RESUMO
Objectives: Bone metabolism is impaired in diabetes mellitus (DM). Our objective is to evaluate the association of bone turnover markers (BTM) and vitamin D receptor (VDR) gene polymorphisms with bone mineral density (BMD) in DM type 1 (T1D) and DM type 2 (T2D). Methods: A total of 165 patients (53 T1D and 112 T2D) were enrolled. BMD was measured by dual-energy X-ray absorptiometry (DEXA). Plasma osteocalcin (OC), beta-CrossLaps (ß-CTX) and N-amino terminal propeptide of type I collagen (P1NP) and VDR gene polymorphisms were evaluated. Results: Participants were 53 T1D (41 years [31-48]) and 112 T2D (60 years [51-66]). BMD were not statistically different between the groups. OC (p<0.001) and P1NP levels (p<0.001) were higher in patients with T1D. The areas under the curve for the prediction of bone pathology were 0.732 (p=0.038) for OC in T1D and 0.697 (p=0.007) in T2D. A significant association was found between lower lumbar BMD and the A allele of BsmI (p=0.03), the A allele of ApaI (p=0.04) and the allele C of the Taql (p=0.046). Also, a significant correlation was found with higher OC levels and the G allele of BsmI (p=0.044), C allele of ApaI (p=0.011), T allele of Taql (p=0.006) and with C allele of FokI (p=0.004). Conclusions: The high negative predictive value of the cut-off point for OC suggests that could be useful in excluding the risk suffering bone loss, allowing offering a personalized clinical approach to prevent this pathology.
RESUMO
Type 2 diabetes mellitus prevalence and morbidity are increasing. Osteoporotic fractures are among the 'non-classical' complications of diabetes and been overlooked for a long time, maybe because of their complex diagnostic and therapeutic approach. The usual tools for preventing fragility fractures (such as the fracture risk assessment tool and bone densitometry) underestimate risk of fractures in type2 diabetic patients. New techniques, such as trabecular bone score or bone turnover markers, could be useful, but greater scientific evidence is required to recommend their use in clinical practice. The special characteristics of their pathophysiology result in decreased bone remodeling with normal or even increased bone mineral density, but with low quality. These changes lead to the occurrence of osteoporotic fractures without evidence of densitometric changes, which could be called 'the diabetic paradox'.