# Long‐Term Growth Outcomes of Children With Type 1 Diabetes According to Glycemic Control and Use of Continuous Glucose Monitoring: A Retrospective Cohort Study

**Authors:** Sujin Kim, Seo Jung Kim, Kyoung Won Cho, Kyungchul Song, Youngha Choi, Hyun Wook Chae, Junghwan Suh

PMC · DOI: 10.1155/pedi/9111583 · Pediatric Diabetes · 2026-03-02

## TL;DR

This study found that better blood sugar control and using continuous glucose monitoring helped children with type 1 diabetes grow taller over five years, especially in boys.

## Contribution

The study shows that CGM use and improved glycemic control are linked to better long-term growth outcomes in children with T1DM.

## Key findings

- Poor glycemic control (HbA1c ≥7.0%) led to a greater decline in height standard deviation scores in males.
- Males using CGM had significantly less decline in height over five years compared to non-CGM users.
- Lower HbA1c levels and CGM use were associated with improved growth outcomes in children with T1DM.

## Abstract

Chronic diseases such as type 1 diabetes mellitus (T1DM) may alter linear growth; however, reports regarding growth in children with T1DM have been inconsistent. This study aimed to investigate the height and growth velocity of patients with T1DM, and whether they were affected by various factors 5 years after the diagnosis.

This retrospective study included patients with T1DM between October 2005 and May 2022, with a follow‐up period of at least 1 year. Patients with diabetes, thyroid disease, celiac disease, or any other chronic disease were excluded. We compared the mean height standard deviation score (H‐SDS) and growth velocity between groups divided based on glycosylated hemoglobin (HbA1c) levels and use of continuous glucose monitoring (CGM) systems.

Among the 150 patients, 45.3% were male, with a mean age at diagnosis of 7.8 ± 3.6 years. At diagnosis, the mean H‐SDS was 0.38 ± 1.11. In males, H‐SDS significantly decreased overtime, with an estimated slope (β) of −0.054 (standard error [SE] = 0.013, 95% confidence interval [CI]: −0.079 to −0.029, p  < 0.01). The decline in H‐SDS was more pronounced in the poorly‐controlled group (mean HbA1c ≥7.0%) compared to the well‐controlled group (mean HbA1c <7.0%; β = −0.081, SE = 0.016, 95% CI: −0.112 to −0.050 vs. β = −0.007, SE = 0.020, 95% CI: −0.047 to −0.033, p  < 0.01). Among males using CGM, the decrease in H‐SDS over the 5‐year follow‐up was significantly less than that observed in the non‐CGM group (β = −0.012, SE = 0.023, 95% CI: −0.057 to −0.034 vs. β = −0.072, SE = 0.015, 95% CI: −0.101 to −0.042, p = 0.03). In the multivariable linear mixed model analysis, younger age at diagnosis (β = −0.009, 95% CI: −0.017 to −0.002, p = 0.02), female (β = 0.067, 95% CI: 0.033 to 0.100, p  < 0.01) and lower HbA1c levels (β = −0.026, 95% CI: −0.038 to −0.015, p < 0.01) were significantly associated with greater improvement in H‐SDS over 5 years.

Glycemic control and CGM use positively affected linear growth in children with T1DM, especially in males. CGM use was associated with improved growth outcomes, which suggests that glucose monitoring may help mitigate the adverse effects of poor glycemic control on growth.

## Linked entities

- **Diseases:** type 1 diabetes mellitus (MONDO:0005147), T1DM (MONDO:0005147), thyroid disease (MONDO:0003240), celiac disease (MONDO:0005130)

## Full-text entities

- **Genes:** GH1 (growth hormone 1) [NCBI Gene 2688] {aka GH, GH-N, GHB5, GHN, IGHD1A, IGHD1B}, GGH (gamma-glutamyl hydrolase) [NCBI Gene 8836] {aka GATD10, GH}, IGF1 (insulin like growth factor 1) [NCBI Gene 3479] {aka IGF, IGF-I, IGFI, MGF}, ALB (albumin) [NCBI Gene 213] {aka FDAHT, HSA, PRO0883, PRO0903, PRO1341}, INS (insulin) [NCBI Gene 3630] {aka IDDM, IDDM1, IDDM2, ILPR, IRDN, MODY10}
- **Diseases:** overweight (MESH:D050177), Diabetes Autoimmunity (MESH:D003922), LMM (MESH:D004195), DKA (MESH:D016883), Peripheral neuropathy (MESH:D010523), Delayed puberty (MESH:D011628), islet autoimmunity (MESH:D007516), obese (MESH:D009765), Wolfram syndrome (MESH:D014929), Nephropathy (MESH:D007674), underweight (MESH:D013851), thyroid disease (MESH:D013959), weight gain (MESH:D015430), MODY (MESH:D003924), long (MESH:D000094024), Chronic diseases (MESH:D002908), maturity-onset diabetes of the young (MESH:C562772), celiac disease (MESH:D002446), H (MESH:D000848), growth impairment (MESH:D006130), diabetic complications (MESH:D048909), hyperglycemia (MESH:D006943), disease (MESH:D004194), DM (MESH:D009223), excess weight (MESH:D015431), Diabetic retinopathy (MESH:D003930), malignant tumors (MESH:D009369), Diabetes (MESH:D003920), COVID-19 (MESH:D000086382), Down syndrome (MESH:D004314), H-SDS (MESH:C000719188)
- **Chemicals:** Glucose (MESH:D005947), C-peptide (MESH:D002096), H (MESH:D006859), SDS (MESH:D012967), glycosylated (-)
- **Species:** Homo sapiens (human, species) [taxon 9606]
- **Mutations:** A1C

## Full text

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## Figures

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## References

36 references — full list in the complete paper: https://tomesphere.com/paper/PMC12952282/full.md

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Source: https://tomesphere.com/paper/PMC12952282