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Abstract VII- Summary & Conclusion Pulmonary fibrosis (PF) is a devastating disorder that belongs to a large family of lung diseases called interstitial lung diseases. It is characterized by chronic inflammation, infiltration of inflammatory cells, generation of reactive oxygen species (ROS), fibroblast proliferation and deposition of collagen into the lung parenchyma. Idiopathic pulmonary fibrosis (IPF) is a specific form of chronic, progressive fibrosing interstitial pneumonia of unknown cause. Patients with pulmonary fibrosis have a median survival of 4 to 5 years after the onset of symptoms. PF can arise from known precipitating factors, including lung exposure to exogenous agents by inhalation or systemically, as with drug-induced pulmonary fibrosis. Amiodarone is one of the most effective antiarrhythmic drugs from class III that is commonly prescribed for treatment of broad spectrum types of arrhythmias. However, pulmonary toxicity is the major side effect of amiodarone and restricts its use. It has been estimated that about 6% of people who are taking amiodarone show toxicity associated with its use, which takes the form of interalveolar or interstitial inflammation or pulmonary fibrosis and the mortality rate is about 5–10%. The mechanism of amiodarone-induced pulmonary side effects is not well known. An in vitro study revealed that amiodarone primarily activates necrotic pathways whereas its metabolite, desethylamiodarone (DES) activates both necrotic and |