2016 Volume 59 Issue 12 Pages 811-818
We encountered a 42-year-old woman with a 3-year history of breast cancer. She underwent total mastectomy of her right breast and axillary lymph node dissection when she was 39 years old. A subtyping analysis demonstrated that the tumor was triple negative. Adjuvant chemotherapy combined with radiotherapy was administered. Even after the standard therapy finished, she hoped to continue the treatment, and therefore chemotherapy was continued. Anti-programmed cell death protein-1 antibody (anti-PD-1 antibody) administration was therefore started. Four weeks after the final administration, she experienced abrupt onset of hyperglycemia and ketoacidosis and was diagnosed with type 1 diabetes mellitus. Her plasma glucose level was 366 mg/dL, HbA1c was 9.5 %, and β-hydroxybutyrate was 7581 μmol/L. Her serum C-peptide level was undetectable, and anti-GAD and anti-IA-2 antibodies were negative. Although anti-PD-1 antibody is highly effective against some cancers that are refractory to standard chemotherapies, there is concern about the development of autoimmune diseases, including type 1 diabetes. Most patients that developed type 1 diabetes after anti-PD-1 therapy exhibited a low or undetectable C-peptide level. Our patient's clinical history and these previous findings suggest that anti-PD-1 antibody may have triggered type 1 diabetes in our patient.