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Idiopathic Pulmonary Fibrosis (IPF) as the name suggests is a progressive disorder with no known aetiology. It is characterised by the thickening of the alveoli due to scarring resulting in cough. It is known to primarily occur in older adults over 60 years of age. The findings of IPF have a known association of Usual Interstitial Pneumonia (UIP) (Raghu et al., 2011; Kawano-Dourado & Kairalla, 2013; Wells, 2013). It has been deemed that the prognosis is generally poor when UIP has been confirmed (King et al., 2001b). The median survival rate of IPF is 50%, typically around two years after diagnosis (Raghu et al., 2011; King et al., 2001b).
Idiopathic Pulmonary Fibrosis (IPF) as the name suggests is a progressive disorder with no known aetiology. It is characterised by the thickening of the alveoli due to scarring resulting in cough. It is known to primarily occur in older adults over 60 years of age. The findings of IPF have a known association of Usual Interstitial Pneumonia (UIP) (Raghu et al., 2011; Kawano-Dourado & Kairalla, 2013; Wells, 2013). It has been deemed that the prognosis is generally poor when UIP has been confirmed (King et al., 2001b). The median survival rate of IPF is 50%, typically around two years after diagnosis (Raghu et al., 2011; King et al., 2001b).
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Progression-Free Survival (PFS) in patients. However, the effects of pirfenidone have not<br />
been extensively investigated till date in patients suffering from advanced stages of IPF.<br />
The early studies on the treatment of IPF using pirfenidone which was conducted in<br />
the early 1990s used the model of bleomycin-induced pulmonary fibrosis in hamsters wherein<br />
the previous research revealed that pirfenidone could actively involved in the reduction of<br />
severe profibrotic lung tissue factors and bronchoalveolar lavage fluid expression.<br />
Pirfenidone is shown to reduce or prevent the accumulation of inflammatory cells,<br />
hydroxyproline, procollagen I and III and Transformation of Growth Factor-Beta (TGF-β) in<br />
the bronchoalveolar lavage and in the lung tissues (Iyer et al., 1995, 1998, 1999a, 2000; Giri<br />
et al., 1999; Schelegle et al., 1997; Mansoor et al., 1999). Similar findings were acquired in<br />
the mice and cats wherein models such as bleomycin and amiodarone are used (Card et al.,<br />
2003; Kakugawa et al., 2004; Tian et al., 2006; Oku et al., 2008b). Pirfenidone is further<br />
shown to reduce the pool of fibrocyte and migrates the cells in the the bleomycin-induced<br />
lung fibrosis lung model (Inomata et al., 2014). Over the recent years, several findings of<br />
experiments involving cell culture revealed that in human lung fibroblasts, the drug is found<br />
to exert effects such as decrease in the proliferation of fibroblasts, reduced TFG-β stimulated<br />
reactions, lessened myofibroblast marker alpha smooth muscle actin (α-SMA) levels, and<br />
reduced heat shock protein 47 expression (Nakayama et al., 2008; Conte et al., 2014).<br />
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