The radiographic manifestations of AIPT are protean, reflective of its cytotoxic and immune mechanisms of injury. Most commonly, AIPT presents as nonspecific interstitial pneumonia (NSIP) with expansion of the pulmonary interstitium by mononuclear inflammatory cells, mild interstitial fibrosis, and hyperplasia of type II pneumocytes. In these patients, symptom onset is usually within months of treatment initiation. At high-resolution chest CT, bilateral lung disease is characterized by scattered regions of ground-glass opacity and interlobular septal thickening with minimal architectural distortion. This can progress to basal predominant fibrosis with honeycombing and traction bronchiectasis in its later stages. Less commonly, AIPT can manifest as bronchiolitis obliterans organizing pneumonia (BOOP) or cryptogenic organizing pneumonia. This results in more patchy interstitial inflammation and loose fibrotic plugs that occlude terminal bronchioles, alveolar ducts, and alveoli on histopathologic specimens. BOOP in isolation is rare, and it more commonly occurs concomitantly with NSIP. Although patients with BOOP often present with similar nonspecific signs and symptoms of progressive dyspnea, dry nonproductive cough, and fever as those patients with NSIP, a CT scan can demonstrate more nodular areas of peripheral consolidation and bronchial wall thickening or dilation. Subpleural nodular opacities may also occur. The radiographic abnormalities typically resolve after stopping amiodarone, but on occasion steroid therapy may be required.