Immune checkpoint inhibitors have emerged as a revolutionary treatment option for patients with various types of malignancy. Although these agents afford a significant improvement in outcomes for melanoma and other previously untreatable malignancies, their novel mechanism of action may predispose patients to immune‐related adverse effects (irAEs). In the tumour neoantigen environment, these irAEs are due to the activation of the immune system by the blockade of suppressive checkpoints, leading to increases in T‐cell activation and proliferation. IrAEs have been reported in almost any organ and at any point in time, even months to years after discontinuation of therapy. Certain populations with distinct physiological changes, genetic risk factors, and specific antigen exposures may be more highly predisposed to develop irAEs. This review discusses the incidence and mechanisms of irAEs and the relationship between host factors and irAE occurrence.
Haploidentical hematopoietic cell transplantation (haplo‐HCT) with posttransplant cyclophosphamide (PTCY) is utilized for patients with hematological disorders but without conventional donors. The effects of new‐onset posttransplant diabetes mellitus (PTDM) following haplo‐HCT are unknown. We examined PTDM incidence and outcomes after haplo‐HCT with PTCY. Patients without diabetes receiving haplo‐HCT (n = 64) were analyzed for PTDM diagnosis (defined as blood glucose ≥ 200 mg/dL). By day 100, 14 (22%) patients developed PTDM (median, 18 days). Hyperglycemia (blood glucose ≥ 200 mg/dL) preceded corticosteroids in 11 (79%) individuals. PTDM patients had increased death/relapse (P = .029). PTDM occurs frequently, precedes corticosteroids, and leads to inferior outcomes following haplo‐HCT. PTDM prophylaxis/treatment may improve HCT survival.
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