Continuous glucose monitoring reduces pubertal hyperglycemia of type 1 diabetes

Abstract

Background Physiologic hyperglycemia of puberty is a major contributor to poor glycemic control in youth with type 1 diabetes (T1D). This study's aim was to determine the effectiveness of continuous glucose monitoring (CGM) to improve glycemic control in pubertal youth with T1D compared to a non-CGM cohort after controlling for age, sex, BMI, duration, and insulin delivery methodology. The hypothesis is that consistent CGM use in puberty improves compliance with diabetes management, leading to increased percentage (%) time in range (TIR70-180 mg/dL) of glycemia, and lowering of HbA1c. Methods A longitudinal, retrospective, case-controlled study of 105 subjects consisting of 51 T1D controls (60.8% male) age 11.5 ± 3.8 y; and 54 T1D subjects (48.1% male) age 11.1 ± 5.0 y with confirmed CGM use for 12 months. Pubertal status was determined by Tanner staging. Results were adjusted for baseline HbA1c and diabetes duration. Results HbA1c was similar between the controls and the CGM group at baseline: 8.2 ± 1.1% vs 8.3 ± 1.2%, p=0.48 respectively; but was significantly lower in the CGM group 12 months later, 8.2 ± 1.1% vs. 8.7 ± 1.4%, p=0.035. Longitudinal change in HbA1c was similar in the prepubertal cohort between the control- and CGM groups: -0.17 ± 0.98% vs. 0.38 ± 1.5%, p=0.17. In contrast, HbA1c increased with advancing age and pubertal status in the pubertal controls but not in the pubertal CGM group: 0.55 ± 1.4 vs -0.22 ± 1.1%, p=0.020. Percent TIR was inversely related to HbA1c in the CGM group, r=-0.6, p=0.0004, for both prepubertal and pubertal subjects. Conclusions CGM use significantly improved glycemic control in pubertal youth with T1D compared to non-CGM users.

Keywords: children; continuous glucose monitoring; hemoglobin A1c; puberty; type 1 diabetes.

Figure 1:

Box plots of the changes in mean hemoglobin A1c concentrations between the controls and the continuous glucose monitoring group during the 12 months of the study. Baseline HbA1c concentrations were not different between the groups but HbA1c was significantly lower in the CGM group at 12 months. The line in each box represents the median, while the ‘o’ and ‘+’ symbols represent the mean for the controls and CGM respectively.

Figure 2:

Graph of the baseline-adjusted hemoglobin A1c (HbA1c) showing the effect of advancing age and pubertal status on the serial HbA1c values in both the CGM users and controls. Among the prepubertal cohort, there was no significant difference in the changes in HbA1c between the CGM and controls: −0.17 ± 0.98% vs. 0.38 ± 1.5%, p=0.17. In contrast, HbA1c increased with age and pubertal status in the pubertal controls, 0.55 ± 1.4% compared to the CGM group, −0.22 ± 1.1% vs, p=0.020.

Figure 3:

Box plots of the differences in HbA1c between the CGM group and controls at various age-based Tanner stages. There were no statistically significant differences in A1c between the CGM and controls for each Tanner stage. This could be due to the small subgroup sample size. For example, though the difference in A1c between the CGM group for Tanner stage IV (n=5) and the controls at Tanner IV (n=4) was clinically significant, it was not statistically significant: 7.5 ± 0.94% vs 9.5 ± 3.02%, p=NS.

Figure 4:

Box plots of the differences in growth velocity between the CGM group and the controls for each age-based Tanner stage. There was no significant difference in growth velocity between the CGM and control groups at each Tanner stage. In contrast, growth velocity was significantly faster at Tanner II compared to Tanner stages III, IV and V (p<0.05) which could be due to the higher number girls in the Tanner II category.

Figure 5:

This scatterplot of the continuous glucose monitoring group shows a significant inverse relationship between hemoglobin A1c and percentage (%) time in range (TIR^{70–180 mg/dL}) of glycemia for three timepoints: baseline, 6 and 12 months, r=−0.6, n=42, p=0.0004.