Other characteristics found to be helpful diagnostically included time interval between symptom onset and diagnosis (based on HRCT finding, on average NSIP was diagnosed a few months earlier than UIP), mean age and gender.3 Pathologic characteristic BEZ235 of NSIP is uniform thickening of alveolar walls with a spectrum of cellular to fibrosing patterns. Recent ATS/ERS review of 305 cases of which 193 had sufficient data for diagnosis, has
suggested NSIP as a separate entity rather than previously thought that it is more a temporary diagnosis. Exclusion of other interstitial lung diseases being of primary concern. NSIP is considered to have good prognosis. Additionally 66 patients were followed up from 0.6 to 19.44 years of which 8 patients passed away (7 from NSIP and 1 from nonrespiratory cause) and 1 patient underwent lung transplantation. Two patients subsequently showed Collagen Vascular Disease (scleroderma and polymyositis). Extensive pathology review of 67 probable cases is summarized as follows: varying amounts of interstitial inflammation and fibrosis uniformly appearing. Two varieties were distinguished: cellular (16% of cases) with mild to moderate chronic inflammatory interstitial infiltrate with little fibrosis and fibrosing (84% of cases) with interstitial thickening by uniform fibrosis of
same age with preservation of alveolar architecture and various amounts of cellular inflammation. Clinical presentation was breathlessness and cough of 6–7 months, mostly women, never-smoker and in 6th decade of life. In cases of histological similarity between NSIP and HP, clinical history of antigen exposure PLX4032 guided diagnosis.6 Pulmonary drug toxicity another cause associated with NSIP is frequently caused by cytotoxic drugs such as cyclophosphamide, bleomycine, carmustine. NSIP has been reported with carmustine toxicity or noncytotoxic drugs such as amiodarone. Other noncytotoxic drugs associated with pulmonary
toxicity include nitrofurantoin, sulfasalazine and gold salts.7 One study compared BAL findings in patients with sarcoidosis versus dipyridamole HP. They noted lymphocytosis consistent with sarcoidosis and Masson bodies have been observed in HP or extrinsic allergic alveolitis.8 Another form of interstitial lung disease that often presents with chronic respiratory symptoms and needs to be distinguished from NSIP is hypersensitivity pneumonitis for antigen avoidance and preventive measures. Hypersensitivity pneumonitis or extrinsic allergic alveolitis is characterized by diffuse parenchymal and airways inflammation due to inhaled antigens previously sensitized to. Symptoms occur 4–8 h after exposure. Studies in England have shown that incidence is 0.9 per 100,000 person years, with mean age of diagnosis of 57, equal male to female ratio and patients less likely to be smokers. HP is classified into acute, sub-acute or intermittent and chronic progressive.