Mineral Metabolism Research Articles

Vitamin D Status in Supplemented Hemodialysis Patients

Introduction: Chronic kidney disease (CKD) causes decreased activity of the enzyme 1-alpha-hydroxylase and calcitriol deficiency with mineral and bone metabolism disorders or secondary hyperparathyroidism. Anticipation of the occurrence of these complications implies the systematic supplementation of all hemodialysis patients, with monitoring of biological parameters. It is in this context that this study was carried out, the general objective of which was to establish the profile of vitamin D concentration in hemodialysis and Ivorian public sector supplemented patients in Abidjan. Patients and Methods: In a cross-sectional study conducted from September to December 2022, we included 89 patients with end-stage CKD treated with hemodialysis at the CNPTIR in Cocody. The collection of epidemio-clinical data was done on the basis of a questionnaire on the one hand and the patients' medical records on the other. The vitamin D concentration was determined by the ELFA immunoassay method on mini Vidas (BIOMERIEUX). Results: The mean age of the patients was 45 ± 13 and 65.17% of them were men. 55.06% of the patients had been treated with dialysis for at least 5 years. 48.31% of the patients had regular supplementation treatment. Of the two types of vitamin D supplementation, 94.38% of the study population was supplemented with cholecalciferol compared to 18% for alfacalcidol with 12% of patients included, using both types. From a biological point of view, it appears that the average concentration of vitamin D in the patients was 26.9 ng/mL, and only 16% have a concentration of less than 20 mg/mL, corresponding to an deficiency vitamin D status. Conclusion: At the end of this cross-sectional study, it emerged that the average in adult hemodialysis subjects followed at the CNPTIR in Cocody had an insufficient vitamin D status. And 37% of the study population with normal vitamin D status. However, these results could be improved by better accessibility to the products, and regular compliance with supplementation.

Extreme soil salinity reduces N and P metabolism and related microbial network complexity and community immigration rate.

Soil microbiomes are well known to suffer from the effects of rising salinity. There are, however, no current understandings regarding its specific effects on microbial metabolic functions associated with nitrogen (N) and phosphorus (P) cycling, particularly in the Yellow River Delta (YRD), one of the largest estuaries in the world. This research examined soil microbiomes at 50 sites in the YRD region to analyze their co-occurrence networks and their relationship with N (nitrification, denitrification, dissimilatory, assimilatory, fixation, and mineralization) and P (solubilization, mineralization, transportation, and regulation) metabolism processes. Our findings indicate a notable reduction in soil multifunctionality as salinity levels increase, with Halofilum-ochraceum playing a significant role in nitrification, whereas Bacteroidetes-SB0662-bin-6 helps solubilize inorganic P in highly saline areas. High soil salinity negatively affected the amoA gene involved in nitrification and increased the nosZ gene involved in denitrification in extreme salinity soil with 8.2g/kg salt content. Extreme salinity significantly reduced the expression of genes involved in inorganic P solubilization, such as ppa and ppx. Additionally, the alkaline P gene phoD exhibited significant decreases in extremely saline soils, thereby impeding the mineralization of organic P. The neutral community models indicated that microbial community immigration rate showed a linear negative relationship with soil EC in the six N and four P processes. Salinization, however, displayed a nonlinear pattern with clearly defined thresholds on the community of microbes involved in N and P cycling. Reduced microbial diversity and interactions are causing a decline in soil multifunctionality, and the soil multifunctionality and network edges jointly limited the microbial community immigration rate involved in N and P cycling. It is crucial to preserve soil microbial functions to support nutrient cycling and predict the ecological effects of soil salinization.

CLINICAL CASE OF FAMILIAL HYPOPHOSPHATEMIC RICKETS IN A CHILD

X-linked hypophosphatemic rickets is an inherited disorder caused by mutations in the PHEX gene (phosphate- regulating proteinwith homology to endopeptidases on the X chromosome). Chronic hypophosphatemia leads to impaired bone mineralization, resulting ingrowth retardation, rickets, and damage to other organs and systems, including maxillofacial abnormalities. Clinically, these manifestationsbecome signifi cant when the child begins to walk.The purpose of the study is to describe a clinical case of congenital hypophosphatemic rickets in a child.Material and methods of the study. clinical, biochemical, genetic and imaging examination of the child Results of the study. The article presents a clinical case of a 9-year-old boy, who was adopted after being removed from an unfavorable psychosocial environment and admitted to the Odesa Regional Children’s Clinical Hospital to clarify the diagnosis and treatment tactics.On admission, the mother reported complaints of delayed psychophysical development, memory impairment, psychosocial dysfunction, deformities of the bones of the upper and lower extremities, chest and skull. The examination revealed a decrease in the level of phosphorus in the blood, increased levels of parathyroid hormone and alkaline phosphatase, and signs of osteomalacia in the x-ray. The diff erential diagnosis included vitamin D-dependent rickets, mucopolysaccharidosis, nanism, hyperparathyroidism, and metaphyseal chondrodystrophy. Based on the data obtained, the fi nal diagnosis was made and appropriate treatment was prescribed.Conclusions. The expanded diff erential diagnosis of rickets with rickets-like diseases contributed to the correct clinical diagnosis. Timely pathogenetic treatment reduces renal tubular phosphorus loss, improves mineral metabolism and quality of life. Prescription of growth hormone will reduce the manifestations of nanism.

Phosphate metabolism: its impact on disorders of mineral metabolism.

Regulatory molecules typically work cooperatively to ensure the efficient functioning of hormonal systems. Examples include LH and FSH in reproductive biology, insulin and glucagon in glucose metabolism. Similarly, calcium and phosphorus are important regulators of skeletal homeostasis. In the circulation, these molecules are under the control of PTH, 1,25(OHD), and FGF23. In turn, these hormones depend upon a mutual and complex interplay among themselves. For example, alterations in calcium metabolism influence phosphorus homeostasis, as occurs in primary hyperparathyroidism (PHPT). Not as well recognized is the influence that abnormalities in phosphorus metabolism can have on calcium homeostasis. In this review, we call attention to the impact that abnormalities in phosphorus can have on calcium metabolism.

Association between proteinuria and mineral metabolism disorders in chronic kidney disease: the Japan chronic kidney disease database extension (J-CKD-DB-Ex)

Chronic kidney disease-mineral and bone disorder (CKD-MBD) are recognized as a systemic disease affecting the prognosis of patients with CKD. Proper management of CKD-MBD is important to improve the prognosis of patients with CKD. Although proteinuria is recognized as a poor prognostic factor in these patients, few reports have examined its association with CKD-MBD. We examined the association between proteinuria and CKD-MBD using data from the Japan Chronic Kidney Disease Database Extension (J-CKD-DB-Ex). Among the patients registered in the J-CKD-DB-Ex, 30,977 with CKD stages G2–G5 who had serum creatinine, albumin, calcium, and phosphate concentrations measured at least once and urinalysis performed were included. The patients were divided into four groups (negative, 1+, 2+, and 3+) according to the degree of proteinuria. The association between proteinuria and CKD-MBD was examined by a logistic regression analysis. In a model adjusted for age, sex, diabetes, and the estimated glomerular filtration rate (eGFR), the odds ratio of the 3 + group compared with the negative group significantly increased to 2.67 (95% confidence interval, 2.29–3.13) for hyperphosphatemia, 2.68 (1.94–3.71) for hypocalcemia, and 1.56 (1.24–1.98) for hypomagnesemia. Proteinuria is associated with hyperphosphatemia, hypocalcemia, and hypomagnesemia in patients with CKD independently of eGFR.

Osteopenia and osteoporosis in patients after bariatric surgery: mechanisms of development, course and prognosis

In recent decades, the medical community around the world has been searching for ways to combat morbid obesity, and despite the variety of methods and techniques, great progress has been noted in recent years in the field of bariatric surgery. Despite its effectiveness, bariatric surgery still has a large number of questions related to the effectiveness of certain methods, their long-term results and the choice of surgery. The purpose of this literature review: to consider the mechanisms of formation, development and course of osteopenia and osteoporosis after bariatric surgery, as well as the frequency of their occurrence depending on the type of bariatric procedure (sleeve gastrectomy, Roux-en-Y gastric bypass, gastric banding, biliopancreatic diversion). To achieve this goal, a literature search on this issue was conducted on the PubMed, eLIBRARY.RU, Google scholar platforms. The material was summarized and analyzed in order to find previously unexplored links in the pathogenesis of osteopenia and osteoporosis and, in general, the mechanisms of mineral metabolism disorders in the postoperative period in patients who underwent bariatric surgeries of varying volumes.

Genetic Variants Affecting Iron Metabolism in Healthy Adults: A Systematic Review to Support Personalized Nutrition Strategies

Background/Objectives: Increased interest in personalized nutrition has led to a growing focus on exploring genetic variants and their impact on nutritional uptake (nutrigenomics). Nevertheless, no systematic review to date has compiled scientific evidence on genetic variants (such as single-nucleotide polymorphisms (SNPs)) affecting mineral metabolism in humans. This review aims to fill this gap and enable optimized personalized nutrition recommendations in health care. Methods: Cochrane, Embase and MEDLINE databases were systematically searched for English and German studies published between 2007 and 2023, focusing on genetic variants linked to nutrition. Studies on overweight, diseased, or underage individuals were excluded. Papers with verified findings were assessed for methodological quality using the Joanna Briggs Institute critical appraisal tool. Results: Twenty-one scientific papers on SNPs associated with mineral metabolism were included. The majority were observational studies (n = 19) conducted on Caucasian populations. Women outnumbered men (37.4%) women, 18.9% men, 43.7% sex not reported. All identified SNPs linked to minerals influenced iron parameters, with the TMPRSS6 gene showing the strongest correlation. Two HFE SNPs (rs1800562 and rs1799945) and one TF SNP (rs1799852) exhibited protective effects, while the other 11 SNPs were linked to increased risk of iron deficiency, suggesting potential benefits from iron supplementation for individuals with those genetic variants. Conclusions: This review provides comprehensive insights into the association between genetic variants and mineral metabolism, and the findings highlight the relevance of genetic makeup in optimizing health through nutritional interventions. The generalizability of the findings may be limited to Caucasians, warranting future research with diverse populations. This review was registered with the International Platform of Registered Systematic Review and Meta-Analysis Protocols (INPLASY) on 12 July 2022, under INPLASY202270068 and funded by the University Centre for Prevention and Sports Medicine at Balgrist University Hospital Zurich and the Swiss Innovation Agency Innosuisse, Switzerland.

Study Of Calcium Magnesium And Phosphorus In Hypothyroidism - A Case Control Study

Background: Thyroid disorders are the most common endocrine abnormality in the world secondary to diabetes mellitus. Thyroid hormones are essential for growth, neuronal development, reproduction and regulation of energy metabolism. It influences the metabolism of all substrates including minerals. Many studies have shown that mineral metabolism is frequently disturbed in thyroid disorders. Materials and Methods: The study was conducted on sixty newly confirmed hypothyroid cases based on the thyroid profile and sixty euthyroid cases were recruited as controls. Blood samples were collected from all the patients for the estimation of serum T3, T4, FT3, FT4, TSH, calcium, phosphorus and magnesium by auto analyzer method. Modified spectrophotometric micro-method was used to measure Serum copper using Bathocuprine Disulphonate Disodium Salt (BCDS) and Guanidine hydrochloride salt. The Statistical software namely SPSS 18.0, and R environment ver.3.2.2 were used for the analysis of the data. Results: It was found that the levels of serum sodium, potassium and calcium were significantly decreased in cases than the controls. Serum magnesium and phosphorus were significantly elevated in cases than controls. Conclusion: Serum calcium, magnesium and phosphorous levels are significantly altered in patients having hypothyroidism. Thyroid diseases have wide spread systemic manifestations including their effects on bone and mineral metabolism. Also thyroid hormone affects the glomerular filtration rate, renal blood flow, tubular reabsorption and excretion of minerals which have direct effect on Calcium, Magnesium and phosphorous level. Thus monitoring of these minerals in hypothyroid patient will be of great benefit in improving clinical manifestation and can be treated appropriately

Targeted Deletion of Fibroblast Growth Factor 23 Rescues Metabolic Dysregulation of Diet-induced Obesity in Female Mice.

Fibroblast growth factor 23 (FGF23) is a bone-secreted protein widely recognized as a critical regulator of skeletal and mineral metabolism. However, little is known about the nonskeletal production of FGF23 and its role in tissues other than bone. Growing evidence indicates that circulating FGF23 levels rise with a high-fat diet (HFD) and they are positively correlated with body mass index (BMI) in humans. In the present study, we show for the first time that increased circulating FGF23 levels in obese humans correlate with increased expression of adipose Fgf23 and both positively correlate with BMI. To understand the role of adipose-derived Fgf23, we generated adipocyte-specific Fgf23 knockout mice (AdipoqFgf23Δfl/Δfl) using the adiponectin-Cre driver, which targets mature white, beige, and brown adipocytes. Our data show that targeted ablation of Fgf23 in adipocytes prevents HFD-fed female mice from gaining body weight and fat mass while preserving lean mass but has no effect on male mice, indicating the presence of sexual dimorphism. These effects are observed in the absence of changes in food and energy intake. Adipose Fgf23 inactivation also prevents dyslipidemia, hyperglycemia, and hepatic steatosis in female mice. Moreover, these changes are associated with decreased respiratory exchange ratio and increased brown fat Ucp1 expression in knockout mice compared to HFD-fed control mice (Fgf23fl/fl). In conclusion, this is the first study highlighting that targeted inactivation of Fgf23 is a promising therapeutic strategy for weight loss and lean mass preservation in humans.

Causal association of serum calcium, phosphate, vitamin D, parathyroid hormone, and FGF23 with the risk of aortic stenosis

Abstract Aim Disorders of mineral metabolism, including elevated levels of serum calcium, phosphate, 25-hydroxyvitamin D (25OH-VitD), parathyroid hormone (PTH), and fibroblast growth factor 23 (FGF23), have been reported in patients with calcific aortic valve stenosis (CAVS). However, evidence of the causal role of mineral metabolism in CAVS is still lacking. We aimed to investigate the causality between mineral metabolism and CAVS. Methods A systematic pipeline combining Mendelian randomization (MR), Steiger directionality test, colocalization analysis, protein-protein network, and enrichment analysis was applied to investigate the causal effect. Genome-wide association study (GWAS) and protein quantitative trait loci data for mineral metabolism markers were extracted from large-scale meta-analyses. Summary statistics for CAVS were obtained from two independent GWAS datasets as discovery and replication cohorts (n=374,277 and 653,867). Results In MR analysis, genetic mimicry of serum FGF23 elevation was associated with increased CAVS risk [ORdiscovery=3.081 (1.649-5.760), Pdiscovery=4.21×10-4; ORreplication=2.280 (1.461-3.558), Preplication=2.82×10-4] without evidence of reverse causation (Psteiger=7.21×10-98). Strong colocalisation association with CAVS was observed for FGF23 expression in the blood (PP.H4 = 0.96). Additionally, we identified some protein-protein interactions between FGF23 and known CAVS causative genes. Serum calcium, phosphate, 25OH-VitD, and PTH failed to show causal effects on CAVS at Bonferroni-corrected significance (all P>0.05/5=0.01). Conclusions Elevated serum FGF23 level is a causal risk factor for CAVS, and its mechanism of action in CAVS development may be independent of its function in regulating mineral metabolism. Hence, FGF23 may serve as a circulating marker and a promising preventive target for CAVS, warranting further investigation.

Changes in heavy metal levels in the oral fluid of young patients with and without plaque-induced gingivitis undergoing treatment with braces

Relevance. Research into the effects of nickel-titanium alloys and heavy metal ions on the development of inflammatory oral diseases is becoming increasingly significant in orthodontics. The relationship between toxic elements and inflammatory responses remains under-researched and controversial. Data on the connection between heavy metals and inflammatory reactions could influence the choice of orthodontic appliance materials and guide the subsequent management and monitoring of patients with braces. The question of the safe use of nickel-titanium alloy braces continues to be a relevant concern.Purpose. To assess the levels of heavy metals in the oral fluid of young patients with braces, both in those who developed plaque-induced gingivitis and those who did not.Materials and Methods. The study involved 50 clinically healthy patients (Groups I and II health categories) with intact teeth, including patients with compensated dental caries (isolated carious lesions – Grade I) and no periodontal diseases (PMA index <20), presenting with dental crowding and malocclusion (K07.2, K07.3). The average age of the patients was 22.1 ± 2.7 years, all of whom were undergoing treatment with metal braces. Oral fluid samples were analyzed for 12 heavy metal elements using inductively coupled plasma mass spectrometry (ICP-MS) in a laboratory setting. Additionally, lysozyme activity and oral fluid pH were measured before appliance placement and six months into orthodontic treatment.Results. Adaptation to braces in young patients is frequently complicated by the development of gingivitis and periodontitis due to impaired oral hygiene and the mechanical pressure exerted on teeth and gums, leading to elemental imbalances. Patients with gingivitis during orthodontic treatment are particularly at risk of developing such imbalances and therefore require timely correction of their mineral metabolism.

Short and long-term effects of kidney donation on mineral and bone metabolism

BackgroundLiving kidney donors (LKD) experience an abrupt decline in glomerular filtration rate (GFR) resulting in abnormalities of mineral and bone metabolism (MBD), and this may have implications for skeletal health. We prospectively studied acute and long term MBD adaptation of LKD from two kidney transplant centers (São Paulo, Brazil and Miami, USA).MethodsRenal function and MBD parameters longitudinally after kidney donation (baseline – D0, day 1, 14, 180 and 360 post-operatively) were measured in 74 patients (40 y, 73% female, 54% Brazilian). A subset of 20 donors from Brazil were reassessed after 10 years of nephrectomy.ResultsAt baseline, Brazilian donors presented lower intact FGF23 (20.8 vs. 80.1 pg/mL, P < 0.01) and higher PTH (47.4 vs. 40.1, P = 0.04) than their US counterparts. GFR decreased to 63% of its baseline levels just after donation but improved 10% during the first year. PTH levels increased on D1, returning to baseline levels on D14, while FGF23 remained higher than baseline over the first year. LKD had a significant reduction of serum phosphate on D1, which returned to baseline levels on D180. A higher fractional excretion of phosphate (FEP) was noted since D14. After 10 years of donation, 20 LKD presented a sustained reduction in GFR (74.8 ± 14mL/min). There was a return to baseline in serum FGF23 [21.8 (18–30) pg/mL] and FEP, accompanied by an increase in serum calcium. PTH remained elevated (57.9 ± 18 pg/mL), whereas serum calcitriol and Klotho were lower than before the donation.ConclusionsThe abrupt decline in kidney mass is associated with an increase in PTH and FGF23 that is not explained by phosphate retention. In a long-term evaluation, LKD showed a sustained drop in GFR, with lower serum calcitriol and Klotho, and higher PTH. The effects of these changes should be investigated in further studies.

Osteoporosis and Normocalcemic Primary Hyperparathyroidism (Conservatively or Surgically Managed).

Asymptomatic primary hyperparathyroidism (PHPT) involves 80-90% of the parathyroid tumor-associated cases of PHPT in the modern medical era, while normocalcemic PHPT (NPHPT) has a prevalence of 0.1-11%. We aimed to analyze the bone status and mineral metabolism in NPHPT amid conservative or surgical management. In this narrative review, we searched PubMed (between January 2020 and July 2024) via different keywords. Fourteen studies from the final analysis (388 patients with NPHPT; 1188 with PHPT; and 803 controls) showed that mean serum calcium levels varied between 2.57 and 2.26 mmol/L in NPHPT. Ten studies identified a similar 24 h urinary calcium in NPHPT versus hypercalcemic PHPT (HPHPT). Except for one study, a mandatory vitamin D analysis was performed, but the 25-hydroxyvitamin D cut-offs varied. Osteoporosis (n = 6 studies; N = 172 with NPHPT) was confirmed in 41.7-100% of NPHPT subjects. In surgery candidates, this rate might be overestimated. A DXA analysis was performed in eight studies (235 subjects with NPHPT, and 455 patients with HPHPT); two studies identified a lower BMD in HPHPT < NPHPT, but the results were not homogenous. A single study analyzed the TBS and found similar results in NPHPT. The prevalence of fractures (n = 9) varied between 7.4% and 42.8% in NPHPT. Bone turnover markers (N = 262 patients, n = 8 studies) showed lower bone formation markers in NPHPT versus PHPT (n = 3). Two studies analyzed the BMD and bone turnover markers following parathyroidectomy (161 patients, including 30 patients with NPHPT; mean ages over 60 years). To conclude, given the wide spectrum of complications associated with PHPT, an early diagnosis and proper management is essential. A more extensive screening in patients with osteoporosis and kidney stones might lead to the discovery of NPHPT, a more recently described form of PHPT. While it is still unclear whether NPHPT is an early stage of HPHPT or a separate entity, recent findings show similar osteoporosis and fracture occurrence, and an improvement in bone metabolism, following parathyroidectomy. More extensive prospective studies are crucial to understand the natural course of the disease, to reach a consensus regarding parathyroidectomy indications and surgery candidates' selection, and to ensure proper personalized management for these patients. With the evolving diagnosis methods, PHPT has become a condition with a changing clinical presentation, which now requires modern evaluation and treatment approaches.

Anticonvulsants impacting bone metabolism: interim results from a cross-sectional study

Background. Despite a wide range of antiepileptic drugs (AEDs) with an improved pharmacological profile, patients often experience a variety of side effects during long-trem anticonvulsant therapy, among which are osteoporotic disorders. Currently, the mechanisms of AED effect on bone metabolism remain poorly understood, which creates certain difficulties in prevention and treatment of AED-induced osteoporosis.Objective: to study bone mineral density and laboratory parameters of bone metabolism in patients with epilepsy and longterm AED administration.Material and methods. A cross-sectional study included two comparison groups: 100 adult patients with epilepsy receiving AEDs for more than 12 months and 58 healthy volunteers without taking AEDs. All participants underwent general clinical examination, computed tomography (CT) densitometry at three time points (L1, L2 and femoral neck) and laboratory tests of mineral metabolism.Results. According to CT-densitometry results, a decrease in bone mineral density was detected in the majority of participants from both study groups. While assessing an impact of osteoporosis risk factors on bone tissue in epileptic patients, low motor activity and duration of AED therapy were the most significant, which was associated with lower bone mineral density indices. The study of laboratory mineral metabolism indicators revealed significant inter-group differences in indicators such as ionized calcium, 25-hydroxy-calciferol, free thyroxine and prolactin (p(U)=0.044, p(U)=0.040, p(U)=0.001, p(U)=0.003, respectively).Conclusion. The intermediate study results showed that long-term anticonvulsant use negatively affected bone metabolism in patients suffering from epilepsy. The data obtained point at need for further in-depth study of AED therapy effect on mineral metabolism.

Seasonal dynamics of indicators of mineral metabolism in horses in the conditions of the Leningrad region

The article analyzes the seasonal dynamics of mineral metabolism indicators in adult horses kept in private stables in the Leningrad region. As a result of the research, knowledge of the concentration and dependence of indicators on the seasonality of the year was obtained. It is important to remember that macro- and microelements are not synthesized in the body, they come from food, water, and air. The degree of their assimilation depends on the state of the respiratory and digestive organs. The most difficult period for animals is winter, when there is a decrease in the resistance of the body as a whole due to poor climatic conditions and minimizing physical activity in the fresh air. All these are predisposing factors for the imbalance of indicators at the level of the whole organism.It is established that in the autumn-winter period there is a decrease in indicators relative to the average annual digital values. Thus, there is a linear relationship between the concentration of calcium and phosphorus in blood serum – the minimum values are observed in winter and are 2.53±0.27 mmol/l and 1.76± 0.11 mmol/l, respectively. And the maximum values are typical for the autumn period and are 3.63±0.29 mmol/l for calcium and 2.33±0.12 mmol/l for phosphorus. Similar dynamics is observed in other indicators of the body's mineral metabolism. Thus, for trace elements such as copper, iron, protein-bound iodine, the minimum values were noted in the spring period. This can be explained by a decrease in the mineral components of the feed itself, as a result of long-term storage, resulting in changes in the chemical composition of vegetable feed with fat oxidation. Microelementoses and osteodystrophic processes are observed in animals. The autumn period is characterized by the highest concentrations of minerals in the blood serum of horses, on average by 8-12% compared with the average annual figures, This is explained by the fact that it was in the summer period that the greatest benefit was obtained from juicy plant substances of feed and proper exercise.This knowledge is necessary to understand the processes occurring in the body of horses at different times of the year and the possibility of correcting mineral supplements based on the data obtained

Prediction of gastrointestinal bleeding hospitalization risk in hemodialysis using machine learning

BackgroundGastrointestinal bleeding (GIB) is a clinical challenge in kidney failure. INSPIRE group assessed if machine learning could determine a hemodialysis (HD) patient’s 180-day GIB hospitalization risk.MethodsAn eXtreme Gradient Boosting (XGBoost) and logistic regression model were developed using an HD dataset in United States (2017–2020). Patient data was randomly split (50% training, 30% validation, and 20% testing). HD treatments ≤ 180 days before GIB hospitalization were classified as positive observations; others were negative. Models considered 1,303 exposures/covariates. Performance was measured using unseen testing data.ResultsIncidence of 180-day GIB hospitalization was 1.18% in HD population (n = 451,579), and 1.12% in testing dataset (n = 38,853). XGBoost showed area under the receiver operating curve (AUROC) = 0.74 (95% confidence interval (CI) 0.72, 0.76) versus logistic regression showed AUROC = 0.68 (95% CI 0.66, 0.71). Sensitivity and specificity were 65.3% (60.9, 69.7) and 68.0% (67.6, 68.5) for XGBoost versus 68.9% (64.7, 73.0) and 57.0% (56.5, 57.5) for logistic regression, respectively. Associations in exposures were consistent for many factors. Both models showed GIB hospitalization risk was associated with older age, disturbances in anemia/iron indices, recent all-cause hospitalizations, and bone mineral metabolism markers. XGBoost showed high importance on outcome prediction for serum 25 hydroxy (25OH) vitamin D levels, while logistic regression showed high importance for parathyroid hormone (PTH) levels.ConclusionsMachine learning can be considered for early detection of GIB event risk in HD. XGBoost outperforms logistic regression, yet both appear suitable. External and prospective validation of these models is needed. Association between bone mineral metabolism markers and GIB events was unexpected and warrants investigation.Trial registrationThis retrospective analysis of real-world data was not a prospective clinical trial and registration is not applicable.Graphical

Complex therapy of mineral metabolism in service dogs

The high physical and functional load of service dogs causes changes not only in body systems, but also in metabolism as a whole. An integrated approach to the study of this problem and the search for a pharmacotherapeutic solution will allow us to correct biochemical changes in the body of dogs and improve the performance and quality of life of animals. The purpose of the study was to study the therapeutic effectiveness of a complex of metabolic stimulants for the correction of mineral metabolism. For the study, 16 service dogs were selected in the area of application of the general search profile, belonging to the Ministry of Internal Affairs of Russia in the Altai Territory. Blood was drawn at the beginning and end of the study to analyze red blood cell counts, hemoglobin, hematocrit, glucose, cholesterol, triglycerides, iron, magnesium, zinc, calcium, phosphorus, and chloride. According to the results of the study, it was established that a violation of homeostasis in service dogs was accompanied by changes in some indicators of red blood, as well as pathology of mineral metabolism. After a course of pharmacotherapy, an increase in red blood cells (up to 7.9±0.22*×1012 cells/l) and hemoglobin (up to 141.66±7.32 g/l) was observed in dogs. Carbohydrate metabolism in both groups was characterized by hypoglycemia (3.34±0.21–3.43±0.28 mmol/l). By the end of the study, the glucose level in the experimental group significantly increased by 31.4% relative to the animals in the control group. By the end of the study, cholesterol levels in dogs in the experimental group decreased more rapidly compared to the control group. The study of the dynamics of mineral metabolism indicators revealed a significant increase in iron levels in the experimental group of animals (up to 25.3±1.9 µmol/l), which was 22.8% higher than the control value. Changes in other indicators of mineral metabolism did not differ significantly between the groups, although dogs receiving stimulating therapy showed positive dynamics of changes in mineral metabolism indicators. The use of a complex of metabolic stimulants “Suiferrovita”, “Strolitin”, “Amber Acid” stabilized red blood counts and contributed to the development of a tendency towards the restoration of mineral metabolism.

Adiposity and Mineral Balance in Chronic Kidney Disease.

Bone homeostasis is balanced between formation and resorption activities and remain in relative equilibrium. Under disease states this process is disrupted, favoring more resorption over formation, leading to significant bone loss and fracture incidence. This aspect is a hallmark for patients with chronic kidney disease mineral and bone disorder (CKD-MBD) affecting a significant portion of the population, both in the United States and worldwide. Further study into the underlying effects of the uremic microenvironment within bone during CKD-MBD are critical as fracture incidence in this patient population not only leads to increased morbidity, but also increased mortality. Lack of bone homeostasis also leads to mineral imbalance contributing to cardiovascular calcifications. One area understudied is the possible involvement of bone marrow adipose tissue (BMAT) during the progression of CKD-MBD. BMAT accumulation is found during aging and in several disease states, some of which overlap as CKD etiologies. Importantly, research has found presence of BMAT inversely correlates with bone density and volume. Understanding the underlying molecular mechanisms for BMAT formation and accumulation during CKD-MBD may offer a potential therapeutic avenue to improve bone homeostasis and ultimately mineral metabolism.

Evaluation of the impact of specific oral health parameters on the quality of life in children with rare disorders of phosphorus-calcium metabolism

Relevance. Understanding the impact of oral health problems on the quality of life in children with rare metabolic disorders that affect mineral metabolism is critically important.Materials and methods. An oral health assessment was conducted on 59 children aged 6 to 17 years with rare diseases affecting mineral metabolism, each with a genetically confirmed diagnosis. The children were divided into two study groups: the first group (24 children) comprised those with bone mineralization disorders (hypophosphatemic rickets, hypophosphatasia), while the second group (35 children) included those with disorders of bone and cartilage formation (osteogenesis imperfecta, Marfan syndrome, achondroplasia, etc.). The clinical condition of the children's dental tissues was assessed by evaluating oral hygiene levels and caries intensity in permanent teeth, using the OHI-S and DMFT indices, respectively. The pufa/PUFA index was used to document complications arising from dental caries. To assess the perception of oral health problems, a survey was administered to parents and legal guardians using the Oral Health-Related Quality of Life (OHRQoL) questionnaire.Results. The average DMFT and OHI-S index values did not show statistically significant differences, with values of 4.26 ± 0.28 and 1.96 ± 0.15 in the first group, and 3.76 ± 0.40 and 1.75 ± 0.10 in the second group, respectively. However, the mean pufa/PUFA index values were significantly higher in children with bone and cartilage formation disorders (p = 0.003), being three times greater than those in the group with bone mineralization disorders, with values of 1.03 ± 0.18 and 0.30 ± 0.11, respectively. This increase was associated with higher correlation coefficients between the DMFT and PUFA indices and the modules for physical discomfort, oral functional status, and emotional well-being, with values of 0.38 and 0.41, and 0.49 and 0.27, compared to 0.07 and 0.02, and 0.29 and -0.21 in the first group. These differences were statistically significant at p &lt; 0.05 and p &lt; 0.005.Conclusion. The study revealed that existing oral health conditions have the greatest impact on the quality of life in children with rare diseases affecting bone and cartilage formation.

7588 Coexistent Toxic Nodular Goiter And Primary Hyperparathyroidism (PHPT), A Combo With Diagnostic And Management Implications

Abstract Disclosure: D. Dave: None. A. Bhan: None. S.D. Rao: None. About 17-84% of patients with PHPT have concomitant thyroid disorders, but the prevalence of coexistent hyperthyroidism in PHPT varies 9-14 %. A vast majority had Graves’ disease with only 3 cases of toxic multinodular goiter (MNG) and PHPT reported in the literature as of 2022 ([1]). We present a rare case of coexistent toxic MNG and PHPT. Case Description: A 68y woman presented with recent 23 kg unintended weight loss and palpitations, but no other symptoms. Denied having kidney stones or fractures. On examination she had fine tremors of hands, MNG without exophthalmos. An ultrasound showed multinodular MNG with cystic lesions. A diagnosis of toxic MNG was made. Laboratory results were: TSH (&amp;lt;0.01 uIU/mL), free T4 1,68 ng/dL (normal: 0.61-1.44 ng/ml), high serum Ca (11.0 - 11.4 mg/dl) over 4y, but PTH was unavailable prior to the visit when it was 107 pg/ml and 89 pg/ml after 3 months of antithyroid therapy. Despite clinical and biochemical euthyroidism after 3 months, serum Ca and PTH levels remained high (11.4 mg/dl and 89 pg/ml respectively). Because she had pulmonary embolism a few years ago, we deferred parathyroidectomy until complete remission of hyperthyroidism. Discussion: Hypercalcemia is the biochemical hallmark of PHPT but can occur in 2-10% of patients with hyperthyroidism alone but only 1% of those will have coexistent PHPT. When these two conditions coexist, hypercalcemia is moderate to severe, and an occasional patient may present with hypercalcemic crisis (2). Prior to the availability of PTH assays, it was a challenge to diagnose coexistent PHPT. Hypercalcemia in hyperthyroidism responds to propranolol but not in PHPT, although the response is variable (3). With the availability of sensitive PTH assays, this maneuver is not necessary. In most cases, current PTH assays distinguish hypercalcemia of hyperthyroidism with suppressed PTH from coexistent PHPT in whom PTH level is non-suppressed or elevated. Monitoring serum Ca and PTH levels during therapy of hyperthyroidism would be useful as normalization of serum Ca and PTH has occasionally been reported (4). In our patient, serum Ca and PTH levels remained high with 3-months of methimazole and atenolol. The impact of both conditions on bone and mineral metabolism are profound, with fractures and kidney stones. Since kidney stones are uncommon in hyperthyroidism, presence of kidney stone in a hyperthyroid hypercalcemic patient should alert the possibility of PHPT. Similarly, significant decrease in bone density in such patient also raises the possibility of PHPT. Prompt diagnosis and appropriate treatment of both conditions is necessary to avoid irreversible complications.