Xiaomin Shi, Mengyu He, Li Ni, Zhijuan Dai, Mengte Shi, Yingying Zhou, Huabing Zhang, Ming Li, Chaoming Wu
<p>A 59-year-old man was diagnosed with Hodgkin lymphoma in May 2020 and began treatment with sintilimab in August 2020. The patient had a normal blood glucose test before receiving treatment with sintilimab, with no family history of diabetes. In September 2020, the patient developed diabetic ketoacidosis after receiving three cycles of sintilimab. Glycated hemoglobin A1c (HbA1c) was 7.0%, and C-peptide level was undetectable. Diabetes-related antibodies, including glutamic acid decarboxylase antibody, insulinoma-associated protein 2 antibodies, and insulin autoantibodies, were all negative. Based on these findings, he was diagnosed with fulminant type 1 diabetes caused by anti-programmed cell death-1 (anti-PD-1) therapy. Additionally, he was also diagnosed with destructive thyroiditis caused by anti-PD-1 therapy at the same time. After discharge, he received insulin therapy, and his glucose level fluctuated between 4 and 20 mmol/L. The treatment regimen for Hodgkin's lymphoma was modified, and sintilimab treatment was stopped. Two months later, the Hodgkin's lymphoma was resolved.</p><p>In November 2021, the patient was admitted to the endocrinology department due to significant weight loss. In the 3 months leading up to his admission, he had lost about 15 kg in weight, with a poor glucose control (often >33.3 mmol/L). He did not report any symptoms of nausea or vomiting. On physical examination, he weighed 47 kg and had a body mass index (BMI) of 16.65 kg/m<sup>2</sup>. On admission, his plasma glucose level was 29.9 mmol/L, and β-hydroxybutyric level was 0.3 mmol/L. Of note, his serum C-peptide was <0.05 ng/mL, while his serum insulin level was >300 mU/L, and his HbA1c level was 10.2%. He was commenced on intravenous regular insulin therapy, and the insulin dose was gradually increased. However, despite continuous intravenous infusion of up to 3200 U of regular insulin daily, his blood glucose was still above 15 mmol/L. Other examinations showed that serum triglyceride was 0.89 mmol/L, adiponectin was 25.15 μg/mL, and insulin-like growth factor-1 was <25 ng/mL. Diabetes-related antibodies were all negative as before.</p><p>We measured his serum insulin receptor antibody by using enzyme linked immunosorbent assay, which was developed in Key Laboratory of Endocrinology of National Health Commission, Peking Union Medical College Hospital. This patient had a positive result on the insulin receptor antibody test. He was therefore diagnosed with type B insulin resistance syndrome (TBIRS). During this admission, he was also diagnosed with Sjogren's syndrome and hemolytic anemia. We commenced him on an immunosuppressive regimen, combining iv rituximab (0.5 g), cyclophosphamide (0.4 g), and glucocorticoids. Glucocorticoids were administered as methylprednisolone 500 mg intravenously for 3 days, followed by a maintenance dose of 50 mg po daily, with a prolonged taper. Hydroxychloroquine was administered in a dose of 0.2 mg po daily continuo
{"title":"Type B insulin resistance syndrome induced by anti-PD-1 therapy","authors":"Xiaomin Shi, Mengyu He, Li Ni, Zhijuan Dai, Mengte Shi, Yingying Zhou, Huabing Zhang, Ming Li, Chaoming Wu","doi":"10.1111/1753-0407.13603","DOIUrl":"https://doi.org/10.1111/1753-0407.13603","url":null,"abstract":"<p>A 59-year-old man was diagnosed with Hodgkin lymphoma in May 2020 and began treatment with sintilimab in August 2020. The patient had a normal blood glucose test before receiving treatment with sintilimab, with no family history of diabetes. In September 2020, the patient developed diabetic ketoacidosis after receiving three cycles of sintilimab. Glycated hemoglobin A1c (HbA1c) was 7.0%, and C-peptide level was undetectable. Diabetes-related antibodies, including glutamic acid decarboxylase antibody, insulinoma-associated protein 2 antibodies, and insulin autoantibodies, were all negative. Based on these findings, he was diagnosed with fulminant type 1 diabetes caused by anti-programmed cell death-1 (anti-PD-1) therapy. Additionally, he was also diagnosed with destructive thyroiditis caused by anti-PD-1 therapy at the same time. After discharge, he received insulin therapy, and his glucose level fluctuated between 4 and 20 mmol/L. The treatment regimen for Hodgkin's lymphoma was modified, and sintilimab treatment was stopped. Two months later, the Hodgkin's lymphoma was resolved.</p><p>In November 2021, the patient was admitted to the endocrinology department due to significant weight loss. In the 3 months leading up to his admission, he had lost about 15 kg in weight, with a poor glucose control (often >33.3 mmol/L). He did not report any symptoms of nausea or vomiting. On physical examination, he weighed 47 kg and had a body mass index (BMI) of 16.65 kg/m<sup>2</sup>. On admission, his plasma glucose level was 29.9 mmol/L, and β-hydroxybutyric level was 0.3 mmol/L. Of note, his serum C-peptide was <0.05 ng/mL, while his serum insulin level was >300 mU/L, and his HbA1c level was 10.2%. He was commenced on intravenous regular insulin therapy, and the insulin dose was gradually increased. However, despite continuous intravenous infusion of up to 3200 U of regular insulin daily, his blood glucose was still above 15 mmol/L. Other examinations showed that serum triglyceride was 0.89 mmol/L, adiponectin was 25.15 μg/mL, and insulin-like growth factor-1 was <25 ng/mL. Diabetes-related antibodies were all negative as before.</p><p>We measured his serum insulin receptor antibody by using enzyme linked immunosorbent assay, which was developed in Key Laboratory of Endocrinology of National Health Commission, Peking Union Medical College Hospital. This patient had a positive result on the insulin receptor antibody test. He was therefore diagnosed with type B insulin resistance syndrome (TBIRS). During this admission, he was also diagnosed with Sjogren's syndrome and hemolytic anemia. We commenced him on an immunosuppressive regimen, combining iv rituximab (0.5 g), cyclophosphamide (0.4 g), and glucocorticoids. Glucocorticoids were administered as methylprednisolone 500 mg intravenously for 3 days, followed by a maintenance dose of 50 mg po daily, with a prolonged taper. Hydroxychloroquine was administered in a dose of 0.2 mg po daily continuo","PeriodicalId":189,"journal":{"name":"Journal of Diabetes","volume":"16 9","pages":""},"PeriodicalIF":3.0,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/1753-0407.13603","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142174192","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Karel Labr, Jindrich Spinar, Jiri Parenica, Lenka Spinarova, Jan Krejci, Filip Malek, Petr Ostadal, Ondrej Ludka, Jiri Jarkovsky, Klara Benesova, Ruzena Labrova, Monika Spinarova