ACTA ENDOCRINOLOGICA (BUC)

Introduction. Vitamin D [25(OH)D] deficiency is prevalent in chronic kidney disease (CKD), related to bone turnover and potentially involved in arterial calcifications. Objective. To evaluate vitamin D status in nondialysis CKD patients and its relationships with bone turnover markers (BTM) and arterial calcifications. Design. Cross-sectional, prospective, multicentric study. Subjects and methods. One hundred twenty-eight CKD patients (median age 61 years, 58% males, median eGFR 29mL/min) were included. Comorbidities, mineral and bone metabolism parameters were evaluated. Total alkaline phosphatase (T-ALP) was used to assess bone turnover. Atherosclerosis was evaluated by carotid intima-media thickness (CIMT), endothelial calcifications by aortic calcification score (ACS), and arterial stiffness by cardio-ankle vascular index (CAVI). Vitamin D deficiency was defined as 25(OH)D <15 ng/mL. Factors associated with vitamin D, T-ALP and vascular parameters were assessed in multivariate regression models. Results. Prevalence of vitamin D deficiency was 63% and median 25(OH)D was 12.8 ng/mL. Older age, female sex and higher parathormone were predictors of vitamin D deficiency. Increased T-ALP was predicted by higher parathormone, suggesting high turnover bone disease. While age was a determinant of all evaluated vascular parameters, lower 25(OH)D was associated only with endothelial calcifications, which correlated with CAVI, suggesting a direct relation between vitamin D deficiency mediated plaques calcification and arterial stiffness. Conclusion. Vitamin D deficiency was highly prevalent in this non-dialysis CKD cohort and was related to age, sex and parathormone. Vitamin D deficiency was associated with increased calcifications of endothelial plaques, which seemed to increase arterial stiffness.

Parathyroid imaging modalities have been used to guide clinicians and surgeons in finding the source of hyperparathyroidism for over 40 years. Primary hyperparathyroidism (PHPT) is generally caused by a parathyroid gland(s) autonomous production of parathyroid hormone (PTH), associated by enlargement of one or more glands. Noninvasive imaging procedures that are used in the management of hyperparathyroidism are anatomical (ultrasound, computer tomography, magnetic resonance imaging) and/or functional (nuclear medicine techniques: planar scintigraphy, single photon emission tomography, positron emission imaging) and/or hybrid imaging.

Introduction. Primary osteoporosis during childhood and adolescence represents an uncommon condition, and secondary forms are more likely to manifest at this age due to chronic disease and adverse effects of medical treatment. Case report. The authors report the case of a young male patient with a history of multiple idiopathic nonvertebral fragility fractures in addition to a family history of maternal osteoporosis and fracture, in whom osteoporosis was confirmed according to 2013 International Society for Clinical Densitometry (ISCD) criteria. Bone markers indicated low bone formation marker osteocalcin. Genetic testing revealed homozygosity for Sp1 COL1A1 gene polymorphism in combination to Fok-I vitamin D receptor (VDR) heterozygous polymorphism, to contribute to low bone mass and increased fracture risk. Severe premenopausal osteoporosis was present in the patient’s mother, who was also tested positive for both gene polymorphisms. Conclusion. This case report highlights the association between COL1A1 and VDR candidate gene polymorphisms and fragility fractures in a family. Individual genetic testing might be of clinical value in idiopathic osteoporosis in young patients, identifying subjects at increased fracture risk.

Background. Weight loss associated with long-term lifestyle changes has significant beneficial effects on metabolic syndrome (MetS) features on obese patients; unfortunately, the weight recidivism rate is high and the weight fluctuations could increase the cardiovascular and metabolic risk. On the other hand, there are many data about the endocrine role of adipose tissue. Objective. Taking into account the imbalance between pro-inflammatory and anti-inflammatory cytokines secreted by adipose tissue on obese patients, this study assessed the effects of one month-long supervised lifestyle change (SLC) program without weight loss on the MetS-associated inflammatory status. Methods. The study included 29 obese adults with MetS. The SLC program included supervised moderate physical activities and diet for one month. The levels of adipocytokines, lipids and inflammatory markers were analyzed before and after one month SLC program, and 2 months later at follow-up. Results. At follow-up, the leptin, vascular endothelial growth factor (VEGF), and hsCRP levels decreased, whereas the interleukin-4 (IL-4) and high-density lipoprotein (HDL) cholesterol levels increased from their baseline levels. So, an SLC program, even in the absence of weight loss, could have an extended antiinflammatory effect by decreasing the proinflammatory adipocytokines. Conclusion. Our data furthermore emphasize the importance of the adipocytokines gender-related variation for a more personalized evaluation protocol on obese patients.

Introduction. Relative adrenal insufficiency (RAI) is common in the setting of critical illness as well as in hemodynamically instable cirrhotic patients with sepsis. Several studies have also shown that RAI is frequent in patients with stable cirrhosis without sepsis. The aim of this study was to prospectively assess the incidence of RAI in patients with stable cirrhosis. Patients and Methods. Forty-seven patients with hemodynamically stable liver cirrhosis without sepsis were prospectively included. RAI, assessed by using low doseshort Synacthen test (LD-SST), was defined as either a basal total cortisol concentration below 3.6 μg/dL or a peak total serum cortisol ≤ 16 μg/dL at 30 min after stimulation. Results. RAI was present in 10 (21.3%) of 47 cirrhotic patients. Peak cortisol level was negatively correlated with the severity of cirrhosis evaluated by Child- Turcotte-Pugh (CTP) (r=-0.46; P=0.001) and Model for End- Stage Liver Disease (MELD) (r=-0.51; P=0.001) scores. The frequency of RAI increased from CTP-A (10%) to CTP-B (30%) to CTP-C (60%). Conclusion. RAI diagnosed by LD-SST is frequent in patients with stable cirrhosis and is related to the severity of liver disease. Further studies are needed to define clinical importance of RAI in stable cirrhotic patients.

Context. Benefits of vitamin D therapies in chronic kidney disease (CKD) are debated. Objective. To compare the effects of medium-term native (VitD) and active (VDRA) vitamin D on parameters of mineral metabolism and arterial function in non-dialysis CKD. Design. Open-label, active comparator, randomized study. Subjects and Methods. Forty-eight adult patients, vitamin D naïve, CKD stage 3 to 5 with increased parathyroid hormone (iPTH) were randomized to receive either oral cholecalciferol 1000UI/day (n=24) or paricalcitol 1mcg/day (n=24) for 6 months. Median changes at end of study vs. baseline in serum calcidiol, iPTH, total alkaline phosphatase (ALP), and cardio-ankle vascular index (CAVI) were the efficacy parameters. Results. Higher increase in calcidiol (15.5 [95%CI 13.3; 17.2] vs. 0.4 [95%CI −6.1; 3.7]ng/mL, p<0.001) were found in VitD group. Conversely, the decline of iPTH (−35.2 [95%CI −83; 9] vs. 13.3 [95%CI −8.1; 35]pg/mL, p=0.008) and ALP (−34 [95%CI −58; −11] vs. −10 [95%CI −23; −2] U/L, p=0.02) were greater after paricalcitol. More subjects experienced iPTH decrease in VDRA group (71% vs. 39%, p=0.03). The variation in CAVI and the incidence of hypercalcemia and hyperphosphatemia were similar. Conclusions. It seems that secondary hyperparathyroidism was more efficiently treated by VDRA, whereas cholecalciferol better corrected the calcidiol deficiency in non-dialysis CKD.