BackgroundObservational studies on osteoporotic fractures in patients with type 2 diabetes indicate their increased incidence compared to those without diabetes, but results are inconsistent. Currently, type 2 diabetes is not considered as an independent risk factor for low-energy fractures in elder subjects. The aim of the study was to assess the association between type 2 diabetes and risk for hip and vertebral fractures in postmenopausal women.Materials and methodsWe searched Medline, Web of Science and Cochrane databases for articles published before September 2013. Studies assessing fractures in women aged >50 diagnosed with type 2 diabetes, regardless of the diabetes treatment, were deemed eligible. To estimate fracture risk meta-analysis in a random effect model was performed. The results were shown by the odds ratio (OR) and 95 % confidence interval (CI). Heterogeneity was tested using a Q-Cochrane test (significance was analyzed with p < 0.10) and I 2 measure.ResultsA total of 15 observational studies (11 cohort and 4 cross-sectional, 263.006 diabetics and 502.115 controls) were included. Thirteen papers provided information on the incidence of hip fractures, and seven on vertebral ones. The meta-analysis revealed type 2 diabetes was associated with higher risk for hip fracture (OR 1.296, 95 % CI (1.069–1.571), but not vertebral fracture (OR = 1.134, 95 % CI (0.936–1.374). There was significant heterogeneity between hip fracture studies. American origin was identified as a potential source of such heterogeneity.ConclusionsThe results of our meta-analysis indicate there is an increased risk for hip fracture in postmenopausal women with type 2 diabetes.

The goal of the study was to investigate the possibility of an association between polymorphisms and single alleles of BsmI, ApaI, TaqI of the vitamin D receptor (VDR) gene with bone mineral density (BMD) and prevalence of vertebral/non-vertebral fractures in a group of postmenopausal Polish women with osteoporosis. The study group comprised of 501 postmenopausal females with osteoporosis (mean age 66.4 ± 8.9), who were diagnosed on the basis of either the WHO criteria or self-reported history of low-energy fractures. The three polymorphisms were determined by PCR (polymerase chain reaction) and RFLP (restriction fragment length polymorphism). BMD at the lumbar spine and femoral neck was assessed by dual energy X-ray absorptiometry (DXA). 285 fractures were reported in the whole group (168 vertebral and 117 non-vertebral). Incidence of non-vertebral fractures was significantly higher in the carriers of single alleles a of ApaI, b of BsmI and T of TaqI VDR gene polymorphisms (p = 0.021, 0.032, 0.020, respectively). No significant associations between allelic variants of the studied polymorphisms and BMD or fracture incidence were found. (1).The presence of single alleles a,b and T of ApaI, BsmI, TaqI VDR gene polymorphisms respectively, might serve as an indicator of non-vertebral fractures. (2). Lack of association between the VDR gene polymorphisms and BMD suggests that VDR contributes to low-energy fractures also through other ways.

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IntroductionPolymorphism in the promoter region of collagen type 1α (COL1A1) +1245G/T (Sp1, rs1800012) was in some studies shown to be relevant for bone mineral density (BMD) and low-energy fracture prediction. The aim of the study was to confirm this finding in a group of postmenopausal women diagnosed with osteoporosis.Material and methodsWe investigated 311 Caucasian women (mean age: 65.2 ±9.39 years) either after low-energy fractures (regardless of the location) or meeting World Health Organization (WHO) criteria for osteoporosis. All patients underwent clinical examination in order to exclude secondary osteoporosis; hip and lumbar spine DEXA was performed (Lunar). The three genotypes of Sp1 polymorphism were determined by RFLP (restriction fragment length polymorphism).ResultsDistribution of COL1A1 genotypes (SS/Ss/ss) agreed with Hardy-Weinberg equilibrium. No relation between COL1A1 genotypes and hip/L1-L4 BMD was found. Fractures were reported in 26.3% of women. Prevalence of low-energy fractures, regardless of the type, was 50.0% in ss genotype carriers, 26.4% in SS homozygotes and 23.7% in Ss heterozygotes. There was no statistically significant recessive or dominant effect of any Sp1 genotype on fracture prevalence (p = 0.613).ConclusionsWe failed to observe that COL1A1 Sp 1 genotypes contribute to BMD determination or are associated with prevalent low-energy fractures in a Polish cohort of postmenopausal osteoporotic women.

IntroductionEducational meetings are one of the most frequently used strategies to change doctors’ professional behavior; however, their effectiveness as a single intervention is limited. This study evaluated the effect of a multifactorial intervention, based on interactive workshops, on the GPs’ knowledge and the delivery rates of preventive procedures in primary care.Material and methodsThe study population comprised 106 GPs working in the Wielkopolska region recruited to the PIUPOZ program (Improving Quality in Primary Care). The intervention in the program consisted of lectures, interactive workshops and an audit, before and three months after the training. Trained medical students directly observed GPs to register which of 12 studied preventive procedures were performed during the consultation in patients aged 40+.ResultsA total of 1060 consultations were recorded, during which 4899 preventive procedures were delivered: 2115 before and 2784 after workshops. The mean number of preventive procedures per patient before and after workshops was 3.84 and 5.25 respectively (p < 0.0001). The most commonly performed preventive procedures were blood pressure, blood glucose and lipid profile measurement. Mean number of correct answers for 16 questions in the initial knowledge test was 8.7 and 12.7 in the final test (p < 0.0001).ConclusionsThe observed number of delivered preventive procedures was below the recommended range. Preventive procedures based on laboratory tests were performed more often than lifestyle counseling.

Graves' (GD) hyperthyroidism leads to reduced bone mineral density (BMD) accompanied by accelerated bone turnover. Ample studies have identified association between estrogen receptor (ESR1) gene polymorphism and decreased BMD and osteoporosis. In contrast, number of publications that link ESR1, BMD and Graves' disease is limited. The purpose of this study was to identify the association between ESR1 polymorphisms and BMD in premenopausal women with GD and to determine whether ESR1 polymorphic variants can predispose to GD. The study included 75 women aged 23-46 years with GD and 163 healthy controls. BMD was measured at lumbar spine and femoral neck. We investigated two SNPs in the ESR1 gene and analyzed genetic variants in the form of haplotypes reconstructed by statistical method. Three out of four possible haplotypes of the PvuII and XbaI restriction fragment length polymorphisms were found in GD patients: px (55.3 %), PX (33.3 %) and Px (11.4 %). Women homozygous for xx of XbaI and for pp of PvuII had the lowest BMD at lumbar spine. Moreover, the px haplotype predisposed to reduced lumbar BMD. No associations were observed for femoral neck BMD. No statistically significant relationship were found between ESR1 polymorphisms or their haplotypes and GD. These results indicate that the PvuII and the XbaI polymorphisms of ESR1 gene are associated with bone mineral density in premenopausal women with GD and may help to estimate the risk of bone loss particularly at lumbar spine. However, none of the ESR1 gene alleles predict the risk of GD in Polish female patients.