Ya-Sian Chang1, Li-Yun Hsiao2, Chien-Yu Lin3, Mu-Chin Shih2, Ming-Chia Hsieh4, Jan-Gowth Chang5. 1. Epigenome Research Center, China Medical University Hospital, Taichung, Taiwan; Department of Laboratory Medicine, China Medical University Hospital, Taichung, Taiwan; Center for Precision Medicine, China Medical University Hospital, Taichung, Taiwan; Department of Medical Laboratory Science and Biotechnology, China Medical University, Taichung, Taiwan. 2. Department of Laboratory Medicine, China Medical University Hospital, Taichung, Taiwan. 3. Graduate Institute of Clinical Medical Science and School of Medicine, China Medical University, Taichung, Taiwan. 4. Departments of Internal Medicine, China Medical University Hospital, Taichung, Taiwan. Electronic address: d94750@mail.cmuh.org.tw. 5. Epigenome Research Center, China Medical University Hospital, Taichung, Taiwan; Department of Laboratory Medicine, China Medical University Hospital, Taichung, Taiwan; Center for Precision Medicine, China Medical University Hospital, Taichung, Taiwan; Graduate Institute of Biomedical Sciences, School of Medicine, China Medical University, Taichung, Taiwan; Department of Bioinformatics and Medical Engineering, Asia University, Taichung, Taiwan. Electronic address: d6781@mail.cmuh.org.tw.
Abstract
AIMS: Patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency or thalassemia have a shorter red blood cell lifespan; therefore, HbA1c is underestimated in these patients. To address these issues, we sought an early indicator for G6PD deficiency or thalassemia in DM patients. METHODS: A total of 4908 patients with DM and 1848 subjects without DM were included in this study. Fasting glucose (FG) levels, HbA1c levels, hemogram profiles and G6PD activities were measured. Genotypic analyses of G6PD deficiency and thalassemia were performed. RESULTS: DM patients with G6PD deficiency had significantly higher FG/HbA1c ratios than did those without G6PD deficiency (26.54 vs. 18.36; p < 0.0001). We divided the FG level into four categories: ≤150, 151-250, 251-350, and ≥351 mg/dL. Among all groups, only patients with DM and G6PD deficiency had higher FG/HbA1c ratios than those of patients with DM alone or DM with thalassemia. To evaluate the reliability of the FG/HbA1c ratio, receiver operating characteristic analyses were performed. The areas under the curve for detecting FG ≤ 150, 151-250, 251-350, and ≥351 mg/dL with G6PD deficiency based on the FG/HbA1c ratio were 0.839 (p < 0.001), 0.888 (p < 0.001), 0.891 (p < 0.001), and 0.640 (p = 0.3954), respectively. G6PD deficiency was confirmed by genetic analysis. We found common mutations that influenced G6PD activity and HbA1c levels. CONCLUSIONS: The FG/HbA1c ratio is a good indicator of DM with G6PD deficiency. If this ratio is determined to be high in a clinical setting, then the clinician must consider whether the patient has a G6PD deficiency, and HbA1c reference values must be adjusted to avoid misdiagnosis and incorrect treatment decisions.
AIMS: Patients with glucose-6-phosphate dehydrogenase (G6PD) deficiency or thalassemia have a shorter red blood cell lifespan; therefore, HbA1c is underestimated in these patients. To address these issues, we sought an early indicator for G6PD deficiency or thalassemia in DMpatients. METHODS: A total of 4908 patients with DM and 1848 subjects without DM were included in this study. Fasting glucose (FG) levels, HbA1c levels, hemogram profiles and G6PD activities were measured. Genotypic analyses of G6PD deficiency and thalassemia were performed. RESULTS:DMpatients with G6PD deficiency had significantly higher FG/HbA1c ratios than did those without G6PD deficiency (26.54 vs. 18.36; p < 0.0001). We divided the FG level into four categories: ≤150, 151-250, 251-350, and ≥351 mg/dL. Among all groups, only patients with DM and G6PD deficiency had higher FG/HbA1c ratios than those of patients with DM alone or DM with thalassemia. To evaluate the reliability of the FG/HbA1c ratio, receiver operating characteristic analyses were performed. The areas under the curve for detecting FG ≤ 150, 151-250, 251-350, and ≥351 mg/dL with G6PD deficiency based on the FG/HbA1c ratio were 0.839 (p < 0.001), 0.888 (p < 0.001), 0.891 (p < 0.001), and 0.640 (p = 0.3954), respectively. G6PD deficiency was confirmed by genetic analysis. We found common mutations that influenced G6PD activity and HbA1c levels. CONCLUSIONS: The FG/HbA1c ratio is a good indicator of DM with G6PD deficiency. If this ratio is determined to be high in a clinical setting, then the clinician must consider whether the patient has a G6PD deficiency, and HbA1c reference values must be adjusted to avoid misdiagnosis and incorrect treatment decisions.