Інформація призначена тільки для фахівців сфери охорони здоров'я, осіб,
які мають вищу або середню спеціальну медичну освіту.


Підтвердіть, що Ви є фахівцем у сфері охорони здоров'я.

"Pain. Joints. Spine." 1 (21) 2016

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Bone quality in diabetic patients

Authors: Jackuliak P., Kuzma M. - Medical Faculty of Comenius University, 5th Department of Internal Medicine, University Hospital, Bratislava, Slovakia; Vanuga P. - National Institute of Endocrinology and Diabetology, Ľubochňa, Slovakia; Killinger Z., Payer J. - Medical Faculty of Comenius University, 5th Department of Internal Medicine, University Hospital, Bratislava, Slovakia

Categories: Rheumatology, Traumatology and orthopedics

Sections: Medical forums

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The article was published on p. 73-74

 

Introduction. Patients with both types of diabetes are known to have an increased risk of fractures. While in type 1 diabetes the major reason is low bone mass, patients with type 2 diabetes are at an increased risk despite increase/-ed bone mineral density (BMD) and this is caused by inferior quality of bone. The association between glyceamic compensation and diabetic complications or comorbidities is well known. Various trials observed that poor glycemic control is associated with higher all types of fracture risk. 

Objective. To determine the role of metabolic compensation measured by A1c haemoglobin (HbA1c) on bone quality measured by trabecular bone score (TBS) and also on BMD in T2DM patients.
Patients and methods. A cross-sectional trial in 56 women patients with T2DM and 30 controls without DM. Mean age of the patients was 51.2 ± 6.1 years. The mean duration of diabetes was 10.3 ± 5.8 yrs. All patients were treated only by oral antidiabetic drugs (metformin and DPP-4), not by insulin. The BMD at lumbar spine (LS), femoral neck (FN) were measured at baseline and after 1 year of treatment by dual energy X-ray absorptiometry (DXA, Hologic). TBS was performed by TBS Insight software (Medimaps, France) from LS DXA scans.
Results. Diabetes was associated with higher BMD than the control group (1.008 ± 0.175 g/cm2 vs 0.961 ± 0.176 g/cm2, p = 0.05). The LS-TBS was lower in T2DM than in control group (1.172 ± 0.120 vs 1.304 ± 0.018, p < 0.001). HbA1c was an important determinant effecting BMD (r = −0.30, p < 0.05) and TBS (r = −0.35, p = 0.01). But the cut-off was 8.5 % for BMD and 7.9 % respectively.
Conclusion. Our datas confirm, that poor glycemic control based on an HbA1c is a important determinat for BMD as a marker of bone quantity and also TBS, a marker of bone quality. It seems that the cut-off levels of HbA1c are others for BMD respectivelly TBS. Reliable HbA1c cut-offs need to be determined in larger prospective studies. Limitations of are trial are, that there can be other factors affecting the correlations like duration of diabetes, treatment modalities, other diabetic complications.   

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