Abstract
Background
Glycated hemoglobin (HbA1c) is a widely used biomarker for assessing long‐term glycemic control in patients suffering from diabetes mellitus. However, certain hematologic conditions, such as hemolytic disorders, can produce misleadingly low HbA1c values, potentially masking poor glycemic control and leading to mismanagement of the patient. This case represents a rare but clinically significant scenario, where G6PD deficiency leads to spuriously low HbA1c level, emphasizing the need for alternative glycemic markers.
Case Presentation
We report the case of a 17‐year‐old male who presented with classic symptoms of hyperglycemia and was diagnosed with type 1 diabetes mellitus (T1DM) based on clinical features, elevated blood glucose, high HbA1c (>14%), and positive glutamic acid decarboxylase (GAD) antibodies. One month after initiating basal–bolus insulin therapy, his follow‐up HbA1c unexpectedly dropped to 3%, despite continuous glucose monitoring (CGM) showing incomplete control of glucose level. Work‐up for nonglycemic factors, specifically those affecting the red blood cells (RBCs) revealed normal hemoglobin electrophoresis but confirmed glucose‐6‐phosphate dehydrogenase (G6PD) deficiency. The intravascular hemolysis associated with G6PD deficiency likely shortened RBC lifespan, producing spuriously low HbA1c values. Fructosamine testing was consistent with ongoing hyperglycemia.
Conclusion
This case underscores the importance of considering alternative glycemic markers, such as fructosamine or CGM metrics, when discordance exists between HbA1c and clinical or CGM findings. Early recognition of G6PD deficiency in diabetic patients with such unusual presentation is critical to ensure accurate monitoring and to guide patient education on avoiding oxidative stress triggers.