Review on Formulation Development: Mucolytic and Expectorant in Pediatric Wet cough.

Mucus hypersecretion is a clinical feature of severe respiratory diseases such as asthma, cystic fibrosis and chronic obstructive pulmonary disease. Airway mucosal infection and/or inflammation associated with these diseases often gives rise to inflammatory products, including neutrophil-derived DNA and filamentous actin, in addition to bacteria, apoptotic cells and cellular debris, that may collectively increase mucus production and viscosity. Coactive agents have been the medication of choice for the treatment of respiratory diseases in which mucus hypersecretion is a clinical complication. The main purpose of coactive drugs is to increase the ability to expectorate sputum and/or decrease mucus hypersecretion. Many coactive drugs are currently available and can be classified according to their putative mechanism of action. Coactive medications include expectorants, mucoregulators, mucolytics and microkinetic. By developing our understanding of the specific effects of coactive agents, we may result in improved therapeutic use of these drugs. The present review provides a summary of the most clin relevant coactive drugs in addition to potential mechanism of action. In healthy individuals, mucus secretion is not excessive and mucus continuously removed by epithelial ciliated cells, then propelled towards the larynx for swallowing [1]. However, an increase in airway mucus secretion can be problematic, especially if the rate of secretion exceeds the rate at which it can be removed by normal ciliary action. Increased mucus secretion (hypersecretion) is a clinical feature of severe respiratory diseases, such as asthma, cystic fibrosis (CF) and chronic obstructive pulmonary disease (COPD). Typically, during infection and/or inflammation, the airway mucosa responds by increasing the volume of mucus hat is secreted. This response is mainly due to hyperplasia and hypertrophy of goblet cells and the submucosal gland, a phenomenon recognized as secretory hyperresponsiveness [2]. The inflammatory process results in loss of cells and ciliary function, destruction of the surfactant layer by airway phospholipases and alteration of the biophysical properties of the mucus [3, 4]. In addition, by-products accumulated during the inflammatory process include neutrophil-derived DNA and filamentous actin (F-actin), dead/apoptotic cells, bacteria and cell debris. Collectively, these factors contribute to mucus purulence, and when expectorated, this mucus is termed sputum [5]. In healthy individuals, mucus secretion is not excessive and mucus continuously removed by epithelial ciliated cells, then propelled towards the larynx for swallowing [1]. However, an increase in airway mucus secretion can be problematic, especially if the rate of secretion exceeds the rate at which it can be removed by normal ciliary action. Increased mucus secretion (hypersecretion) is a clinical feature of severe respiratory diseases, such as asthma, cystic fibrosis (CF) and chronic obstructive pulmonary disease (COPD). Typically, during infection and/or inflammation, the airway mucosa responds by increasing the volume of mucus hat is secreted. This response is mainly due to hyperplasia and hypertrophy of goblet cells and the submucosal gland, a phenomenon recognized as secretory hyperresponsiveness [2]. The inflammatory process results in loss of cells and ciliary function, destruction of the surfactant layer by airway phospholipases and alteration of the biophysical properties of the mucus [3, 4]. In addition, by-products accumulated during the inflammatory process include neutrophil-derived DNA and filamentous actin (F-actin), dead/apoptotic cells, bacteria and cell debris. Collectively, these factors contribute to mucus purulence, and when expectorated, this mucus is termed sputum [5].