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Anti-programmed Cell Death Protein-1 Therapy in Intrahepatic Cholangiocarcinoma Induced Type 1 Diabetes: A Case Report and Literature Review.

Abstract
Immune checkpoint inhibitors, widely used in the treatment of malignancies, can improve the prognosis of patients, while it also can induce various immune-related adverse events, and type 1 diabetes induced by anti-programmed cell death protein-1 is a rare but severe complication. Here we reported a case of type 1 diabetes induced by anti-PD-1 which was to treat intrahepatic cholangiocarcinoma. The case was a 61-year-old female who developed diabetes and ketoacidosis symptoms at the 16th week after anti-PD-1 therapy. Her blood glucose was 30.32 mmol/L, HBA1c was 8.10%, and C-peptide was <0.10 ng/ml. The patient was diagnosed as fulminant type 1 diabetes mellitus complicated with ketoacidosis induced by anti-PD-1, and was treated with massive fluid rehydration, intravenous infusion of insulin and correction of acid-base electrolyte disorder. Hepatectomy was performed after stabilization, and the patient was treated with long-term insulin. Through the case report and literature review, this study aims to improve oncologists' understanding of anti-PD-1 induced type 1 diabetes, so as to make early diagnosis and treatment of the complications and ensure medical safety.
AuthorsZhi-Kai Zheng, Jiong-Liang Wang, Wen-Xuan Li, Tian-Qing Wu, Min-Shan Chen, Zhong-Guo Zhou
JournalFrontiers in public health (Front Public Health) Vol. 10 Pg. 917679 ( 2022) ISSN: 2296-2565 [Electronic] Switzerland
PMID35784237 (Publication Type: Case Reports, Review, Research Support, Non-U.S. Gov't)
CopyrightCopyright © 2022 Zheng, Wang, Li, Wu, Chen and Zhou.
Chemical References
  • Insulins
Topics
  • Bile Duct Neoplasms (complications, drug therapy)
  • Bile Ducts, Intrahepatic
  • Cell Death
  • Cholangiocarcinoma (complications, drug therapy)
  • Diabetes Mellitus, Type 1 (complications, diagnosis)
  • Female
  • Humans
  • Insulins (adverse effects)
  • Ketosis (complications)
  • Middle Aged

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