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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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observed that only 21% of these patients exhibited a gradually continuous path without<br />
confirmation of acute decompensation (Fernández Pérez et al., 2010).<br />
2.2.7.3 Rapidly Progressive IPF<br />
A subgroup of patients with IPF were recognized by Selman and coworkers , who<br />
exhibited a quickly continuous disease (< 6 mo of symptoms prior to first appearance) and<br />
displayed reduced survival in contrast to patients subsequent to the gradually continuous<br />
clinical path (Selman et al., 2007). These were essentially massive cigarette smoking men<br />
(Selman et al., 2007). The patients with a hastened clinical path impressively exhibited a<br />
gene expression description that varied from those with obtuse development and extended<br />
survival in spite of having related lung functions, chest imaging and histologic observations<br />
during the period of diagnosis. It was demonstrated by Boon and colleagues that lung<br />
molecular indications during the period of diagnosis may recognize patients with substantial<br />
IPF in contrast with those having quickly continuous disease (Boon et al., 2009).<br />
2.2.7.4 Acute Exacerbations of IPF<br />
Intervals of acute respiratory decrease are witnessed in patients with IPF either due to<br />
familiar complications, like infections, or of unrevealed reason (i.e., acute aggravation of<br />
IPF). Our comprehension of these occurrences has enhanced due to the creation of<br />
predefined norms for acute aggravation and disease development in patients with IPF. It is<br />
described that the acute aggravation of IPF causes the emergence of quick decline (within<br />
few days to weeks) in symptoms, lung function, and radiographic occurrence (bilateral<br />
ground-glass opacities and fusion overlapping a reticular pattern on HRCT) in the lack of<br />
infection, pulmonary embolism, heart failure or other recognizable reason (Collard et al.,<br />
2007b; Tomioka et al., 2007; Silva et al., 2007). A very poor result is exhibited in patients<br />
with acute aggravations of IPF.<br />
2.2.8 Diagnosis<br />
The IPF conclusive diagnosis of needs:(a) the expulsion of diffuse parenchymal lung<br />
diseases of known reason (connective tissue diseases, drug toxicity, environmental or<br />
occupational exposure) or other described clinical establishments and (b) the existence of a<br />
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