Chest
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Cough is a common symptom of diseases such as asthma and COPD and also presents as a disease in its own right. Treatment options are limited; a recent meta-analysis concluded that over-the-counter remedies are ineffective, and there is increasing concern about their use in children. Transient receptor potential cation channel, subfamily A, member 1 (TRPA1) channels are nonselective cation channels that are activated by a range of natural products (eg, allyl isothiocyanate), a multitude of environmental irritants (eg, acrolein, which is present in air pollution, vehicle exhaust, and cigarette smoke), and inflammatory mediators (eg, cyclopentenone prostaglandins). ⋯ Inhalational exposure to irritating gases, fumes, dusts, vapors, chemicals, and endogenous mediators can lead to the development of cough. The respiratory tract is innervated by primary sensory afferent nerves, which are activated by mechanical and chemical stimuli. Recent data suggest that activation of TRPA1 on these vagal sensory afferents by these irritant substances could lead to central reflexes, including dyspnea, changes in breathing pattern, and cough, which contribute to the symptoms and pathophysiology of respiratory diseases.
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Mounier-Kuhn syndrome (MKS) is a condition characterized by tracheobronchomegaly resulting from the loss or atrophy of musculoelastic fibers within the airway wall. Concomitant tracheobronchomalacia is seen in most patients with MKS, often leading to significant respiratory compromise due to bronchiectasis, increased dead space, and impaired secretion clearance. ⋯ An aggressive approach that targets central airway stabilization may improve outcomes for patients with MKS.
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Tobacco smoke is a major risk factor in the development of COPD. Secondhand smoke (SHS) exposure is a known risk factor in asthma, bronchitis, and coronary artery disease. Elastin is a recognized target for injury in COPD, and the amino acids desmosine and isodesmosine (D/I), which are specific for elastin degradation, are elevated in COPD. This study determined whether exposure to SHS affects elastin degradation in asymptomatic individuals. ⋯ Results indicate a tissue matrix effect of degradation of body elastin from SHS exposure and possible lung structure injury, which may result in COPD. Long-term studies of individuals exposed to SHS for the development of COPD are warranted.
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We report five cases of asthma unmasked by anti-tumor necrosis factor (TNF)-α-blocking drugs. Asthma symptoms appeared within an average of 4 months (range 1-24 months) after starting the anti-TNF-α treatment for inflammatory disease. The patients did not appear to be predisposed to asthma except for one patient who had asthma during childhood. ⋯ Asthma control was achieved with inhaled steroids, allowing anti-TNF-α treatment to continue. The biotherapy was maintained for the fifth patient in association with inhaled steroids. The pathophysiologic mechanisms are unknown but are probably more complex than the T helper 1/T helper 2 imbalance suggested in the literature, and further studies are required.