Context primary hyperparathyroidism (PHPT) has been related to bone loss. Dual-energy X-ray absorptiometry (DXA) cannot distinguish between trabecular and cortical bone compartments but the recently developed 3D-DXA software might overcome this issue. Objective to examine the differences in DXA-derived areal bone mineral density (aBMD) and 3D-DXA parameters at the hip site between patients with PHPT and a healthy control group. Design cross-sectional pilot study Setting hospital Patients 80 adults (59.5 ± 9.1 yrs), 40 with PHPT and 40 healthy age- and sex-matched healthy controls. Measures aBMD (g/cm²) of the femoral neck, trochanter, shaft and total hip was assessed using DXA. Cortical surface (sBMD, mg/cm²), cortical volumetric BMD (vBMD, mg/cm³), trabecular vBMD (mg/cm³), integral vBMD (mg/cm³) and cortical thickness (mm) was assessed using 3D-DXA software. Results mean-adjusted values showed lower aBMD (7.5% to 12.2%, effect size: 0.51-1.01) in the PHPT group compared to the control group (all p<0.05). 3D-DXA revealed bone impairment (3.7% to 8.5%, effect size: 0.47-0.65) in patients with PHPT, mainly in cortical parameters (all p<0.05). However, differences in trabecular vBMD were not statistically significant (p=0.055). The 3D mapping showed lower cortical sBMD, cortical vBMD and cortical thickness at the trochanter and diaphysis in the PHPT group (p<0.05) compared to the control group. In both groups, the presence of osteopenia or osteoporosis is related to lower cortical bone. Conclusions aBMD and cortical 3D parameters are impaired in patients with PHPT versus healthy controls. The vBMD of the trabecular compartment seems to be affected though to a lower extent.

Background/Objectives: Patients with chronic hypoparathyroidism are at increased risk of kidney complications. Also, chronic kidney disease is associated with increased cardiovascular risk. The aim was to analyze the factors that influence kidney function, including cardiovascular diseases (CVD), in a cohort of patients with chronic hypoparathyroidism. Methods: This was a retrospective longitudinal study that included 100 patients with chronic hypoparathyroidism. Results: The estimated glomerular filtration rate (eGFR) was associated with the duration of disease (p = 0.014). During follow-up, a significant decrease in eGFR was observed over time (p < 0.001), and changes in the eGFR were associated with the duration of disease (p < 0.001). We found that the eGFR was lower in patients with urolithiasis (p = 0.003), hypertension (p < 0.001), type 2 diabetes (p = 0.031) and dyslipidemia (p < 0.001). In total, 14% of patients had a chronic kidney disease (CKD), and these patients had a longer duration of disease (p < 0.001). The percentage of patients with urolithiasis (p = 0.003), nephrocalcinosis (p = 0.008), hypertension (p = 0.005), type 2 diabetes (p < 0.001), dyslipidemia (p < 0.001), coronary heart disease (p = 0.008), and arrhythmia (p < 0.001) was higher in patients with CKD. Logistic regression models showed that disease duration was associated with CKD (OR = 1.11; 95% CI [1.03–1.22]; p = 0.008). We used ROC curves to assess the usefulness of disease duration as a marker of CKD, and the AUC was 0.850 (95% CI 0.763–0.937, p < 0.001). A duration of disease > 15.5 years had a sensitivity of 85.7% and a specificity of 71.9% for a diagnosis of CKD. Conclusions: The duration of disease appears to be a predictor of the presence of renal dysfunction in patients with chronic hypoparathyroidism. In addition, the coexistence of CVD factors could result in greater renal damage.

Frailty is a multidimensional syndrome of reduced physiological reserve that is particularly prevalent in individuals with type 2 diabetes. Identifying objective biochemical markers to complement clinical screening tools, such as the FRAIL scale, is an increasingly important unmet need. Periostin, a matricellular protein involved in tissue remodeling, bone metabolism, and chronic complications of diabetes, has emerged as a potential candidate. In this cross-sectional study of 137 adults with type 2 diabetes (65 ± 8 years), participants were classified as robust, pre-frail, or frail according to FRAIL scores. Frailty correlated positively with age (p < 0.001), BMI (p = 0.006), waist circumference (p = 0.01), and diabetes duration (p = 0.040), and negatively with TBS (p = 0.001), HDL-c (p = 0.040), and eGFR (p = 0.009). A stronger positive correlation was observed with serum periostin (p < 0.001). Frail individuals showed higher periostin levels than pre-frail (p = 0.006) and robust participants (p = 0.008), independent of age. Periostin demonstrated moderate discriminatory capacity for frailty status (AUC = 0.710; p < 0.001), while adding periostin to clinical variables resulted in a numerical increase in overall model discrimination (AUC = 0.900 vs. 0.858). A threshold of >1307 pmol/L yielded 77.8% sensitivity and 66.7% specificity. These preliminary findings indicate that periostin is significantly associated with frailty in type 2 diabetes and may represent a complementary biochemical biomarker of frailty status, warranting further validation in longitudinal studies.