What is it about?
In a diabetic crisis, there is often a notable elevation of tumor markers, which may indicate a potential relationship between diabetes and future tumor risk. Diabetes, as a metabolic disorder characterized by chronic hyperglycemia and insulin resistance, may promote tumor development through various mechanisms. For example, prolonged high blood sugar can lead to oxidative stress, chronic inflammation, and cellular damage, creating an environment conducive to tumor cell mutation and proliferation. Additionally, abnormal secretion of insulin and insulin-like growth factors is closely linked to the proliferation of tumor cells. Elevated tumor markers, such as carcinoembryonic antigen (CEA), cancer antigen 19-9 (CA19-9), and alpha-fetoprotein (AFP), may be more common in diabetic patients. While these markers may rise as a non-specific response during a diabetic crisis, their elevation suggests that individuals with diabetes may be at higher risk for developing cancer in the future. Therefore, in addition to focusing on blood glucose control during a diabetic crisis, it is important for diabetic patients to regularly monitor tumor markers in order to detect potential malignancies at an early stage.
Featured Image
Photo by Rinke Dohmen on Unsplash
Why is it important?
This study may deepen the discussion of the clinical findings on the observed higher prevalence of tumor markers in diabetic crises such as diabetic ketoacidosis and hyperosmolar hyperglycemic state. It warrants further follow-up in these groups of patients, establishes related cut-offs for alerts, provides more sensitive markers for blood sampling for early prevention, and intensifies the importance of glycemic control and screening the population at higher risks for diabetes and tumors.
Perspectives
Read the Original
This page is a summary of: The Effect of Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic on the Metabolic Tumor Markers: A Real-World Retrospective Study, Diabetes Metabolic Syndrome and Obesity, November 2024, Taylor & Francis,
DOI: 10.2147/dmso.s487398.
You can read the full text:
Resources
Contributors
The following have contributed to this page