Distal renal tubular acidosis (RTA) is a rare adverse reaction to immune checkpoint inhibitors, which only occurs in a small number of cases. To the best of our knowledge, distal RTA caused by sintilimab, a programmed cell death protein 1 (PD-1) inhibitor, has not been previously reported. In the present study, the case of a 62-year-old man with metastatic cardiac carcinoma treated with sintilimab anti-PD-1 therapy was reported. After the fourth administration of sintilimab, the treatment course was interrupted by metabolic hyperchloraemic acidosis with hypokalaemia. Following urine and blood tests, immunotherapy-induced distal RTA was suspected. Treatment with sintilimab and chemotherapy was stopped, and treatment with sodium bicarbonate and potassium citrate was started, which resulted in an adequate response. The present study provides the first case of distal RTA secondary to sintilimab treatment.
Introduction In recent years, oral antineoplastic agents are commonly used in antitumor therapy. The interaction between drugs may affect the efficacy of drugs or lead to adverse reactions. We describe the case of a patient who presented acute liver injury, possibly induced by the concomitant use of metoprolol and dacomitinib. Case report A 62-year-old male patient with non-small cell lung cancer was admitted for anti-cancer treatment. He regularly took metoprolol tartrate 12.5 mg, 2/day for hypertension. He was treated with dacomitinib according to EGFR Exon21 L858R positive. After 3 days of dacomitinib, the patient's alanine aminotransferase (ALT) and glutathione aminotransferase (AST) increased, and the heart rate and systolic blood pressure of the patient decreased significantly. The patient was diagnosed with acute liver injury. Management and outcomes Dacomitinib was discontinued and glutathione, magnesium isoglycyrrhizinate were given to treat acute liver injury. Two days after discontinued dacomitinib, the patient's heart rate increased, but the ALT and AST of the patient elevated again. Metoprolol tartrate was subsequently discontinued and the ALT and AST gradually decreased and the patient discharged from the hospital eight days later with his liver function improved. Discussion To our knowledge, this is the first case in the literature of acute liver injury possibly induced by the interaction between metoprolol and dacomitinib. The interaction most likely arose because dacomitinib is a CYP2D6 strong inhibitor and could therefore impair the metabolism of metoprolol (a CYP2D6 substrate) and increase its serum concentration. Therefore, hepatic function should be carefully monitored in patients treated with dacomitinib and metoprolol and other inhibitors or inducers of CYP2D6.
Immune-related adverse events following treatment with immune checkpoint inhibitors (ICIs) can occur at any time during therapy, with onset occurring most frequently during the first 3 months of treatment. However, they rarely occur after treatment cessation. An awareness of delayed immune-related events following the termination of immunotherapy is paramount for optimal tumour management. The present study reports a case of a 69-year-old male patient with right lung adenocarcinoma. He suffered from psoriasis for ~40 years and was suspected of developing immune checkpoint inhibitor-related pneumonitis (CIP) 6 months after the cessation of treatment with the anti-programmed cell death-1 receptor antibody sintilimab. The present case study is, to the best of our knowledge, the first case of late-onset CIP after the cessation of sintilimab. Subsequently, the report also reviews previously reported cases of late-onset CIP after the cessation of ICI treatment. The present report highlights the finding that CIP can develop, although rarely reported, months or even years after the termination of immunotherapy. Therefore, CIP should always be considered as one of the possibilities and addressed accordingly once the pulmonary infection is ruled out. Careful monitoring, timely diagnosis and administration of corticosteroids are essential in controlling this condition, particularly for patients with pre-existing autoimmune diseases.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
customersupport@researchsolutions.com
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.
Copyright © 2025 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.