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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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Source: Adopted from Bendstrup (2014)<br />
2.2.2 Etiology<br />
The basic issue of patients exhibiting pulmonary fibrosis is its diminishing features.<br />
The etiology of pulmonary fibrosis comprehension will give long-term typical reduction and<br />
potential alteration of the disease. There are presently various familiar hazards till date that<br />
are related with pulmonary fibrosis which will be explained below.<br />
2.2.2.1 Radiation and chemotherapy-induced lung injury<br />
The treatment of breast, lung, oesophageal and lymphoid cancers is done using<br />
Thoracic Radiation Therapy (RT). A general dose-restricting obstacle of RT nevertheless is<br />
the evolution of pulmonary interstitial damage and infection, frequently described to as<br />
radiation pneumonitis and appearance of fibrotic foci (Burkhardt, 1989; Carver et al., 2007;<br />
Vågane et al., 2008). In RT-originated fibrosis various procedures have been recognized,<br />
comprising enhanced Reactive Oxygen Species (ROS), alveolar injury (Ghafoori et al., 2008)<br />
and the toxic impact of ROS on parenchymal cells (Beinert et al., 1999; Rødningen et al.,<br />
2008), obstruction of multiplication-related transcription components (Lemay & Haston,<br />
2008), and the inflow of infection cells, like lymphocytes and macrophages (Johnston et al.,<br />
2004; Westermann et al., 1999). Dysregulated pro-inflammatory and pro-fibrotic cytokines,<br />
IL-6, MMPs, TGFβ (Barthelemy-Brichant et al., 2004; Matej et al., 2007; Hill, 2005; Molteni<br />
et al., 2007; Yang et al., 2007) and chemokines (Johnston et al., 2002) moreover additionally<br />
decrease the anti-inflammatory cytokines subsequent to radiation (Haase et al., 2007) can also<br />
intensify the infection and wound-healing reaction. Genetic determinants of RT-originated<br />
fibrosis have been exhibited by animal prototypes (Sharplin & Franko, 1989; Lemay &<br />
Haston, 2008) comparable to the analogous genotype-associated relations in humans<br />
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