Impact of Asthma and Corticosteroid Exposure on Glycemic Markers in Overweight and Obese Children.
4 affiliations
- 1Department of Pediatric Medicine, Division of Pulmonology, Sidra Medicine, Doha, Qatar.
- 2College of Medicine, Qatar University, Doha, Qatar.
- 3Department of Pediatric Medicine, Division of Endocrinology and Diabetes, Sidra Medicine, Doha, Qatar.
- 4Department of Pediatrics, Weill Cornell Medicine, Doha, Qatar.
Abstract
Purpose
Corticosteroids are the cornerstone of asthma management, yet they are associated with hyperglycemia and insulin resistance. This study evaluated associations between asthma characteristics and glycemic markers in children with overweight or obesity and examined whether corticosteroid exposure modifies these associations.Methods
This cross-sectional study included 199 children aged 6-17 years with overweight or obesity from the Middle East and North Africa region. They were divided into two groups: with asthma (OO-A) (N = 100) and without asthma (OO) (N = 99). Asthma phenotype was classified as type 2 (blood eosinophils ≥ 300 cells/µL, FeNO ≥ 30 ppb, or confirmed allergy) or non-type 2 asthma. Asthma severity was classified based on FEV₁% predicted: mild (≥ 80%), moderate (60% to < 80%), and severe (< 60%). Linear and logistic regression models assessed associations between asthma characteristics and glycemic markers in the circulation before and after adjusting for corticosteroid use.Results
Asthma was associated with higher HbA1c (β = 0.152, p = 0.007) and prediabetes (HbA1c ≥ 5.7%) (OR = 2.69, p = 0.026) only when not adjusting for corticosteroid use. Mediation analysis showed that corticosteroid exposure may account for 45.4% of the total effect of asthma on HbA1c (p = 0.024). The OO group had a higher prevalence of insulin resistance (HOMA-IR ≥ 2.5) (p = 0.029). Type 2 asthma was associated with higher HbA1c without corticosteroid adjustment (β = 0.176, p = 0.002), which was attenuated after corticosteroid adjustment (β = 0.116, p = 0.057). Severe asthma remained significantly associated with higher HbA1c in both models regardless of corticosteroid adjustment (β = 0.347-0.409, p < 0.05). No consistent associations were found with other glycemic markers.Conclusion
The asthma-HbA1c association in children with overweight/obesity may be largely mediated by corticosteroid use. Severe asthma may have a direct association with HbA1c independent of steroid use. Given the cross-sectional design and limited sample sizes, these findings require confirmation in larger longitudinal studies with more precise assessments of corticosteroid exposure and other confounders to clarify causal pathways and to evaluate whether optimizing asthma management while minimizing corticosteroid exposure could reduce long-term metabolic risk in this vulnerable population.
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BibTeX
@article{noor2026impact,
title = {{Impact of Asthma and Corticosteroid Exposure on Glycemic Markers in Overweight and Obese Children.}},
author = {Safa Noor and Alaa Abdelhamid and Yaman Al-Haneedi and Omar Tluli and Harshita Shailesh and Elwaseila Hamdoun and Mutasim Abu-Hasan and Ibrahim A Janahi},
journal = {Diabetes, metabolic syndrome and obesity : targets and therapy},
year = {2026},
month = oct,
doi = {10.2147/dmso.s614951},
url = {https://europepmc.org/article/MED/42921507},
note = {CC BY},
}
RIS
TY - JOUR
TI - Impact of Asthma and Corticosteroid Exposure on Glycemic Markers in Overweight and Obese Children.
AU - Safa Noor
AU - Alaa Abdelhamid
AU - Yaman Al-Haneedi
AU - Omar Tluli
AU - Harshita Shailesh
AU - Elwaseila Hamdoun
AU - Mutasim Abu-Hasan
AU - Ibrahim A Janahi
PY - 2026
DA - 2026/10/19
JO - Diabetes, metabolic syndrome and obesity : targets and therapy
DO - 10.2147/dmso.s614951
UR - https://europepmc.org/article/MED/42921507
AB - Purpose Corticosteroids are the cornerstone of asthma management, yet they are associated with hyperglycemia and insulin resistance. This study evaluated associations between asthma characteristics and glycemic markers in children with overweight or obesity and examined whether corticosteroid exposure modifies these associations.Methods This cross-sectional study included 199 children aged 6-17 years with overweight or obesity from the Middle East and North Africa region. They were divided into two groups: with asthma (OO-A) (N = 100) and without asthma (OO) (N = 99). Asthma phenotype was classified as type 2 (blood eosinophils ≥ 300 cells/µL, FeNO ≥ 30 ppb, or confirmed allergy) or non-type 2 asthma. Asthma severity was classified based on FEV₁% predicted: mild (≥ 80%), moderate (60% to < 80%), and severe (< 60%). Linear and logistic regression models assessed associations between asthma characteristics and glycemic markers in the circulation before and after adjusting for corticosteroid use.Results Asthma was associated with higher HbA1c (β = 0.152, p = 0.007) and prediabetes (HbA1c ≥ 5.7%) (OR = 2.69, p = 0.026) only when not adjusting for corticosteroid use. Mediation analysis showed that corticosteroid exposure may account for 45.4% of the total effect of asthma on HbA1c (p = 0.024). The OO group had a higher prevalence of insulin resistance (HOMA-IR ≥ 2.5) (p = 0.029). Type 2 asthma was associated with higher HbA1c without corticosteroid adjustment (β = 0.176, p = 0.002), which was attenuated after corticosteroid adjustment (β = 0.116, p = 0.057). Severe asthma remained significantly associated with higher HbA1c in both models regardless of corticosteroid adjustment (β = 0.347-0.409, p < 0.05). No consistent associations were found with other glycemic markers.Conclusion The asthma-HbA1c association in children with overweight/obesity may be largely mediated by corticosteroid use. Severe asthma may have a direct association with HbA1c independent of steroid use. Given the cross-sectional design and limited sample sizes, these findings require confirmation in larger longitudinal studies with more precise assessments of corticosteroid exposure and other confounders to clarify causal pathways and to evaluate whether optimizing asthma management while minimizing corticosteroid exposure could reduce long-term metabolic risk in this vulnerable population.
SN - 1178-7007
ER -