Pulmonary pharmacology & therapeutics
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Patients with chronic cough often report symptoms arising in the throat, in response to non-specific stimuli. Accordingly, the concept of a 'hypersensitivity' of the larynx in chronic cough has evolved over the past ten years. ⋯ The mechanisms underlying laryngeal hypersensitivity in chronic cough are currently unclear, however recent studies provide new clinical and physiological techniques to aid detection and monitoring of laryngeal hypersensitivity. This review provides an overview of the current state of knowledge in this field.
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Chronic cough is regarded as a challenging clinical problem due to its frequency and often limited therapeutic options. Chronic cough that remains refractory to usual medical treatment causes significant quality of life impairment. ⋯ Recent additions in the treatment of chronic cough have been significant as they consider cough to have a unifying diagnosis of cough hypersensitivity with or without the presence of a neuropathic basis. Effective treatments for refractory chronic cough that target these areas include behavioural treatment such as speech pathology and pharmaceutical treatment with neuromodulating medications such as gabapentin.
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Pulm Pharmacol Ther · Oct 2015
Meta AnalysisEffect of exogenous pulmonary surfactants on mortality rate in neonatal respiratory distress syndrome: A network meta-analysis of randomized controlled trials.
The utilization of multiple natural and synthetic products in surfactant replacement therapies in treatment of neonatal respiratory distress syndrome (NRDS) prompted us to take a closer looks at these various therapeutic options and their efficacies. The purpose of our study was to evaluate the effects of six exogenous pulmonary surfactants (EPS) (Survanta, Alveofact, Infasurf, Curosurf, Surfaxin and Exosurf) on mortality rate in NRDS by a network meta-analysis. ⋯ Our study demonstrated that Surfaxin could effectively reduce the mortality rate of infants with NRDS and may have a better efficacy in NRDS treatment, compared to Survanta, Alveofact, Infasurf, Curosurf and Exosurf.
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Pulm Pharmacol Ther · Aug 2015
Randomized Controlled Trial Comparative StudyEffect of an anti-reflux medical device in the control of deflation cough: A placebo-controlled comparative study with an antacid drug in chronic coughers.
Deflation cough (DC), i.e. the cough-like expiratory expulsive efforts evoked by maximal lung emptying, is partially inhibited by prior intake of an antacid. We wished to compare the effects of an anti-reflux medical device (Gastrotuss(®)) and of a widely used antacid drug (Maalox(®)) on the number of expiratory thrusts evoked by maximal lung emptying in chronic cough patients. ⋯ Pre-treatment with anti-reflux agents with a substantially different composition are equally effective in inhibiting DC. The liking of the two compounds used in the present experiments differed considerably and may be important to improve adherence to treatment in patients undergoing long-term therapy for reflux-related symptoms.
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Pulm Pharmacol Ther · Jun 2015
Nintedanib modulates surfactant protein-D expression in A549 human lung epithelial cells via the c-Jun N-terminal kinase-activator protein-1 pathway.
Idiopathic pulmonary fibrosis (IPF) is a progressive disease with a high mortality rate. Signalling pathways activated by several tyrosine kinase receptors are known to be involved in lung fibrosis, and this knowledge has led to the development of the triple tyrosine kinase inhibitor nintedanib, an inhibitor of vascular endothelial growth factor receptor (VEGFR), platelet-derived growth factor receptor (PDGFR), and fibroblast growth factor receptor (FGFR), for the treatment of IPF. Pulmonary surfactant protein D (SP-D), an important biomarker of IPF, reportedly attenuates bleomycin-induced pulmonary fibrosis in mice. ⋯ Increased expression of SFTPD mRNA and SP-D protein in the lungs of nintedanib-treated mice was also observed. In this work, we demonstrated that nintedanib up-regulated SP-D expression in A549 cells via the JNK-AP-1 pathway and did not affect cell proliferation. This is the first report describing SP-D induction by nintedanib.