The effectiveness of immunosuppressive cyclosporin in attenuating the progression of interstitial lung diseases

Interstitial lung diseases (ILDs) are a group of diseases that affects the lung parenchymal tissue causing irreversible damage through fibrosis and chronic inflammation, consequentially depriving gas exchange in affected individuals (1). The effects in ILDs are observed largely in the lung interstitium and differentiating them from one other is challenging as they often share comparable physiological, clinical and radiological features (2). Their aetiologies exist either in known or unknown forms. Known aetiology of ILDs include those that may have genetic predisposition which includes pulmonary manifestation of existent rheumatoid arthritis (RA) (3) or other autoimmune diseases also known as interstitial pneumonia with autoimmune features (IPAF) (4), connective tissue diseases (CTDs) such as scleroderma (systemic sclerosis), inflammatory myositis (polymyositis and dermatomyositis), Sj？gren syndrome and other undifferentiated CTD (5). Environmental factors such as bioaerosol induce hypersensitivity pneumonitis, while exposure to bird proteins, hay dust, molds and mycobacterium can also induce ILD to varying degrees. Occupation associated ILDs include asbestosis or silicosis while drugs such as amiodarone, methotrexate and nitrofurantoin are known to affect lung interstitium causing ILDs (6). Tobacco smoking is also linked to ILDs in some forms of desquamative interstitial pneumonia (DIP) and respiratory bronchiolitis-associated interstitial lung disease (RB-ILD) and pulmonary langerhans’ cell histiocytosis (LCH) (7,8). There are however ILDs whose aetiologies are still unknown or are complex, these mainly constitutes the rare forms of ILDs such lymphangioleiomyomatosis (LAM) and granulomatous such as Sarcoidosis (2,9)