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Background: Our previous research in an experimental model of current environmental human exposure to cadmium (Cd) (female rats fed a diet containing Cd at 1 and 5 mg/kg for up to 2 years) revealed that chronic treatment with this toxic element destroyed the metabolism of the bone tissue, decreased mineralisation, and weakened bone biomechanical properties, whereas the co-administration of a 0.1% chokeberry (Aronia melanocarpa L. (Michx.) Elliott berry) extract (AME) ameliorated the osteotoxic action of Cd. Methods: In this study, it was explored whether the unfavourable effect of Cd and the protective action of AME might be mediated by the impact on the metabolism of bone essential elements such as calcium (Ca) and inorganic phosphorus (Pi), including the pathways of its regulation by calciotropic hormones (parathormone—PTH, calcitonin—CT, and 1,25-dihydroxyvitamin D3—1,25(OH)2D3) and Klotho. Results: Low-level Cd treatment (1 mg/kg) caused only a temporary elevation in the serum PTH concentration and a decline in the concentration of CT. Moderate treatment with Cd (5 mg/kg) destroyed the body homeostasis of both mineral elements (lowered their concentrations in the serum and enhanced urinary loss), influenced the serum concentrations of Klotho and calciotropic hormones, as well as reduced the concentrations of 25-hydroxyvitamin D 1alpha-hydroxylase (1alpha-OHase) and 1,25(OH)2D3 in the kidney. The application of AME during Cd intoxication improved the pathways involved in maintaining Ca and Pi homeostasis and allowed subjects to maintain the proper levels of these elements in the serum and urine. Conclusions: In conclusion, Cd at low-to-moderate exposure may exert an unfavourable impact on bone by influencing the pathways involved in regulating Ca and Pi metabolism and destroying the body status of these minerals. It seems that the possible mechanism of the osteoprotective effect of AME during chronic intoxication with this toxic element involves normalization of the concentrations of calciotropic hormones and Klotho in the serum and improvement of the homeostasis of Ca and Pi. This study provided further evidence that chokeberry products may be an effective strategy in counteracting the unfavourable effects of chronic low-to-moderate exposure to Cd. [ABSTRACT FROM AUTHOR]

Background: Parathyroidectomy has been shown to reduce cardiovascular risk factors in some studies, although findings on these parameters remain inconsistent. Objectives: This study aimed to evaluate inflammatory and cardiovascular risk markers in patients with Primary Hyperparathyroidism (PHPT) before and one month after successful parathyroidectomy (PTX). Methods: We retrospectively analyzed PHPT patients who visited the outpatient clinic between 2015 and 2020. Patient demographics, hemogram data, calcium, parathormone (PTH), vitamin D, high-density lipoprotein (HDL), mean platelet volume (MPV), neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and monocyte-to-HDL ratio (MHR) were recorded and compared pre- and postoperatively. Results: The analysis revealed significant postoperative increases in platelet, MPV, HDL, PLR, and vitamin D levels (p = 0.001, p = 0.001, p = 0.001, p = 0.024, p = 0.001, respectively). Conversely, PTH, calcium, NLR, and MHR levels significantly decreased (p = 0.001, p = 0.001, p = 0.011, p = 0.019, respective-ly). Correlation analysis demonstrated a negative association between postoperative PTH and vitamin D (p = 0.010, r = -0.292**) and a positive association between postoperative PTH and both calcium (p = 0.008, r = 0.309**) and NLR (p = 0.046, r = 0.227**). Multivariable regression analysis demonstrated that postoperative PTH levels were significantly associated with calcium (B = 39.82, Beta = 0.321, p = 0.0469), NLR (B = 110.02, Beta = 0.428, p = 0.0384), baseline comorbidity scores (B = -30.54, Beta = -0.287, p = 0.0361), and preoperative inflammation levels (B = 25.69, Beta = 0.311, p = 0.0386). Conclusion: Our findings highlight a potential link between PHPT and inflammatory-cardiovascular risk, with parathyroidectomy exerting a beneficial effect within the first month post-surgery. The study also suggests that these risk factors may be modifiable with timely surgical intervention. Clinical trial number: Not applicable. [ABSTRACT FROM AUTHOR]

Background: Teriparatide (TPT) acts against severe primary (postmenopausal) osteoporosis (MOP), and it requires continuation with another anti-resorptive drug to conserve or enhance the effects on fracture risk reduction. Objective: To analyse the sequential pharmacotherapy in MOP who were treated upon a 24-month daily 20 µg TPT protocol (24-mo-TPT) followed by another 12 months of anti-resorptive drugs (12-mo-AR) amid real-life settings. Hypotheses: 1. TPT candidates had a more severe fracture risk profile versus those who did not fulfil the TPT criteria according to the national protocol of TPT initiation; 2. Patients treated with TPT improved their DXA profile after 24 mo; 3. After 1 year of therapy since the last TPT injection, the improved bone profile and fracture risk at the end of the TPT protocol were conserved; 4. The mineral metabolism assays and fracture risk status were similar at TPT initiation between those who finished the 24 mo protocol and those who prematurely stopped it. Methods: This was a longitudinal, retrospective, multicentre study in MOP. The entire cohort (group A) included the TPT group (B) versus the non-TPT group (non-B). Group B included subjects who finished 24-mo-TPT (group P) and early droppers (ED), and then both continued 12-mo-AR. Results: Group B (40.5%) from cohort A (N = 79) vs. non-B had lower T-scores, increased age and years since menopause. A similar profile of demographic features, BTM, and prevalent fractures (73%, respectively, 57%) was found in group P (72%) vs. ED (21.8%). Group P: osteocalcin was statistically significantly higher at 12 mo (+308.39%), respectively, at 24 mo (+171.65%) vs. baseline (p < 0.001 for each), while at 12-mo-AR became similar to baseline (p = 0.615). The cumulative probability of transient hypercalcemia-free follow-up of protocol had the highest value of 0.97 at 6 mo. An incidental fracture (1/32) was confirmed under 24-mo-TPT. BMD had a mean percent increase at the lumbar spine of +8.21% (p < 0.001), of +12.22% (p < 0.001), respectively, of +11.39% (p < 0.001). The pharmacologic sequence for 12-mo-AR included bisphosphonates (24.24% were oral BP) or denosumab (13%). BTM showed a suppression at 12-mo-AR (p < 0.05), while all BMD/T-scores were stationary. No incidental fracture was registered during 12-mo-AR. Conclusions: All research hypotheses were confirmed. This study in high-risk MOP highlighted an effective sequential pharmacotherapy in reducing the fracture risk as pinpointed by BMD/T-score measurements and analysing the incidental fractures profile. [ABSTRACT FROM AUTHOR]

Background/Objectives: Kenny–Caffey syndrome 2 (KCS2) is a rare cause of hypoparathyroidism, inherited in an autosomal dominant mode, resulting from pathogenic variants of the FAM111A gene, which is implicated in intracellular pathways regulating parathormone (PTH) synthesis and skeletal and parathyroid gland development. Methods: The case of a boy is reported, presenting with the characteristic and newly identified clinical, biochemical, radiological, and genetic abnormalities of KCS2. Results: The proband had noticeable dysmorphic features, and the closure of the anterior fontanel was delayed until the age of 4 years. Biochemical evaluation at several ages revealed persistent hypocalcemia, high normal phosphorous, and inappropriately low normal PTH. To exclude other causes of short stature, the diagnostic approach revealed low levels of IGF-1, and on CNS MRI, small pituitary gland and empty sella. Nocturnal levels of growth hormone were normal. MRI also revealed bilateral symmetrical microphthalmia and torturous optic nerves. Skeletal survey was compatible with cortical thickening and medullary stenosis of the long bones. Genomic data analysis revealed a well-known pathogenic variant of the FAM111A gene (c.1706G>A, p. R569H), which is linked with KCS2 or nanophthalmos. Conclusions: KCS2, although a rare disease, should be included in the differential diagnosis of hypoparathyroidism and short stature. Understanding the association of pathogenic variants with KCS2 phenotypic variability will allow the advancement of clinical genetics and personalized long-term follow-up and will offer insights into the role of the FAM111A gene in the disease pathogenesis and normal embryogenesis of implicated tissues and organs. [ABSTRACT FROM AUTHOR]

Abstract Background Parathyroidectomy has been shown to reduce cardiovascular risk factors in some studies, although findings on these parameters remain inconsistent. Objectives This study aimed to evaluate inflammatory and cardiovascular risk markers in patients with Primary Hyperparathyroidism (PHPT) before and one month after successful parathyroidectomy (PTX). Methods We retrospectively analyzed PHPT patients who visited the outpatient clinic between 2015 and 2020. Patient demographics, hemogram data, calcium, parathormone (PTH), vitamin D, high-density lipoprotein (HDL), mean platelet volume (MPV), neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and monocyte-to-HDL ratio (MHR) were recorded and compared pre- and postoperatively. Results The analysis revealed significant postoperative increases in platelet, MPV, HDL, PLR, and vitamin D levels (p = 0.001, p = 0.001, p = 0.001, p = 0.024, p = 0.001, respectively). Conversely, PTH, calcium, NLR, and MHR levels significantly decreased (p = 0.001, p = 0.001, p = 0.011, p = 0.019, respective-ly). Correlation analysis demonstrated a negative association between postoperative PTH and vitamin D (p = 0.010, r = -0.292**) and a positive association between postoperative PTH and both calcium (p = 0.008, r = 0.309**) and NLR (p = 0.046, r = 0.227**). Multivariable regression analysis demonstrated that postoperative PTH levels were significantly associated with calcium (B = 39.82, Beta = 0.321, p = 0.0469), NLR (B = 110.02, Beta = 0.428, p = 0.0384), baseline comorbidity scores (B = -30.54, Beta = -0.287, p = 0.0361), and preoperative inflammation levels (B = 25.69, Beta = 0.311, p = 0.0386). Conclusion Our findings highlight a potential link between PHPT and inflammatory-cardiovascular risk, with parathyroidectomy exerting a beneficial effect within the first month post-surgery. The study also suggests that these risk factors may be modifiable with timely surgical intervention. Clinical trial number Not applicable.

Previous studies have shown the protective effects of vitamin D supplementation against urinary tract infection (UTI). However, there are a few contradictory studies on the negative effect of vitamin D supplementation on UTI. Our objective was to establish whether there existed a relationship between serum vitamin D levels and UTIs in children. This study compared the serum 25-hydroxy vitamin D [25(OH)D] levels of children diagnosed with UTIs with those of healthy children (control group). We found a high rate of 25(OH)D deficiency in both the control and case groups (90% and 66.7%, respectively). Therefore, we added the laboratory parameters calcium, phosphate, and parathormone (PTH) to our analysis. We assessed the medical records of 60 patients diagnosed with UTIs and 20 healthy controls. The mean serum 25(OH)D level and PTH level were significantly higher in the patient group than in the control group. The PTH level was significantly lower in the acute pyelonephritis (APN) group than in the control group (p=0.016). Phosphate levels in the APN group were significantly lower than those in the control and cystitis groups (p=0.04, p=0.006 respectively). Because there was no correlation between 25(OH)D level and UTI, we concluded that 25(OH)D had no effect on UTI. [ABSTRACT FROM AUTHOR]

Purpose: Cardiometabolic disorders are non-classical complications of hypercalcemic primary hyperparathyroidism (HC-PHPT), but whether this risk connotes normocalcemic PHPT (NC-PHPT) remains to be elucidated. We investigated cardiometabolic alterations in both forms of PHPT, looking for their association with indices of disease activity. Methods: Patients with HC-PHPT (n = 17), NC-PHPT (n = 17), and controls (n = 34) matched for age, sex, and BMI were assessed for glucose, lipid, blood pressure alterations, and history of cardiovascular events to perform a case–control study at an ambulatory referral center for Bone Metabolism Diseases. Results: NC-PHPT, in comparison to controls, showed similar glucose (mean ± SD, 88 ± 11 vs 95 ± 22 mg/dl), total cholesterol (199 ± 25 vs 207 ± 36 mg/dl), and systolic blood pressure levels (SBP, 132 ± 23 vs 132 ± 19 mmHg), together with a comparable frequency of glucose alterations (6% vs 9%), lipid disorders (41% vs 50%) and hypertension (53% vs 59%, p = NS for all comparisons). Conversely, all these abnormalities were more prevalent in HC-PHPT vs controls (p < 0.05). When compared to NC-PHPT, HC-PHPT showed higher glucose (113 ± 31 mg/dl), total cholesterol (238 ± 43 mg/dl), and SBP levels (147 ± 15 mmHg) as well as an increased frequency of glucose (41%) and lipid alterations (77%) and a higher number of cardiovascular events (18% vs 0%, p < 0.05 for all comparisons). Among indices of PHPT activity, calcium levels displayed a significant correlation with glucose (R = 0.46) and SBP values (R = 0.60, p < 0.05). Conclusion: NC-PHPT is not associated with cardiovascular alterations. The predominant pathogenetic role of hypercalcemia in the development of cardiometabolic disorders could account for the absence of such alterations in NC-PHPT. [ABSTRACT FROM AUTHOR]

Background and Objectives: Uric acid (UA) and the markers of mineral bone metabolism and inflammation are commonly altered in patients with chronic kidney disease (CKD) and are associated with the risk of cardiovascular complications and death. Studies point to a link between high serum UA and mineral bone homeostasis and inflammation, but controversy remains. The aim of this study was to evaluate the relationship between UA levels and mineral bone metabolism and inflammation biomarkers in a sample of Mexican patients with CKD 3a–5. Materials and Methods: This cross-sectional study included 146 Mexican patients with CKD 3a–5. In addition, 25 healthy subjects were included in the study with the aim of generating reference data for comparisons. Metabolic parameters including UA serum concentrations, mineral bone metabolism (parathormone (PTH), fibroblast growth factor 23 (FGF23), calcium, and phosphate), and inflammation (interleukin (IL)-1β, IL-6, and tumor necrosis factor-alpha (TNF-α)) biomarkers were measured in all of the samples and compared as a function of the estimated glomerular function rate (eGFR) or UA levels. Results: Intact PTH, FGF23, and cytokines were higher in advanced CKD stages. Patients with hyperuricemia had significantly higher values of FGF23 and TNF-α compared with those without hyperuricemia. The eGFR was found to be significantly and negatively correlated with all markers. Uric acid was significantly correlated with phosphate, iPTH, FGF23, and TNF-α, whereas iPTH was significantly correlated with FGF23, TNF-α, and FGF23. Finally, a multivariate analysis confirmed the relationship of eGFR with all the tested biomarkers, as well as other relationships of iPTH with UA and TNF-α and of FGF23 with UA and TNF-α. Conclusions: This study supports the relationship between uric acid and levels of mineral bone metabolism and inflammation biomarkers in patients with CKD at middle to advanced stages. In the follow-up of patients with CKD, monitoring and controlling UA levels through nutritional or pharmacological interventions could help in the prevention of alterations related to mineral bone metabolism. [ABSTRACT FROM AUTHOR]

Background/Objectives: Type II diabetes mellitus (T2DM) is recognized as a condition of mild chronic inflammation, marked by increased levels of acute-phase proteins and various inflammatory indicators. These inflammatory substances, along with inflammation of adipose tissue and the secretion of adipocytokines, can contribute to insulin resistance and β cell dysfunction. By influencing both innate and adaptive immunity, vitamin D can inhibit the production of inflammatory cytokines and help mitigate the low-grade chronic inflammation associated with T2DM. Several strategies have been proposed to increase vitamin D levels effectively and safely, but the recent and strong ones have common tactics. Short-term high doses increase the level acutely, and long-term lower doses maintain sufficient levels. Methods: The aim of our work was to determine and verify the effectiveness of high doses of vitamin D to safely increase its level in patients with type 2 diabetes mellitus, as well as the effect of these doses on selected metabolic parameters. Data from 20 studies (vitamin D group n = 612, and control group n = 592) regarding the influence of vitamin D supplementation with doses above 4000 IU on serum 25(OH)D, fasting blood glucose (FBG), hemoglobin A1c (HbA1c), blood pressure, serum calcium, and parathormone were pooled. Results: Vitamin D supplementation significantly improved serum 25(OH)D levels, with an average increase after intervention versus baseline at 177.09%. Our studies suggest that vitamin D supplementation may benefit various parameters in T2DM patients, including glycemic control, blood pressure, and PTH levels. Conclusions: Vitamin D supplementation may have beneficial effects on various parameters in type 2 diabetes patients, including glycemic control, blood pressure, and parathormone levels. However, the results are only sometimes consistent across all studies. Further examination is needed. [ABSTRACT FROM AUTHOR]

Objective: We used machine learning to develop and validate a multivariable algorithm allowing the accurate and early prediction of postoperative hypocalcemia risk. Background: Postoperative hypocalcemia is frequent after total thyroidectomy. An early and accurate individualized prediction of the risk of hypocalcemia could guide the selective prescription of calcium supplementation only to patients most likely to present with hypocalcemia after total thyroidectomy. Methods: This retrospective study enrolled all patients undergoing total thyroidectomy in a single referral center between November 2019 and March 2022 (derivation cohort) and April 2022 and September 2022 (validation cohort). The primary study outcome was postoperative hypocalcemia (serum calcium under 80 mg/L). Exposures were multiple clinical and biological variables prospectively collected and analyzed with various machine learning methods to develop and validate a multivariable prediction algorithm. Results: Among 610/118 participants in the derivation/validation cohorts, 100 (16.4%)/26 (22%) presented postoperative hypocalcemia. The most accurate prediction algorithm was obtained with random forest and combined intraoperative parathyroid hormone measurements with 3 clinical variables (age, sex, and body mass index) to calculate a postoperative hypocalcemia risk for each patient. After multiple cross-validation, the area under the receiver operative characteristic curve was 0.902 (0.829--0.970) in the derivation cohort, and 0.928 (95% CI: 0.86; 0.97) in the validation cohort. Postoperative hypocalcemia risk values of 7% (low threshold) and 20% (high threshold) had, respectively, a sensitivity of 92%, a negative likelihood ratio of 0.11, a specificity of 90%, and a positive of 7.6 for the prediction of postoperative hypocalcemia. Conclusions: Using machine learning, we developed and validated a simple multivariable model that allowed the accurate prediction of postoperative hypocalcemia. The resulting algorithm could be used at the point of care to guide clinical management after total thyroidectomy. [ABSTRACT FROM AUTHOR]

(1) Background and Objectives: Vitamin D is implicated in the pathogenesis of Chronic Kidney Disease—Mineral and Bone Disorder (CKD-MBD) in hemodialysis (HD) patients, including the development of secondary hyperparathyroidism (SHP). While cholecalciferol supplementation is recommended for vitamin D deficiency correction, its impact on CKD-MBD remains inconsistent. The aim of this observational prospective study was to assess the effect of cholecalciferol in achieving high–normal serum 25-hydroxycholecalciferol (25(OH)D > 75 ng/mL) levels and its impact on CKD-MBD biochemical markers, including 1,25-dihydroxycholecalciferol (1,25(OH)2D) and parathormone (PTH) in HD patients. The study also evaluated the maintenance dosage required to sustain 25(OH)D levels within the 50–75 ng/mL range. (2) Materials and Methods: A total of 22 HD patients with baseline 25(OH)D levels 30–50 ng/mL received cholecalciferol (70,000 IU/week) to achieve the target serum 25(OH)D > 75 ng/mL. Baseline data on calcium, phosphate, 1–84 PTH, 25(OH)D, and 1,25(OH)2D serum levels were compared with the data when 25(OH)D > 75 ng/mL was targeted or when the highest 25(OH)D levels were noted. (3) Results: Cholecalciferol significantly improved vitamin D status in HD patients, with 73% reaching the target 25(OH)D level >75 ng/mL in a median time of 7.5 weeks, with a median total dose of 525,000 IU. This was associated with a significant rise in 1,25(OH)2D, decrease in 1–84 PTH, and no significant effect on calcium and phosphate levels. The median maintenance dose of cholecalciferol was established at 30,000 IU/week. (4) Conclusions: The findings support the use of cholecalciferol targeting high normal 25(OH)D levels to improve biochemical markers of CKD-MBD in HD patients. [ABSTRACT FROM AUTHOR]

The expression of several key molecules is altered in parathyroid tumors due to gene mutations, the loss of heterozygosity, and aberrant gene promoter methylation. A set of genes involved in parathyroid tumorigenesis has been investigated in sporadic parathyroid adenomas (PAds). Thirty-two fresh PAd tissue samples surgically removed from patients with primary hyperparathyroidism (PHPT) were collected and profiled for gene, microRNA, and lncRNA expression (n = 27). Based on a gene set including MEN1, CDC73, GCM2, CASR, VDR, CCND1, and CDKN1B, the transcriptomic profiles were analyzed using a cluster analysis. The expression levels of CDC73 and CDKN1B were the main drivers for clusterization. The samples were separated into two main clusters, C1 and C2, with the latter including two subgroups of five PAds (C2A) and nineteen PAds (C2B), both differing from C1 in terms of their lower expression of CDC73 and CDKN1B. The C2A PAd profile was also associated with the loss of TP73, an increased expression of HAR1B, HOXA-AS2, and HOXA-AS3 lncRNAs, and a trend towards more severe PHPT compared to C1 and C2B PAds. C2B PAds were characterized by a general downregulated gene expression. Moreover, CCND1 levels were also reduced as well as the expression of the lncRNAs NEAT1 and VLDLR-AS1. Of note, the deregulated lncRNAs are predicted to interact with the histones H3K4 and H3K27. Patients harboring C2B PAds had lower ionized and total serum calcium levels, lower PTH levels, and smaller tumor sizes than patients harboring C2A PAds. In conclusion, PAds display heterogeneous transcriptomic profiles which may contribute to the modulation of clinical and biochemical features. The general downregulated gene expression, characterizing a subgroup of PAds, suggests the tumor cells behave as quiescent resting cells, while the severity of PHPT may be associated with the loss of p73 and the lncRNA-mediated deregulation of histones. [ABSTRACT FROM AUTHOR]

A cross-sectional study was performed in healthy adults (mean age 28 y, 67% women) whose habitual diet was an omnivore, lacto-ovo vegetarian, or vegan diet. The total sample (n = 297) was divided into two groups according to the parathormone (PTH) cut-off value of 65 pg/mL of either normal-PTH (n = 228) or high-PTH (n = 69). Vitamin D status (25-hydroxycholecalciferol, 25-OHD), PTH, and bone formation (bone alkaline phosphatase, BAP) and bone resorption (N-telopeptides of type I collagen, NTx) markers were determined. Hematocrit, erythrocytes, hemoglobin, platelets, serum iron, serum transferrin, transferrin saturation, and serum ferritin were also measured. In the total sample, 25-OHD and PTH were negatively correlated, and all subjects with high PTH presented vitamin D insufficiency (25-OHD < 75 nmol/L). High bone remodeling was observed in the high-PTH group, with significantly higher NTx and marginally higher BAP compared to the normal-PTH group. Hematocrit and ferritin were significantly lower in the high-PTH compared to the normal-PTH group. However, serum iron was higher in the high-PTH group, which was only observed for the lacto-ovo vegetarian and vegan subjects. It is concluded that both low vitamin D and low iron status are associated with elevated PTH and bone resorption, more in vegetarians than omnivores, which is in line with the hypothesis that chronic iron deficiency in adulthood mainly predisposes to osteoporosis in postmenopausal women and the elderly. [ABSTRACT FROM AUTHOR]

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Background: This study checked whether vitamin D (Vit-D) supplementation improves the efficacy of resistance training (RT) in terms of increasing muscle strength and lean body mass (LBM), and influencing cardiorespiratory fitness (VO2max) in Vit-D-deficient middle-aged healthy men. Methods: Participants (n = 28) were quasi-randomly assigned to one of two groups, which, in a double-blind manner, supplemented their diet daily with either Vit-D (8000 IU; VD) or placebo (PLC) during participation in a 12-week supervised RT program. Results: During the intervention, serum Vit-D concentrations increased 2.6-fold (p < 0.001) in the VD group, while no changes occurred in the PLC group. Muscle strength gains (p < 0.001) as measured in seven exercises performed on RT equipment and increases (p < 0.001) in LBM were similar in the two groups. Total fat mass, percent total fat, and percent android fat decreased (p < 0.05) to a similar extent in both groups, but there was no change in VO2max in either group. Conclusions: In conclusion, in healthy Vit-D-insufficient middle-aged men engaged in resistance training, Vit-D supplementation increases serum 25(OH)D levels but does not enhance gains in muscle strength and LBM, or decreases in fat mass and fat percentage, and does not affect cardiorespiratory fitness. [ABSTRACT FROM AUTHOR]

Continuous venovenous hemofiltation (CVVH) with citrate anticoagulation has been shown to be associated with substantial losses of calcium and negative calcium balance in ICU patients, which may lead to excessive bone loss and osteoporosis. The aim of this study is to investigate whether plasma parathormone monitoring can identify patients with negative calcium balance during CVVH. This is a retrospective single-center study of all adult ICU patients treated with citrate CVVH from 2021 to 2023. PTH was measured routinely once per week. Calcium excretion in ultrafiltrate fluid and CVVH calcium balance were measured daily. In total, 274 PTH measurements were performed in 111 patients. In 61 measurements (22%), PTH was higher than the upper limit of normal (>8 pmol/L). If PTH was higher than normal, plasma ionized calcium was less than 1.16 mmol/L in 77% of cases and hypercalcemia was never present. In a subgroup of patients treated with CVVH for at least 36 h in the preceding 72 h, PTH values were similar for quartiles by cumulative calcium balance. Increased plasma concentrations of PTH are frequently found in ICU patients treated with citrate CVVH, but no association was found between PTH and the CVVH calcium balance over the last 72 h.

Atypical parathyroid tumor is a rare disease that can be challenging to distinguish from parathyroid adenoma. Atypical parathyroid tumor shows some laboratory and histopathological features with parathyroid cancer. This study attempts to compare clinical, laboratory, radiologic, and histopathological characteristics in atypical parathyroid tumor and parathyroid adenoma. This was a retrospective study based on the database of eighty-two subjects who underwent surgery for primary hyperparathyroidism at a tertiary referral center between 2010 and 2021. Forty-one patients with atypical parathyroid tumor were matched by age and gender to controls with parathyroid adenoma. Clinical, laboratory, radiologic, and characteristics were obtained from the hospital database. Forty-five (54.8%) of primary hyperparathyroidism patients were symptomatic, 36 (90%) had nephrolithiasis, 6 (15%) had fracture, and 3 (7.5%) had hypercalcemic crisis. Atypical parathyroid tumor patients present with significantly increased serum calcium, parathormone, and alkaline phosphatase levels (P <.001, all). No significant difference was observed in the results of bone mineral density, T-scores, and Z-scores. The size of adenoma was significantly greater in the atypical parathyroid tumor group (24 (8.8–70) mm vs. 12 (3.8–32) mm, P = 0.005). Our study revealed that increased preoperative serum calcium, parathormone, alkaline phosphatase concentrations, and parathyroid adenoma size on ultrasound may have predicted the atypical parathyroid tumor. [ABSTRACT FROM AUTHOR]

The primary objective of this study was to use artificial neural network (ANN) to predict the post operative hypocalcemia and severity of hypocalcemia following total thyroidectomy. The secondary objective was to determine the weightage for the factors predicting the hypocalcemia with the ANN. A single center, retrospective case series included treatment-naive patients undergoing total thyroidectomy for benign or malignant thyroid nodules from January 2020 to December 2022. Artificial neural network (ANN) - Multilayer Perceptron (MLP) used to predict post-operative hypocalcemia in ANN. Multivariate analysis was used construct validity. The data of 196 total thyroidectomy cases was used for training and testing. The mean incorrect prediction during training and testing was 3.18% (± σ = 0.65%) and 3.66% (± σ = 1.88%) for hypocalcemia. The cumulative Root-Mean-Square-Error (RMSE) for MLP model was 0.29 (± σ = 0.02) and 0.32 (± σ = 0.04) for training and testing, respectively. Area under ROC was 0.98 for predicting hypocalcemia 0.942 for predicting the severity of hypocalcemia. Multivariate analysis showed lower levels of post operative parathormone levels to be predictor of hypocalcemia (p < 0.01). The maximum weightage given to iPTH (100%) > Need for sternotomy (28.55%). Our MLP NN model predicted the post-operative hypocalcemia in 96.8% of training samples and 96.3% of testing samples, and severity in 92.8% of testing sample in 10 generations. however, it must be used with caution and always in conjunction with the expertise of the surgical team. Level of Evidence – 3b. [ABSTRACT FROM AUTHOR]

Objectives: The study was carried out to assess the effect of zinc supplementation on changes in calcium homeostasis, and parathyroid gland, bone, and skeletal muscle histology in rats exposed to subchronic oral glyphosate-based herbicide (GBH, GOBARA®) toxicity. Methods: Sixty male Wistar rats in 6 equal groups (DW, Z, G1, G2, ZG1, ZG2) were used: DW and Z were given 2 mL/kg distilled water and 50 mg/kg of zinc chloride (2%), respectively; G1 and G2 received 187.5 mg/kg and 375 mg/kg of glyphosate (in GBH), respectively; ZG1 and ZG2 were pretreated with 50 mg/kg of zinc chloride before receiving glyphosate, 1 hour later, at 187.5 and 375 mg/kg, respectively. Treatments were by gavage once daily for 16 weeks. Serum calcium, vitamin D, and parathormone were estimated. Histopathological examination of parathyroid gland, femoral bone and biceps femoris muscle was done. Results: GBH exposure caused significant (P =.0038) decrease in serum calcium concentration in G1, significant (P =.0337) decrease in serum vitamin D concentration in G1, significant increases in parathormone in G1 (P =.0168) and G2 (P =.0079) compared to DW. Significant (P >.05) changes did not occur in the other parameters of G2 compared to DW. Dose-dependent effect in GBH exposure was not observed after comparing G1 and G2. Necrotic changes occurred in parathyroid gland cells, osteocytes, and muscle cells in G1 and G2. In ZG1 and ZG2, significant (P >.05) variations in the parameters were not observed and tissue lesions were absent. Conclusion: Subchronic GBH exposure impaired calcium homeostasis observed as hypocalcemia, hypovitaminemia D, and secondary hyperparathyroidism and caused tissue damage in parathyroid gland, bone, and muscle of rats and these were mitigated by zinc chloride pretreatment. [ABSTRACT FROM AUTHOR]

Chronic kidney disease (CKD) stands as a prominent non-communicable ailment, significantly impacting life expectancy. Physiopathology stands mainly upon the triangle represented by parathormone–Vitamin D–Fibroblast Growth Factor-23. Parathormone (PTH), the key hormone in mineral homeostasis, is one of the less easily modifiable parameters in CKD; however, it stands as a significant marker for assessing the risk of complications. The updated “trade-off hypothesis” reveals that levels of PTH spike out of the normal range as early as stage G2 CKD, advancing it as a possible determinant of systemic damage. The present review aims to review the effects exhibited by PTH on several organs while linking the molecular mechanisms to the observed actions in the context of CKD. From a diagnostic perspective, PTH is the most reliable and accessible biochemical marker in CKD, but its trend bears a higher significance on a patient’s prognosis rather than the absolute value. Classically, PTH acts in a dichotomous manner on bone tissue, maintaining a balance between formation and resorption. Under the uremic conditions of advanced CKD, the altered intestinal microbiota majorly tips the balance towards bone lysis. Probiotic treatment has proven reliable in animal models, but in humans, data are limited. Regarding bone status, persistently high levels of PTH determine a reduction in mineral density and a concurrent increase in fracture risk. Pharmacological manipulation of serum PTH requires appropriate patient selection and monitoring since dangerously low levels of PTH may completely inhibit bone turnover. Moreover, the altered mineral balance extends to the cardiovascular system, promoting vascular calcifications. Lastly, the involvement of PTH in the Renin–Angiotensin–Aldosterone axis highlights the importance of opting for the appropriate pharmacological agent should hypertension develop.

We aimed to provide an in-depth analysis with respect to three turning points in pancreas involvement in primary hyperparathyroidism (PHP): hypercalcemia-induced pancreatitis (HCa-P), MEN1 (multiple endocrine neoplasia)-related neuroendocrine tumors (NETs), and insulin resistance (IR). This was a comprehensive review conducted via a PubMed search between January 2020 and January 2024. HCa-P (n = 9 studies, N = 1375) involved as a starting point parathyroid NETs (n = 7) or pancreatitis (n = 2, N = 167). Case report-focused analysis (N = 27) showed five cases of pregnancy PHP-HCa-P and three reports of parathyroid carcinoma (female/male ratio of 2/1, ages of 34 in women, men of 56). MEN1-NET studies (n = 7) included MEN1-related insulinomas (n = 2) or MEN1-associated PHP (n = 2) or analyses of genetic profile (n = 3), for a total of 877 MEN1 subjects. In MEN1 insulinomas (N = 77), the rate of associated PHP was 78%. Recurrence after parathyroidectomy (N = 585 with PHP) was higher after less-than-subtotal versus subtotal parathyroidectomy (68% versus 45%, p < 0.001); re-do surgery was 26% depending on surgery for pancreatic NETs (found in 82% of PHP patients). MEN1 pathogenic variants in exon 10 represented an independent risk factor for PHP recurrence. A single pediatric study in MEN1 (N = 80) revealed the following: a PHP rate of 80% and pancreatic NET rate of 35% and 35 underlying germline MEN1 pathogenic variants (and 3/35 of them were newly detected). The co-occurrence of genetic anomalies included the following: CDC73 gene variant, glucokinase regulatory protein gene pathogenic variant (c.151C>T, p.Arg51*), and CAH-X syndrome. IR/metabolic feature-focused analysis identified (n = 10, N = 1010) a heterogeneous spectrum: approximately one-third of adults might have had prediabetes, almost half displayed some level of IR as reflected by HOMA-IR > 2.6, and serum calcium was positively correlated with HOMA-IR. Vitamin D deficiency was associated with a higher rate of metabolic syndrome (n = 1). Normocalcemic and mildly symptomatic hyperparathyroidism (n = 6, N = 193) was associated with a higher fasting glucose and some improvement after parathyroidectomy. This multilayer pancreas/parathyroid analysis highlighted a complex panel of connections from pathogenic factors, including biochemical, molecular, genetic, and metabolic factors, to a clinical multidisciplinary panel. [ABSTRACT FROM AUTHOR]

Aim: To investigate the effects of short-term oral intake of spironolactone on parathyroid hormone (PTH) and calcium levels, as well as other biochemical and clinical parameters in normotensive female patients with polycystic ovary syndrome (PCOS). Method: 32 PCOS patients were studied at baseline and three months after regular intake of a daily dose of 50 mg or 100 mg spironolactone. PTH, calcium and other biochemical tests as well as clinical parameters were evaluated at baseline and after three months. Results: Body mass index and serum PTH levels decreased significantly after treatment (p: 0.021 andp: 0.043, respectively). Mean high-density lipoprotein was significantly decreased after treatment (p: 0.011). No significant change was observed in calcium, phosphorus, total cholesterol, triglycerides, and fasting blood glucose levels. Serum testosterone and dehydroepiandrosterone sulphate decreased significantly after 3 months of therapy (p: 0.000 andp: 0.006; respectively). Conclusions: In our study, taking spironolactone at a dose of 100 mg/day lowered PTH levels and had a positive effect on weight loss and insulin resistance. New studies are needed to investigate the effects of treatment with spironolactone on bone and metabolism. It is recommended to monitor dyslipidemia while taking the drug. [ABSTRACT FROM AUTHOR]

Background and Objectives: Uric acid (UA) and the markers of mineral bone metabolism and inflammation are commonly altered in patients with chronic kidney disease (CKD) and are associated with the risk of cardiovascular complications and death. Studies point to a link between high serum UA and mineral bone homeostasis and inflammation, but controversy remains. The aim of this study was to evaluate the relationship between UA levels and mineral bone metabolism and inflammation biomarkers in a sample of Mexican patients with CKD 3a–5. Materials and Methods: This cross-sectional study included 146 Mexican patients with CKD 3a–5. In addition, 25 healthy subjects were included in the study with the aim of generating reference data for comparisons. Metabolic parameters including UA serum concentrations, mineral bone metabolism (parathormone (PTH), fibroblast growth factor 23 (FGF23), calcium, and phosphate), and inflammation (interleukin (IL)-1β, IL-6, and tumor necrosis factor-alpha (TNF-α)) biomarkers were measured in all of the samples and compared as a function of the estimated glomerular function rate (eGFR) or UA levels. Results: Intact PTH, FGF23, and cytokines were higher in advanced CKD stages. Patients with hyperuricemia had significantly higher values of FGF23 and TNF-α compared with those without hyperuricemia. The eGFR was found to be significantly and negatively correlated with all markers. Uric acid was significantly correlated with phosphate, iPTH, FGF23, and TNF-α, whereas iPTH was significantly correlated with FGF23, TNF-α, and FGF23. Finally, a multivariate analysis confirmed the relationship of eGFR with all the tested biomarkers, as well as other relationships of iPTH with UA and TNF-α and of FGF23 with UA and TNF-α. Conclusions: This study supports the relationship between uric acid and levels of mineral bone metabolism and inflammation biomarkers in patients with CKD at middle to advanced stages. In the follow-up of patients with CKD, monitoring and controlling UA levels through nutritional or pharmacological interventions could help in the prevention of alterations related to mineral bone metabolism.

(1) Background and Objectives: Vitamin D is implicated in the pathogenesis of Chronic Kidney Disease—Mineral and Bone Disorder (CKD-MBD) in hemodialysis (HD) patients, including the development of secondary hyperparathyroidism (SHP). While cholecalciferol supplementation is recommended for vitamin D deficiency correction, its impact on CKD-MBD remains inconsistent. The aim of this observational prospective study was to assess the effect of cholecalciferol in achieving high–normal serum 25-hydroxycholecalciferol (25(OH)D > 75 ng/mL) levels and its impact on CKD-MBD biochemical markers, including 1,25-dihydroxycholecalciferol (1,25(OH)2D) and parathormone (PTH) in HD patients. The study also evaluated the maintenance dosage required to sustain 25(OH)D levels within the 50–75 ng/mL range. (2) Materials and Methods: A total of 22 HD patients with baseline 25(OH)D levels 30–50 ng/mL received cholecalciferol (70,000 IU/week) to achieve the target serum 25(OH)D > 75 ng/mL. Baseline data on calcium, phosphate, 1–84 PTH, 25(OH)D, and 1,25(OH)2D serum levels were compared with the data when 25(OH)D > 75 ng/mL was targeted or when the highest 25(OH)D levels were noted. (3) Results: Cholecalciferol significantly improved vitamin D status in HD patients, with 73% reaching the target 25(OH)D level >75 ng/mL in a median time of 7.5 weeks, with a median total dose of 525,000 IU. This was associated with a significant rise in 1,25(OH)2D, decrease in 1–84 PTH, and no significant effect on calcium and phosphate levels. The median maintenance dose of cholecalciferol was established at 30,000 IU/week. (4) Conclusions: The findings support the use of cholecalciferol targeting high normal 25(OH)D levels to improve biochemical markers of CKD-MBD in HD patients.

Disorders of the mineral balance often determine the symptoms, the severity of the course and the prognosis of many diseases. Primary hyperparathyroidism (PHPT) is a common endocrine disease caused by increased secretion of parathyroid hormone as a result of primary damage to the parathyroid glands. Diagnosis of PHPT is often difficult. Clinical signs of PHPT appear months or years after the onset of the disease, however, the presence of hypercalcemia serves as an early indication of the disease of the thyroid gland. Often, patients are observed for a long time by related specialists (rheumatologists, traumatologists-orthopedists, oncologists), which gives rise to a lot of problems consisting in the lack of adequate treatment and its result, the progression of the disease, disability, and a decrease in the quality of life. Often, patients are observed for a long time by related specialists (rheumatologists, orthopedic traumatologists, oncologists) under the “masks” of various pathologies (osteoporosis, recurrent urolithiasis, etc.), which gives rise to a lot of problems, consisting in an erroneous diagnosis, lack of adequate treatment and its result, progression of the disease, disability, and a decrease in the quality of life. Late diagnosis of PHPT leads to the development of severe complications (osteoporetic fractures, renal failure) and an increased risk of premature death. A clinical case of late diagnosis of PHPT at the stage of pronounced bone complications of the disease, which proceeded under the guise of osteoarthritis, is considered. According to the results of laboratory and instrumental studies, the following were revealed: hypercalcemia, a significant increase in the concentration of PTH, adenoma of the left lower parathyroid gland, hyperparathyroid osteodystrophy, and a decrease in bone mineral density. Surgical treatment was performed – selective parathyroidectomy with the development of hypocalcemia in the early postoperative period, which was stopped by taking calcium supplements and active vitamin D metabolites and is designed to help practitioners of various specialties to understand the issues of diagnosis of PHPT and effective care for patients.

Abstract Bone marrow fibrosis represents an important structural change in the marrow that interferes with some of its normal functions. The aetiopathogenesis of fibrosis is not well established except in its primary form. The present review consolidates current understanding of marrow fibrosis. We searched PubMed without time restriction using key words: bone marrow and fibrosis as the main stem against the terms: growth factors, cytokines and chemokines, morphology, megakaryocytes and platelets, myeloproliferative disorders, myelodysplastic syndrome, collagen biosynthesis, mesenchymal stem cells, vitamins and minerals and hormones, and mechanism of tissue fibrosis. Tissue marrow fibrosis-related papers were short listed and analysed for the review. It emerged that bone marrow fibrosis is the outcome of complex interactions between growth factors, cytokines, chemokines and hormones together with their facilitators and inhibitors. Fibrogenesis is initiated by mobilisation of special immunophenotypic subsets of mesenchymal stem cells in the marrow that transform into fibroblasts. Fibrogenic stimuli may arise from neoplastic haemopoietic or non-hematopoietic cells, as well as immune cells involved in infections and inflammatory conditions. Autoimmunity is involved in a small subset of patients with marrow fibrosis. Megakaryocytes and platelets are either directly involved or are important intermediaries in stimulating mesenchymal stem cells. MMPs, TIMPs, TGF-β, PDGRF, and basic FGF and CRCXL4 chemokines are involved in these processes. Genetic and epigenetic changes underlie many of these conditions.

Abstract Background Hepatitis C virus (HCV) infection is linked to a higher mortality rate in hemodialysis (HD) patients. We aimed to see if HCV eradication using interferon-free direct acting antivirals (DAAs) can affect bone-mineral and anemia biochemical parameters such as serum calcium (Ca++), phosphorus (PO4 +), parathormone (PTH), fibroblast growth factor 23 (FGF23), hemoglobin (HB), and ferritin in HD patients and also peripheral insulin resistance by monitoring serum fasting insulin and HOMA insulin resistance (HOMA-IR). Methods Three hundred and thirty-four adults on regular HD with positive HCV genotype 4 (191 male and 143 female) were included; 157 of them had seroconversion during HD. All were hepatitis B virus (HBV) negative and received treatment with DAAs. All cases were examined for body mass index (BMI), HB, ferritin level, transferrin saturation (TSAT), Ca++, PO4 +, PTH, FGF23, serum albumin, alanine transaminase (ALT), fasting insulin level, and HOMA-IR at the beginning and then were measured after 6 and 12 months from a sustained virological response (SVR). Results After 6 and 12 months from SVR, there was a significant increase in serum Ca despite no change in oral calcium dose requirement over that period (p = 0001), a significant increase in HB, serum iron (p = 0001), and a significant reduction in serum ferritin, PO4, PTH, and FGF23 (p = 0001). Both fasting insulin level and HOMA-IR were statistically significantly dropped. Conclusion HCV eradication with interferon-free DAAs showed a statistically significant impact on hemodialysis patients regarding hemoglobin, ferritin level, bone-mineral parameters, and improvement in peripheral insulin resistance.

Aims: Abnormalities of mineral metabolism (MM) have been related to cardiovascular disorders. There are no reports on the prognostic role of MM after an acute coronary syndrome (ACS). We aim to assess the prognostic role of MM after an ACS. Methods and results: Plasma levels of components of MM [fibroblast growth factor 23 (FGF23), calcidiol, parathormone, klotho, and phosphate], high‐sensitivity C‐reactive protein, and N‐terminal‐pro‐brain natriuretic peptide were measured in 1190 patients at discharge from an ACS. The primary outcome was a combination of acute ischaemic events, heart failure (HF) and death. Secondary outcomes were the separate components of the primary outcome. Age was 61.7 ± 12.2 years, and 77.1% were men. Median follow‐up was 5.44 (3.03–7.46) years. Two hundred and ninety‐four patients developed the primary outcome. At multivariable analysis FGF23 (hazard ratio, HR 1.18 [1.08–1.29], P < 0.001), calcidiol (HR 0.86 [0.74–1.00], P = 0.046), previous coronary or cerebrovascular disease, and hypertension were independent predictors of the primary outcome. The predictive power of FGF23 was homogeneous across different subgroups of population. FGF23 (HR 1.45 [1.28–1.65], P < 0.001) and parathormone (HR 1.06 1.01–1.12]; P = 0.032) resulted as independent predictors of HF. FGF23 (HR 1.21 [1.07–1.37], P = 0.002) and calcidiol (HR 0.72 [0.54–0.97), P = 0.028) were independent predictors of death. No biomarker predicted acute ischaemic events. FGF23 predicted independently the primary outcome in patients with estimated glomerular filtration rate > 60 mL/min/1.73 m2. Conclusions: FGF23 and other components of MM are independent predictors of HF and death after an ACS. This effect is homogeneous across different subgroups of population, and it is not limited to patients with chronic kidney disease. [ABSTRACT FROM AUTHOR]

Sustainable healthy diets are promoted, and consequently vegetarian diets are currently increasing. However, scientific information on their effects on bone health is scarce. A cross-sectional study was performed in adults (66% women) classified into three groups: omnivores (n = 93), lacto-ovo vegetarians (n = 96), and vegans (n = 112). Nutrient intake, body composition, physical activity, vitamin D status (25-hydroxycholecalciferol, 25-OHD), parathormone (PTH), and bone formation (bone alkaline phosphatase, BAP) and resorption (N-telopeptides of type I collagen, NTx) markers were determined. Lacto-ovo vegetarians and especially vegans showed lower protein, fat, calcium, phosphorous, vitamin D, retinol, iodine, and zinc intakes, and higher carbohydrate, fibre, carotenes, magnesium, and vitamin K intakes compared to omnivores. Body composition was similar in the three groups that performed vigorous physical activity regularly. Body bone mass and muscle mass were positively correlated with BAP, and time performing physical activity with 25-OHD. The prevalence of vitamin D deficiency or insufficiency (25-OHD < 75 nmol/L) was 93.7% in the studied population, and vitamin D deficiency (25-OHD < 25 nmol/L) was significantly higher in vegans. Vegetarians of both groups had increased PTH and NTx with vegans showing significantly higher PTH and NTx than omnivores. Conclusion: Adult vegetarians, especially vegans, should reduce the risk of bone loss by appropriate diet planning and vitamin D supplementation. [ABSTRACT FROM AUTHOR]

Aim:Peyronie’s disease’s (PD) etiology is still unclear. Many factors that may cause the disease are being investigated. The objective of our study was to clarify the effect of serum parathormone and ionized calcium levels on the pathophysiology of PD.Methods:The study was designed as a cross-sectional study. Demographic data, physical examinations, laboratory tests, and medical and sexual histories of patients between January 2017 and June 2020 were analyzed. Patients were divided into PD and control groups.Results:By measuring serum calcium and parathormone levels of patients, we analyzed 38 PD and 40 control group patients and revealed that i) parathormone (p=0.321) and ionized calcium (p=0.286) levels are not related to PD, and ii) cardiovascular disease (p=0.037), diabetes mellitus (p=0.0001), and hypertension (p=0.001) are significantly associated with PD, whereas smoking, alcohol consumption, and dyslipidemia status are not.Conclusion:The study shows that there is no relationship between serum parathormone and ionized calcium levels and the etiology of PD.

Our objective was to overview the novel aspects in the field of adrenal gland neoplasms, namely, the management of bone status with respect to primary aldosteronism (PA). In the current narrative review, a PubMed study was conducted from inception until June 2023. The inclusion criteria were: human (clinically relevant) studies of any study design (at least 10 patients per study); English papers; and the following combination of key words within the title and/or abstract: "aldosterone" AND "bone", "skeleton", "osteoporosis", "fracture", "calcium", "parathyroid", "DXA", "osteocalcin", "P1NP", "alkaline phosphatase", "bone marker", "trabecular bone score", or "FRAX". The exclusion criteria were in vitro or animal studies, reviews, and case reports/series. We screened 1027 articles and finally included 23 studies (13 of case-control type, 3 cross-sectional, 5 prospective, 1 observational cohort, and 1 retrospective study). The assessments provided in these studies were as follows: nine studies addressed Dual-Energy X-ray Absorptiometry (DXA), another study pointed out a bone microarchitecture evaluation underlying trabecular bone score (TBS), and seven studies investigated the bone turnover markers (BTMs) profile. Moreover, 14 studies followed the subjects after adrenalectomy versus medical treatment, and 21 studies addressed secondary hyperparathyroidism in PA patients. According to our study on published data during a period of almost 40 years (n = 23, N = 3965 subjects aged between 38 and 64, with a mean age 56.75, and a female-to-male ratio of 1.05), a higher PTH in PA versus controls (healthy persons or subjects with essential hypertension) is expected, secondary hyperparathyroidism being associated in almost half of the adults diagnosed with PA. Additionally, mineral metabolism anomalies in PA may include lower serum calcium and higher urinary calcium output, all these three parameters being reversible under specific therapy for PA, regardless medical or surgical. The PA subgroup with high PTH seems at higher cardiovascular risk, while unilateral rather than bilateral disease was prone to this PTH anomaly. Moreover, bone mineral density (BMD) according to central DXA might show a higher fracture risk only in certain adults, TBS being a promising alternative (with a still unknown perspective of diabetes' influence on DXA-TBS results in PA). However, an overall increased fracture prevalence in PA is described in most studies, especially with respect to the vertebral site, the fracture risk that seems correctable upon aldosterone excess remission. These data recommend PA as a cause of secondary osteoporosis, a treatable one via PA intervention. There is still an area of debate the way to address BMTs profile in PA, the case's selection toward specific bone evaluation in every day practice, and further on, the understanding of the potential genetic influence at the level of bone and mineral complications in PA patients. [ABSTRACT FROM AUTHOR]

Introduction: Secondary hyperparathyroidism, as a result of chronic kidney disease could be treated medically or surgically. When pharmacotherapy fails, patients undergo surgery - parathyroidectomy, the curative treatment of secondary hyperparathyroidism (SHPT). There are currently 3 accepted surgical techniques, each with supporters or opponents - total parathyroidectomy, subtotal parathyroidectomy and parathyroidectomy with immediate autotransplantation. Methods: In this paper we described our experience on a series of 160 consecutive patients diagnosed with secondary hyperparathyroidism who underwent surgery, in 27 cases it was totalization of the intervention (patients with previously performed subtotal parathyroidectomy or with supernumerary glands and SHPT recurrence). We routinely perform total parathyroidectomy, the method that we believe offers the best results. Results: The group of patients was studied according to demographic criteria, paraclinical balance, clinical symptomatology, pre- and postoperative iPTH (intact parathormone) values, SHPT recurrence, number of reinterventions. In 31 cases we found gland ectopy and in 15 cases we discovered supernumerary parathyroids. A percentage of 96.24% of patients with total parathyroidectomy did not show recurrence. Discussions: After analyzing the obtained results, our conclusion was that total parathyroidectomy is the intervention of choice for patients suffering from secondary hyperparathyroidism when pharmacotherapy fails in order to prevent recurrence of the disease and to correct the metabolic parameters. [ABSTRACT FROM AUTHOR]

Introduction: Clinical hypocalcemia (CH) following total thyroidectomy (TT) is a potentially life-threatening condition if left untreated. This study aimed at evaluating the accuracy of parathyroid hormone (PTH) measured in the early morning of the first postoperative day (POD-1) in predicting CH, and determining the cutoff values of PTH that can predict the development of CH. Methods: We performed a retrospective review of patients undergoing TT between February 2018 and July 2022. Serum PTH, calcium, and albumin levels were measured on morning (6-8 AM) of postoperative day one (POD-1), and serum calcium level was measured from POD-2 onwards. We performed ROC curve analysis to determine the accuracy of PTH in predicting postoperative CH, and cutoff values of PTH to predict CH. Results: Ninety-one patients, 52 (57.1%) with benign and 39 (42.9%) with malignant goiter were included. The incidence of biochemical, and clinical hypocalcemia was 24.2% and 30.8%, respectively. In our study serum, PTH measured in the early morning of first postoperative day following TT was found to have good accuracy (AUC = .88) in predicting CH. A PTH value of ≥27.15 pg/mL was found to have a 96.4% sensitivity in ruling out CH, while a serum PTH value <10.65 pg/mL had a specificity of 95.2% in predicting CH. Discussion: Patients with a serum PTH value of ≥27.15 pg/mL can be discharged without any supplements, those with PTH <10.65 pg/mL should be started on calcium and calcitriol supplements, while patients having PTH values between 10.65 and 27.15 pg/mL should be monitored for the development of signs and/or symptoms of hypocalcemia. [ABSTRACT FROM AUTHOR]

Our study aimed to determine and analyze the serum levels of 25 (OH) vitamin D and parathyroid hormone (PTH) to assess vitamin D deficiency as a risk factor for increased morbidity of acute respiratory infections (ARI) in childhood. The changes in the serum parathormone level were used as a criterion for vitamin D sufficiency since an optimal level of 25 (OH) vitamin D is required for normal PTH values. The study included 87 children divided into four subgroups, respectively – children with acute bronchopneumonia (n=49), children with acute laryngotracheitis (n=11), children with acute bronchiolitis (n=16), and a control group (n=11). Subnormal Vit. D levels were found in the individual groups: in the bronchopneumonia group, 18 children showed evidence of insufficiency; in the group of children with laryngotracheitis, five children showed insufficiency, and one child had Vit.D deficiency; children with acute bronchiolitis showed abnormalities in vit. D levels: seven children with insufficiency and two children - with deficiency. The preliminary results showed that Vit. D status deviations are more common in children with acute respiratory infections than in healthy children. [ABSTRACT FROM AUTHOR]

Osteoporosis, which is considered a significant burden for society, has been an actual health problem in recent years and is attracting the attention of researchers. The prevalence of osteoporosis, which is considerd as a widespread metabolic disease of the skeletal system, increases with age. Early diagnosis of osteoporosis, which ranks fourth after cardiovascular diseases, oncological diseases and diabetes, leads to improvement of the life quality of population. An imbalance between osteoclasts and osteoblasts leads to changes in the amount of biochemical markers of bone turnover in blood and urine, which are important in osteoporosis. These substances include the main components of mineral metabolism and hormones. The presented article provides detailed information about biochemical markers that play an important role in bone density changes. [ABSTRACT FROM AUTHOR]

Bone marrow fibrosis represents an important structural change in the marrow that interferes with some of its normal functions. The aetiopathogenesis of fibrosis is not well established except in its primary form. The present review consolidates current understanding of marrow fibrosis. We searched PubMed without time restriction using key words: bone marrow and fibrosis as the main stem against the terms: growth factors, cytokines and chemokines, morphology, megakaryocytes and platelets, myeloproliferative disorders, myelodysplastic syndrome, collagen biosynthesis, mesenchymal stem cells, vitamins and minerals and hormones, and mechanism of tissue fibrosis. Tissue marrow fibrosis-related papers were short listed and analysed for the review. It emerged that bone marrow fibrosis is the outcome of complex interactions between growth factors, cytokines, chemokines and hormones together with their facilitators and inhibitors. Fibrogenesis is initiated by mobilisation of special immunophenotypic subsets of mesenchymal stem cells in the marrow that transform into fibroblasts. Fibrogenic stimuli may arise from neoplastic haemopoietic or non-hematopoietic cells, as well as immune cells involved in infections and inflammatory conditions. Autoimmunity is involved in a small subset of patients with marrow fibrosis. Megakaryocytes and platelets are either directly involved or are important intermediaries in stimulating mesenchymal stem cells. MMPs, TIMPs, TGF-β, PDGRF, and basic FGF and CRCXL4 chemokines are involved in these processes. Genetic and epigenetic changes underlie many of these conditions. Highlights: Fibrosis of the marrow is always secondary to a primary event which may be clonal or non clonal. Megakaryocytes and platelets form the central arm in myelofibrosis. Haemopoietic stem cells, clonal or activated in various inflammatory processes, immune cells and megakaryocytes (clonal or activated) interact with mesenchymal stem cells of GLI+ and Lep+ subsets that differentiate into myofibroblasts, -fibroblasts and fibrocytes. At each of these steps different cytokines, vitamins, hormones and minerals interact to produce the fibrocollagenous matrix. TGF-β and CXCL4 are important growth factors and chemokines assist this process. PDGFα, VEGF, angiopoietin, bFGF-, BMP pathway and inflammatory/oxidative cytokine pathways and tissue oxygen sensing mechanism via HID1α are also involved in the process in specific cases. Vitamins, hormones, minerals, and protease/anti-protease balance finally determine the extent of fibrosis. Many signals converge to produce TGF-β that stimulates marrow fibrosis. There may be a healthy noradrenergic input to the marrow vasculature that prevents fibrosis. Epigenetic regulation of fibrosis is getting increasing attention for understanding the process and directing targeted therapy. Addressing these signals with various targeted therapies alone or in combination are being developed (e.g ruxolotinib in PMF) [ABSTRACT FROM AUTHOR]

Aim: In primary hyperparathyroidism patients, avoiding hypoparathyroidism and hypocalcemia after surgery is essential. We aimed to evaluate if the delta parathormone percent value (ΔPTH%) can identify patients with an increased risk of developing hypocalcemia after parathyroid surgery for primary hyperparathyroidism. Material and methods: Eighty patients with parathyroid adenomas who underwent single parathyroidectomy were analyzed, and demographical data, preoperative, and postoperative laboratory data were collected were included in the study. Postoperative hypocalcemia was defined as a corrected calcium value below 8.5 mg/dL calculated from the blood values taken on the first postoperative day. The ΔPTH value was calculated by finding the difference between the preoperative PTH value and the postoperative PTH value, and the percentage of ΔPTH was calculated by dividing the ΔPTH value by the preoperative PTH (ΔPTH = Preoperative PTH – Postoperative PTH, and ΔPTH% = ΔPTH / Preoperative PTH). Results: Postoperative hypocalcemia developed in 7.5% of the patients. Hypocalcemic patients had higher ΔPTH and ΔPTH% values. The selection of 130.95 ng/L as ΔPTH level cutoff level divided patients with and without postoperative hypocalcemia with 83.3% sensitivity and 62.2% specificity. As for ΔPTH%, a cut-off value of 71.4% had 100.0% sensitivity, 56.8% specificity, and a 16-fold increase in odds of postoperative hypocalcemia. Conclusion: ΔPTH and ΔPTH% values are helpful predictors of postoperative hypocalcemia after parathyroidectomy and can be used as a guiding tool.

Introduction. Urolithiasis is not a simple disease, but it is a group of metabolic and endocrine disorders in the organism, coupled with changes in the urinary tract. Objectives. Research on the etiopathogenesis of urolithiasis; to analyze parathyroid hormones, to determine citrates in urine; their influence on the occurrence of urolithiasis. Research and the role of infection in the occurrence of urolithiasis, clinical symptoms, diagnostic methods, prevention methods and as well as preventive measures. Materials and methods. The research was conducted on our patients at the Urology Clinic, University Clinical Center of Kosovo, in Pristina. The work was prospective; in our research, we included 102 patients. Results. Our research has increased Parathormone in 5, 88% of cases. We had hypocitraturia in 57, 84% of cases. Hypocyturia then affects the creation of conditions for the crystallization and aggregation of stoneforming substances. Urolithiasis includes both sexes, primarily men 66, 7%, and women 33.3%. With X2- test we obtained a significant difference with statistical significance in the number of cases by gender (X2 = 11.3, P = 0.001). The most attacked age group was 40-49 years old. Symptoms are dominated by colic, nephralgia, dysuria, and hematuria. In this research, we have 22.5% of positive results of urine cultures. Conclusion. Therefore, there is still no explanation about the pathogenesis of urolithiasis, and with the knowledge of the etiopathogenesis of urolithiasis, symptoms, clinic, metabolic disorders and pathomorphology of urolithiasis, prophylactic measures can be taken, and urolith recurrence can be prevented.

We aimed to investigate correlation between perioperative biochemical values and adenoma volume, the effects of perioperative biochemical values and clinicopathological variables on postoperative hypocalcemia after parathyroidectomy. A retrospective study planned in tertiary university hospital on patients undergone surgery for primer hyperparathyroidism. Preoperative calcium (first, close to surgery, maximum), PTH (first, close to surgery, maximum), alkaline phosphatase (ALP) and phosphorus (P) values, postoperative calcium (early, late), postoperative PTH (early, late), 24-hour urinary calcium calculation, time from the first diagnosis of elevated calcium until surgery, preoperative hypercalcemia treatments, excised parathyroid gland, histopathologic diagnosis, maximum diameter and volume of the excised parathyroid on histopathologic examination, postoperative intravenous calcium supplement were analyzed. 73 patients were included in the study. The median age of the patients was 54 years (range, 18-82), and 83.6% were female. In univariate analysis, patients who were administrated intravenous (IV) calcium supplement had higher preoperative PTH (p=0.024). adenoma volume correlated moderate with preoperative PTH first (r=0.396, p=0.001), preoperative maximum parathormone (r=0.380, p=0.001), preoperative PTH CS (r=0.432, p [Med-Science 2023; 12(1.000): 271-7]

IntroductionSecondary hyperparathyroidism, as a result of chronic kidney disease could be treated medically or surgically. When pharmacotherapy fails, patients undergo surgery - parathyroidectomy, the curative treatment of secondary hyperparathyroidism (SHPT). There are currently 3 accepted surgical techniques, each with supporters or opponents – total parathyroidectomy, subtotal parathyroidectomy and parathyroidectomy with immediate autotransplantation.MethodsIn this paper we described our experience on a series of 160 consecutive patients diagnosed with secondary hyperparathyroidism who underwent surgery, in 27 cases it was totalization of the intervention (patients with previously performed subtotal parathyroidectomy or with supernumerary glands and SHPT recurrence). We routinely perform total parathyroidectomy, the method that we believe offers the best results. ResultsThe group of patients was studied according to demographic criteria, paraclinical balance, clinical symptomatology, pre- and postoperative iPTH (intact parathormone) values, SHPT recurrence, number of reinterventions. In 31 cases we found gland ectopy and in 15 cases we discovered supernumerary parathyroids. A percentage of 96.24% of patients with total parathyroidectomy did not show recurrence.DiscussionsAfter analyzing the obtained results, our conclusion was that total parathyroidectomy is the intervention of choice for patients suffering from secondary hyperparathyroidism when pharmacotherapy fails in order to prevent recurrence of the disease and to correct the metabolic parameters.

Serum calcium homeostasis is mainly regulated by parathormone (PTH) secreted by the parathyroid gland. Besides PTH and Gcm2, a master gene for parathyroid differentiation, many genes are expressed in the gland. Especially, calcium-sensing receptor (CaSR), vitamin D receptor (VDR), and Klotho function to prevent increased secretion of PTH and hyperplasia of the parathyroid gland under chronic hypocalcemia. Parathyroid-specific dual deletion of Klotho and CaSR induces a marked enlargement of the glandular size. The parathyroid develops from the third and fourth pharyngeal pouches except murine species in which the gland is derived from the third pouch only. The development of the murine parathyroid gland is categorized as follows: (1) formation and differentiation of the pharyngeal pouches, (2) appearance of parathyroid domain in the third pharyngeal pouch together with thymus domain, (3) migration of parathyroid primordium attached to the top of thymus, and (4) contact with the thyroid lobe and separation from the thymus. The transcription factors and signaling molecules involved in each of these developmental stages are elaborated. In addition, mesenchymal neural crest cells surrounding the pharyngeal pouches and parathyroid primordium and invading the parathyroid parenchyma participate in the development of the gland. [ABSTRACT FROM AUTHOR]

Background/aim: The pathology of laryngomalacia is still not clear. The aim of this study was to investigate the relationship between vitamin D levels and laryngomalacia, and to evaluate vitamin D levels according to the classification of laryngomalacia. Materials and methods: This retrospective study was conducted in the Kahramanmaraş Sütçü İmam University Medicine Faculty's Otorhinolaryngology Clinic between June 2014 and January 2021. Laryngomalacia was classified. Laboratory tests for all patients included calcium (Ca), phosphorus (P), parathormone (PTH), blood urea nitrogen (BUN), creatinine (Cre), alanine transaminase (ALT), and 25-hydroxy vitamin D (25-OH-D). Results: Evaluations were performed for 64 infants with laryngomalacia, including 41 male and 23 female infants with a mean age of 4.6 ± 3.0 months, and a control group of 64 healthy infants with a mean age of 4.5 ± 2.8 months. A statistically significant difference was determined between the laryngomalacia group and the control group with respect to 25-OH-D and PTH levels (p < 0.001). When data were examined according to laryngomalacia types, a statistically significant difference was determined between the groups for 25-OH-D, Ca, P, PTH, and ALT values. The 25-OH-D level was statistically significantly lower in the severe laryngomalacia group than in the mild and control groups (p < 0.001). A statistically significant difference was determined between the moderate and severe laryngomalacia groups and the control group regarding PTH levels (p < 0.001). Conclusion: Vitamin D deficiency may have a role in the etiology of laryngomalacia, and this view is supported by the finding that there was a decrease in vitamin D levels associated with laryngomalacia classification. In addition, the reduction in PTH levels in infants with laryngomalacia may be explained by the change in Ca metabolism. It would be appropriate for further studies to investigate the response to vitamin D replacement therapy in patients with moderate and severe laryngomalacia. [ABSTRACT FROM AUTHOR]