Abstract
Laboratory HbA1c does not always predict diabetes complications and our aim was to establish a glycaemic measure that better reflects intracellular glucose exposure in organs susceptible to complications. Six months of continuous glucose monitoring data and concurrent laboratory HbA1c were evaluated from 51 type 1 diabetes (T1D) and 80 type 2 diabetes (T2D) patients. Red blood cell (RBC) lifespan was estimated using a kinetic model of glucose and HbA1c, allowing the calculation of person-specific adjusted HbA1c (aHbA1c). Median (IQR) RBC lifespan was 100 (86-102) and 100 (83-101) days in T1D and T2D, respectively. The median (IQR) absolute difference between aHbA1c and laboratory HbA1c was 3.9 (3.0-14.3) mmol/mol [0.4 (0.3-1.3%)] in T1D and 5.3 (4.1-22.5) mmol/mol [0.5 (0.4-2.0%)] in T2D. aHbA1c and laboratory HbA1c showed clinically relevant differences. This suggests that the widely used measurement of HbA1c can underestimate or overestimate diabetes complication risks, which may have future clinical implications.
Highlights
High glucose exposure in specific organs is a critical factor for the development of diabetes complications (Marcovecchio, 2017; Giacco and Brownlee, 2010)
While variation in Red blood cell (RBC) glucose uptake is likely relevant to the risk of diabetes complications in susceptible organs, variation in red cell lifespan can affect haemoglobin glycation and HbA1c values, in turn compromising the accuracy of this glycaemic marker in predicting risk of complications
As illustrated in the figure, those with the shorter RBC lifespan of 80 days showed around 22 mmol/mol (2%) lower laboratory HbA1c than adjusted HbA1c (aHbA1c)
Summary
High glucose exposure in specific organs ( eye, kidney, and nerve) is a critical factor for the development of diabetes complications (Marcovecchio, 2017; Giacco and Brownlee, 2010). While raised intracellular glucose is responsible for diabetes complications (Giacco and Brownlee, 2010; Brownlee, 2005), extracellular hyperglycaemia selectively damages cells with limited ability to adjust cross-membrane glucose transport effectively (Brownlee, 2005). While variation in RBC glucose uptake is likely relevant to the risk of diabetes complications in susceptible organs, variation in red cell lifespan can affect haemoglobin glycation and HbA1c values, in turn compromising the accuracy of this glycaemic marker in predicting risk of complications. This explains the inability to clinically rely on laboratory HbA1c in those with haematological disorders
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