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ABSTRACT Drug-induced lung disease (DILD) encompasses a broad, highly heterogeneous group of conditions that may occur as a result of exposure to numerous agents, such as antineoplastic drugs, conventional or biological disease-modifying antirheumatic drugs, antiarrhythmics, and antibiotics. Between 3% and 5% of prevalent cases of interstitial lung diseases are reported as DILDs. The pathogenesis of lung injury in DILD is variable, multifactorial, and often unknown. Acute presentation is the most common, can occur from days to months after the start of treatment, and ranges from asymptomatic to acute respiratory failure. The CT patterns are varied and include ground-glass opacities, organizing pneumonia, and diffuse alveolar damage. Notably, there are no clinical manifestations or CT patterns specific to DILD, which makes the diagnosis quite challenging and necessitates a high index of suspicion, as well as the exclusion of alternative causes such as infection, cardiac-related pulmonary edema, exacerbation of a preexisting ILD, and neoplastic lung involvement. Discontinuation of the offending medication constitutes the cornerstone of treatment, and corticosteroid treatment is usually necessary after the onset of clinical manifestations. The prognosis varies widely, with high mortality rates in severe cases. A history of medications related to pulmonary toxicity in patients with new-onset respiratory symptoms should prompt consideration of DILD as a potential underlying cause.

Targeted therapy and immunotherapy have markedly improved prognosis of advanced melanoma patients. With expanded use of these drugs, a range of cutaneous adverse events has emerged. Although the vast majority of adverse events are low-grade, they many cause significant morbidity and can affect patients' quality of life. Early diagnosis and prompt intervention may prevent unnecessary discontinuation of life-saving anticancer therapies. In this article, we review the cutaneous adverse events of small molecules and monoclonal antibodies used for the therapy of melanoma and discuss their pathophysiology and recommendations for prevention and management of these adverse events.

Abstract: Therapeutic antibodies targeting the programmed cell death protein 1 (PD‐1) pathway function as immune checkpoint inhibitors, allowing the immune system to recognize tumors which otherwise escape immune surveillance. However, these agents can also elicit an autoimmune response by inhibiting the ability of non‐neoplastic tissues and regulatory cells to suppress the immune system. Here we present a fatal case of active myocarditis in a 55‐year‐old man with non‐small‐cell lung cancer which occurred following monotherapy with the PD‐1 inhibitor nivolumab (Opdivo). He presented with acute right‐sided heart failure and died 1 day after admission. Postmortem examination revealed multiple gelatinous lesions in the myocardium of the interventricular septum and the bilateral atria and ventricles which had microscopic features diagnostic of myocarditis. Subsequent studies failed to identify an infectious cause. Immune checkpoint inhibitors are an increasingly common addition to anticancer regimens and they should be considered in the evaluation of acute myocarditis. [ABSTRACT FROM AUTHOR]