For last week’s practice question, we quizzed participants on the sudden onset of hyperglycemia. 66% of respondents chose the best answer. We want to clarify and share this important information, so you can pass it on to people living with diabetes and your colleagues, plus prepare for exam success!
Before we start though, if you don’t want any spoilers and haven’t tried the question yet, you can answer it by clicking here.
A 58-year-old man without a history of diabetes is receiving treatment with an immune checkpoint inhibitor for metastatic melanoma. Four months after beginning therapy, he presents with polyuria, weight loss, nausea, and fatigue. Laboratory findings include:
- Plasma glucose: 465 mg/dL
- Blood ketones: Positive
- Arterial pH: 7.18
- C-peptide: Undetectable
Which mechanism most likely explains this sudden hyperglycemia?
- A. Progressive insulin resistance caused chronically elevated cortisol levels
- B. Autoimmune destruction of pancreatic beta cells
- C. Glucocorticoid-induced hepatic glucose production
- D. Pancreatic exocrine insufficiency from chronic pancreatitis
Getting to the Best Answer
Answer A is incorrect. 9.84% chose this answer, “Progressive insulin resistance caused chronically elevated cortisol levels.” This answer is incorrect. Insulin resistance due to elevated cortisol levels gradually elevates glucose levels and is not usually associated with severe insulin deficiency, undetectable C-peptide, or DKA.
Answer B is correct. 66.14% of you chose this answer, “Autoimmune destruction of pancreatic beta cells.” You chose the best answer. Great Job! Immune checkpoint inhibitors can precipitate rapid-onset autoimmune diabetes, often presenting as diabetic ketoacidosis (DKA). Beta-cell destruction is typically abrupt, resulting in profound insulin deficiency requiring lifelong insulin therapy.
Answer C is incorrect. 19.29% of respondents chose this: “Glucocorticoid-induced hepatic glucose production.” Answer C is incorrect. Although corticosteroids commonly cause hyperglycemia, they generally produce insulin resistance rather than complete beta-cell destruction or absent C-peptide. There is no indication this patient is receiving glucocorticoids.
Finally, Answer D is incorrect. 4.72% chose this answer, “Pancreatic exocrine insufficiency from chronic pancreatitis.” Pancreatitis-related diabetes (type 3c diabetes) usually develops over time and is associated with exocrine pancreatic dysfunction, malabsorption, and a history of pancreatic disease—not sudden autoimmune beta-cell destruction and DKA following immunotherapy.
For More Info on Cancer and Diabetes, we have 2 great resources for you.
- Decoding the Cancer and Diabetes Connection Article by Beverly Thomassian
- Cancer and Diabetes Webinar (1.5 CEs) Airing July 21, at 11:30am. .
We hope you appreciate this week’s rationale! Thank you so much for taking the time to answer our Question of the Week and participate in this fun learning activity!
Want to Learn More about this Question?
Join us July 21st for our
Level 5 | Cancer & Diabetes Webinar
Explore the unexpected link between cancer and diabetes — and master glucose management strategies for people with diabetes undergoing treatment.
Individuals with cancer often experience hyperglycemia secondary to treatment, which can increase the risk of infection and other complications. Recent research has also identified a significant link between diabetes and cancer. This course uses a case study approach to explore this connection and provide practical strategies for managing steroid-induced hyperglycemia and improving quality of life for people navigating both conditions.
Course Topics:
- Discuss the relationship between cancer, hyperglycemia, and insulin resistance
- State 3 benefits of normalizing glucose levels during chemotherapy
- Using a case study approach, discuss strategies to improve glucose levels and quality of life
