida (PNE), and ascertained its safety for use. Presence of secondary metabolites, and safety of PNE (10-2000 mg/kg) were evaluated by preliminary phytochemical screening, and by Irwin's test respectively. Percentage reduction in cough count, percentage increase in latency of cough, and percentage protection offered by PNE were established by the citric acid-induced cough, acetylcholine- and Histamine-induced bronchoconstriction models. Dunkin-Hartley guinea pigs were treated with 100-500 mg/kg PNE or reference drugs, dihydrocodiene, atropine, mepyramine. Expectorant property of PNE (100-1000 mg/kg) was determined using the tracheal phenol red secretion; with ammonium chloride as a reference medication. Percentage maximal possible analgesic effect in the tail immersion test and the total nociceptive score in acetic acid-induced abdominal writhes, after treatment of BALB/c mice with PNE (100-500 mg/kg), diclofenac, and morphine were also estimated. Phytochemical screening revealed the presence of tannins, alkaloids, glycosides, saponins, steroids, terpenoids and anthraquinones. PNEdid not cause any extract-related physical, pharmacological and CNS toxicities or mortality; sedation was observed at doses 1000-2000 mg/kg. It showed significant dose-dependent reduction in cough count, and increased cough latency. PNE (1000 mg/kg) enhanced tracheal phenol red secretion. PNE (100-500 mg/kg) significantly and dose dependently increased tail withdrawal latencies, and nociceptive score. PNE has antitussive, expectorant, and analgesic properties, with an LD50>2000 mg/kg.
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PMID:Antitussive, expectorant and analgesic effects of the ethanol seed extract of Picralima nitida (Stapf) Th. & H. Durand. 2716 49

A 45-year-old female who had undergone Nissen fundoplication for long-standing laryngopharyngeal reflux (LPR) developed episodes of coughing and throat clearing. Strobovideolaryngoscopy demonstrated evidence of LPR with a reflux finding score of 11. A cough workup including a chest X-ray and pulmonology consultation was negative. Consultation with a nutritionist revealed Histamine intolerance. Histamine-free diet resulted in marked improvement in patient's symptoms and examination.
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PMID:Histamine Sensitivity: An Uncommon Recognized Cause of Living Laryngopharyngeal Reflux Symptoms and Signs-A Case Report. 3284 4


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