Side effects of immune-checkpoint inhibitors: Can multiple side effects be seen in a patient?

Abstract

Introduction Nivolumab is a human immunoglobulin G4 monoclonal antibody that inhibits programmed cell death-1 activity by binding to the programmed cell death-1 receptors. Cancer cells express increased number of programmed cell death-1 ligands and this allows them to escape the cytotoxic effects of the T cells. Therefore, the negative programmed cell death-1 receptor signal regulates T-cell proliferation and activation is disrupted. However, this change in the activity of the T cells can cause them to lose their ability to recognize host cells. The immune response enabled by these agents has led to side effects, commonly known as “immune-related adverse events.” Case report We report a case of a 66-year-old male patient who was treated with nivolumab for recurrent renal cell carcinoma presented with hepatitis and adrenalitis. Three weeks after starting nivolumab, the patient had abdominal pain and weakness, and then aspartate and alanine transaminase levels were found to be elevated. Management and outcome Hepatitis was predicted to be due to nivolumab, because other causes were excluded. He started using oral methylprednisolone and then, hepatitis improved. However, while receiving methylprednisolone treatment, fludrocortisone was started with the pre-diagnosis of adrenalitis due to the persistence of fatigue, weakness, and hyponatremia and hyperkalemia. With both treatments, the patient's symptoms and sodium and potassium level returned to normal. Discussion This case emphasizes the need for patient's education and awareness of immune-related adverse events, and the importance of understanding the management of life-threatening complications of the checkpoint inhibitors, because these side effects require prompt recognition and treatment.

The Uncharted Landscape of Rare Endocrine Immune-Related Adverse Events

“…Twenty-seven studies with detailed patients’ features have been published from 2013 to 2022 and are included in Table 1 [ 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 , 35 , 36 , 37 , 38 , 39 ]. These studies describe a total of 29 patients who experienced PAI following ICI therapy for various types of malignancy.…”

“…Three patients (10.3%) were treated with anti-CTLA-4 monotherapy, 20 patients (69%) were treated with anti-PD-1/L1 monotherapy, and the remaining six patients (20.7%) were treated with anti-CTLA-4 and anti-PD-1 combination therapy. In at least eight cases [ 16 , 21 , 23 , 24 , 27 , 34 , 37 ], ICIs were chosen as the first-line systematic therapy for advanced disease, whereas, in four cases ICI, treatment was combined with a tyrosine kinase inhibitor [ 13 , 22 , 27 , 29 ], which has also been implicated for PAI development [ 40 ]. The ICI-induced PAI was diagnosed from 10 days to 1 year post ICI initiation.…”