Elevated HbA1c Is Associated with Altered Cortical and Trabecular Microarchitecture in Girls with Type 1 Diabetes.


Journal

The Journal of clinical endocrinology and metabolism
ISSN: 1945-7197
Titre abrégé: J Clin Endocrinol Metab
Pays: United States
ID NLM: 0375362

Informations de publication

Date de publication:
01 04 2020
Historique:
received: 07 08 2019
accepted: 22 11 2019
pubmed: 26 11 2019
medline: 5 1 2021
entrez: 26 11 2019
Statut: ppublish

Résumé

Skeletal fragility is a significant complication of type 1 diabetes (T1D), with an increased risk of fracture observed starting in childhood. Altered bone accrual and microarchitectural development during the critical peripubertal years may contribute to this fragility. To evaluate differences in skeletal microarchitecture between girls with T1D and controls and to assess factors associated with these differences. Cross-sectional comparison. Girls ages 10-16 years, 62 with T1D and 61 controls. Areal bone mineral density (BMD) measured by dual-energy x-ray absorptiometry did not differ between girls with and without T1D. At the distal tibia, trabecular BMD was 7.3 ± 2.9% lower in T1D (P = 0.013), with fewer plate-like and axially-aligned trabeculae. Cortical porosity was 21.5 ± 10.5% higher, while the estimated failure load was 4.7 ± 2.2% lower in T1D (P = 0.043 and P = 0.037, respectively). At the distal radius, BMD and microarchitecture showed similar differences between the groups but did not reach statistical significance. After stratifying by HbA1c, only those girls with T1D and HbA1c > 8.5% differed significantly from controls. P1NP, a marker of bone formation, was lower in T1D while CTX and TRAcP5b, markers of bone resorption and osteoclast number, respectively, did not differ. The insulin-like growth factor 1 (IGF-1) Z-score was lower in T1D, and after adjustment for the IGF-1 Z-score, associations between T1D status and trabecular microarchitecture were largely attenuated. Skeletal microarchitecture is altered in T1D early in the course of disease and among those with higher average glycemia. Suppressed bone formation and lower circulating IGF-1 likely contribute to this phenotype.

Identifiants

pubmed: 31761940
pii: 5639696
doi: 10.1210/clinem/dgz221
pmc: PMC7064304
pii:
doi:

Substances chimiques

Biomarkers 0
Blood Glucose 0
Glycated Hemoglobin A 0
hemoglobin A1c protein, human 0

Banques de données

ClinicalTrials.gov
['NCT02140424']

Types de publication

Journal Article Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Subventions

Organisme : NIDDK NIH HHS
ID : K23 DK105350
Pays : United States
Organisme : NICHD NIH HHS
ID : K24 HD071843
Pays : United States
Organisme : NCRR NIH HHS
ID : S10 RR023405
Pays : United States
Organisme : NCRR NIH HHS
ID : UL1 RR025758
Pays : United States

Informations de copyright

© Endocrine Society 2019. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

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Auteurs

Deborah M Mitchell (DM)

Endocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts.
Pediatric Endocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts.

Signe Caksa (S)

Endocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts.

Taïsha Joseph (T)

Endocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts.

Mary L Bouxsein (ML)

Endocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts.
Center for Advanced Orthopaedic Studies, Beth Israel Deaconness Medical Center and Harvard Medical School, Boston, Massachusetts.

Madhusmita Misra (M)

Pediatric Endocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts.
Neuroendocrine Unit, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts.

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Classifications MeSH