Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We describe in six men, recurrent episodes recurring over months or years, of sudden, brief complete obstruction to respiration followed by dyspnoea with loud inspiratory stridor lasting two to five minutes. Attacks occurred during wakefulness and/or sleep. In one patient an episode was witnessed endoscopically: the initial obstruction was seen to be caused by complete laryngeal closure. The false vocal cords then opened, but the vocal cords remained adducted and caused inspiratory stridor. The similarity of the attacks described by the other patients suggests that they were all caused by laryngeal closure. Furthermore, they could simulate the episodes by voluntarily adducting their vocal cords. The symptoms were usually preceded by a sensation of throat irritation and in four cases symptoms of upper respiratory infection were present. Associated features present in some of the patients included post-nasal discharge, snoring, sleep apnoea and gastro-oesophageal reflux. None was hypocalcaemic. Although stimulation of laryngeal receptors is known to produce reflex laryngeal closure, cough is the usual response during wakefulness. Treatment aimed at reducing upper airway irritation and voluntary inhibition of coughing appeared successful in reducing the incidence and severity of the episodes. Recognition of the condition is important as it may be confused with other causes of acute dyspnoea and it appears to respond to specific management.
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PMID:Brief upper airway (laryngeal) dysfunction. 228 83

Gastroesophageal reflux disease (GERD) may cause, trigger or exacerbate many pulmonary diseases. The physiological link between GERD and pulmonary disease has been extensively studied in chronic cough and asthma. A primary care physician often encounters patients with extra esophageal manifestations of GERD in the absence of heartburn. Patients may present with symptoms involving the pulmonary system; noncardiac chest pain; and ear, nose and throat disorders. Local irritation in the esophagus can cause symptoms that vary from indigestion, like chest discomfort and abdominal pain, to coughing and wheezing. If the gastric acid reaches the back of the throat, it may cause a bitter taste in the mouth and/or aspiration of the gastric acid into the lungs. The acid can cause throat irritation, postnasal drip and hoarseness, as well as recurrent cough, chest congestion and lung inflammation leading to asthma and/or bronchitis/ pneumonia. This clinical review examines the potential pathophysiological mechanisms of pulmonary manifestations of GERD. It also reviews relevant clinical information concerning GERD-related chronic cough and asthma. Finally, a potential management strategy for GERD in pulmonary patients is discussed.
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PMID:Pulmonary manifestations of gastroesophageal reflux disease. 1964 41

Patients with gastroesophageal reflux disease (GERD) display enhanced laryngeal reflex reactivity to stimuli that may be due to sensitization of the laryngeal C-fibers by acid and pepsin. Menthol, a ligand of transient receptor potential melastatin-8 (TRPM8), relieves throat irritation. However, the possibility that GERD induces laryngeal C-fiber hypersensitivity to cigarette smoke (CS) and that menthol suppresses this event has not been investigated. We delivered CS into functionally isolated larynxes of 160 anesthetized rats. Laryngeal pH 5-pepsin treatment, but not pH 5-denatured pepsin, augmented the apneic response to CS, which was blocked by denervation or perineural capsaicin treatment (a procedure that blocks the conduction of C fibers) of the superior laryngeal nerves. This augmented apnea was partially attenuated by capsazepine [an transient receptor potential vanilloid 1 (TRPV1) antagonist], SB-366791 (a TRPV1 antagonist), and HC030031 [a transient receptor potential ankyrin 1 (TRPA1) antagonist] and was completely prevented by a combination of TRPV1 and TRPA1 antagonists. Local application of menthol significantly suppressed the augmented apnea and this effect was reversed by pretreatment with AMTB (a TRPM8 antagonist). Our electrophysiological studies consistently revealed that laryngeal pH 5-pepsin treatment increased the sensitivity of laryngeal C-fibers to CS. Likewise, menthol suppressed this laryngeal C-fiber hypersensitivity and its effect could be reversed by pretreatment with AMTB. Our results suggest that laryngeal pH 5-pepsin treatment increases sensitivity to CS of both TRPV1 and TRPA1, which are presumably located at the terminals of laryngeal C-fibers. This sensory sensitization leads to enhanced laryngeal reflex reactivity and augmentation of the laryngeal C-fiber responses to CS, which can be suppressed by menthol acting via TRPM8.
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PMID:Menthol suppresses laryngeal C-fiber hypersensitivity to cigarette smoke in a rat model of gastroesophageal reflux disease: the role of TRPM8. 2553 33