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Licensed Unlicensed Requires Authentication Published by De Gruyter July 8, 2020

Continuous glucose monitoring reduces pubertal hyperglycemia of type 1 diabetes

Benjamin Udoka Nwosu, Shamima Yeasmin, Sanaa Ayyoub, Shwetha Rupendu, Tony R. Villalobos-Ortiz, Gabrielle Jasmin, Sadichchha Parajuli, Bita Zahedi, Emily Zitek-Morrison, Laura C. Alonso and Bruce A. Barton

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.


Corresponding author: Professor Benjamin Udoka Nwosu, Department of Pediatrics, Division of Endocrinology, University of Massachusetts Medical School, 55 Lake Avenue North, Worcester, MA, 01655, USA, Phone: +774 441 7784, Fax: 774 441 8055, E-mail:

Acknowledgment

No funding received.

  1. Research funding: None declared.

  2. Author contributions: All the authors have accepted responsibility for the entire content of this submitted manuscript and approved submission.

  3. Competing interests: Authors state no conflict of interest.

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Supplementary Material

The online version of this article offers supplementary material (https://doi.org/10.1515/jpem-2020-0057).

Received: 2020-02-10
Accepted: 2020-05-08
Published Online: 2020-07-08
Published in Print: 2020-07-28

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