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Diabetes mellitus (DM) is associated with an increased risk of fractures due to deterioration of bone quality, which can be referred to as "diabetic osteodystrophy." Furthermore, the risk of fracture is increased in DM, even if bone mineral density is normal or high and is associated with increased morbidity if a fracture develops. In addition to the pathophysiological mechanisms of DM, diabetesrelated complications and drugs used in the treatment of DM may also affect bone health. Moreover, the increased risk of falling due to microvascular complications, hypoglycemia, and postural hypotension also contributes to the development of fractures. Individuals with DM should be screened for osteoporosis with recommendations similar to those of the general population. When diagnosing osteoporosis and deciding on treatment, it should be kept in mind that DM may be an important risk factor, and lower threshold values of the T score should be used. [ABSTRACT FROM AUTHOR]

Pyrethroid insecticides are currently a widely used class of pesticides. It is therefore important to determine the mechanism of disorders in some mammalian systems due to prolonged exposure to these pesticides and to justify means to prevent poisoning complications. The study was conducted on 30 female rats aged 3 months for 120 days. Intoxication was modeled using α-cypermethrin at a dose of 10 mg/kg. The prevention of intoxication complications was carried out with an adaptogenic complex consisting of the flavonoid quercetin, vitamins C and D3, and minerals (Ca, Mn, Zn, Cu, Se, Mg) at a dose of 500 mg/kg. Assessment of intoxication and preventive efficacy of the adaptogen was performed by determining the duration of the estrous cycle, ovarian organ index, degree of atrophy of the alveolar process in the jaws, as well as density, content of mineral and organic components in the bones. Hepatotoxicity markers were determined in the blood serum, osteoresorption markers in the alveolar bone homogenate, inflammation indicators in the liver, and antioxidant system status in all tissues. Prolonged exposure to α-cypermethrin was associated with a prolongation of the estrous cycle due to a reduction in the diestrus stage and a decrease in the ovarian organ index along with a significant increase in blood estradiol levels. In intoxicated animals, the degree of atrophy of the alveolar process increased and the density of femurs and vertebrae decreased due to a decrease in the weight fraction of the mineral component in the bones. In the bone tissue of the alveolar process, an increase in the activity of elastase and markers of oxidative stress (an increase in the content of malondialdehyde and a decrease in catalase activity), as well as a compensatory increase in the alkaline phosphatase activity were found. In the rat liver, an increase in the acid phosphatase activity and the inhibition of antioxidant defense were observed. An increase in the elastase activity and a decrease in the catalase activity with an increase in the malondialdehyde content were found in the serum of the animals. The use of an adaptogen under conditions of α-cypermethrin intoxication contributed to the normalization of the estrous cycle, ovarian organ index and blood estradiol levels. In the tissue of the femur and vertebrae of rats, the treatment by the prophylactic complex led to an increase in bone density due to an increase in the content of the mineral component, and a decrease in the degree of atrophy of the jaws, in the tissue of which the activation of the enzymatic link of antioxidant defense and a decrease in the activity of destructive elastase too were found. The developed adaptogen prevented the development of oxidative stress and inflammation in the blood serum and liver in the animals. The results of the research indicate a negative effect of α-cypermethrin on the sexual function in female rats, on the state of bone tissue along with the hepatotoxic effect of the pesticide. The proposed agent for the prevention of α-cypermethrin intoxication effectively prevented endocrine disruption in the ovaries, bone destruction and inflammation in the liver.

Pyrethroid insecticides are currently a widely used class of pesticides. It is therefore important to determine the mechanism of disorders in some mammalian systems due to prolonged exposure to these pesticides and to justify means to prevent poisoning com- plications. The study was conducted on 30 female rats aged 3 months for 120 days. Intoxication was modeled using α-cypermethrin at a dose of 10 mg/kg. The prevention of intoxication complications was carried out with an adaptogenic complex consisting of the flavonoid quercetin, vitamins C and D3, and minerals (Ca, Mn, Zn, Cu, Se, Mg) at a dose of 500 mg/kg. Assessment of intoxication and preventive efficacy of the adaptogen was performed by determining the duration of the estrous cycle, ovarian organ index, degree of atrophy of the alveolar process in the jaws, as well as density, content of mineral and organic components in the bones. Hepatotoxicity markers were determined in the blood serum, osteoresorption markers in the alveolar bone homogenate, inflammation indicators in the liver, and antioxidant system status in all tissues. Prolonged exposure to α-cypermethrin was associated with a prolongation of the estrous cycle due to a reduction in the diestrus stage and a decrease in the ovarian organ index along with a significant increase in blood estradiol levels. In intoxicated animals, the degree of atrophy of the alveolar process increased and the density of femurs and vertebrae decreased due to a decrease in the weight fraction of the mineral component in the bones. In the bone tissue of the alveolar process, an increase in the activity of elastase and markers of oxidative stress (an increase in the content of malondialdehyde and a decrease in catalase activity), as well as a compensatory increase in the alkaline phosphatase activity were found. In the rat liver, an increase in the acid phosphatase activity and the inhibition of antioxidant defense were observed. An increase in the elastase activity and a decrease in the catalase activity with an increase in the malondialdehyde content were found in the serum of the animals. The use of an adaptogen under conditions of α-cypermethrin intoxication contributed to the normalization of the estrous cycle, ovarian organ index and blood estradiol levels. In the tissue of the femur and vertebrae of rats, the treatment by the prophylactic complex led to an increase in bone density due to an increase in the content of the mineral component, and a decrease in the degree of atrophy of the jaws, in the tissue of which the activation of the enzymatic link of antioxidant defense and a decrease in the activity of destructive elastase too were found. The developed adaptogen prevented the development of oxidative stress and inflammation in the blood serum and liver in the animals. The results of the research indicate a negative effect of α-cypermethrin on the sexual function in female rats, on the state of bone tissue along with the hepatotoxic effect of the pesticide. The proposed agent for the prevention of α-cypermethrin intoxication effectively prevented endocrine disruption in the ovaries, bone destruction and inflammation in the liver. [ABSTRACT FROM AUTHOR]

Objective To investigate the changes of OAT expression in bone cells in chronic renal failure (CRF) and involved mechanism, and to explore the effect of OAT expression on bone metabolism. Methods Randomly divide the rats into a control group (n=6) and a model group (n=6) .The model group established a rat chronic renal failure model using "single nephrectomy+adenine gavage" method, and the red blood cell ( RBC) and hemoglobin ( HGB) of the rat body were measured using a blood routine analyzer; Measure indicators such as creatinine (Cr), urea nitrogen (BUN), uric acid (UA), blood calcium (Ca2+), and blood phosphorus (P3+) using a fully automated biochemical analyzer; Pathological examination of rat kidneys; X-ray examination of rat tibia; Immunohistochemical examination of bone tissue OAT1 level. Results The bone density of the model group rats is lower than that of the control group; The calcium and phosphorus metabolism of rats in the model group was in metabolic disorder, and the OAT1 value of bone tissue binding was much lower than that of the control group (P= 0.001 8), which was statistically significant. (P=0.001 8) Conclusion Chronic renal failure affected the binding ability of OAT1 in bone tissue, leading to the metabolic disorder for calcium absorption and phosphorus metabolism, thus aggravating renal osteodystrophy (P<0.05). [ABSTRACT FROM AUTHOR]

Simple Summary: Mineral and bone disorder (MBD) is usually prevalent in pediatric patients with chronic kidney disease (CKD) and is correlated with meaningful morbidity. CKD may cause disorders in bone remodeling/modeling, which are more evident in the growing skeleton, expressing as short stature, bone pain and deformities, fractures, slipped epiphyses and ectopic calcifications. Although evaluation of bone health is a crucial part in the clinical care of children with CKD, it persists as a significant challenge for pediatricians. Intense changes in mineral and bone metabolism are frequent in chronic kidney disease (CKD) and represent an important cause of morbidity and reduced quality of life. These disorders have conventionally been defined as renal osteodystrophy and classified based on bone biopsy, but due to a lack of bone biopsy data and validated radiological methods to evaluate bone morphology in children, it has been challenging to effectively assess renal osteodystrophy in pediatric CKD; the consequence has been the suboptimal management of bone disorders in children. CKD–mineral and bone disorder (CKD-MBD) is a new expression used to describe a systemic disorder of mineral and bone metabolism as a result of CKD. CKD-MBD is a triad of biochemical imbalances in calcium, phosphate, parathyroid hormone, and vitamin D; bone deformities and soft tissue calcification. This literature review aims to explore the pathogenesis, diagnostic approach, and treatment of CKD-MBD in children and the effects of renal osteodystrophy on growing skeleton, with a specific focus on the biological basis of this peculiar condition. [ABSTRACT FROM AUTHOR]

This article presents a rare clinical observation of a bone form of primary hyperparathyroidism in a 16-year-old adolescent complicated by a pathological fracture of the right femur. The features of the given case are: late diagnosis of primary hyperparathyroidism in an adolescent with clinical manifestations; complication of the disease with a pathological fracture, which required two-stage treatment, open repositioning and metal plate osteosynthesis; difficulties in the organization of the examination and treatment of the patient, related to the detection of covid-19 and his stay in an infectious department; the need for tactical decision on the sequence of surgical treatment of the fracture and its cause - primary hyperparathyroidism.

The health and productivity of animals, as well as farmers' financial well-being, can be significantly impacted by cattle illnesses. Accurate and timely diagnosis is therefore essential for effective disease management and control. In this study, we consider the development of models and algorithms for diagnosing diseases in cattle based on Sugeno's fuzzy inference. To achieve this goal, an analytical review of mathematical methods for diagnosing animal diseases and soft computing methods for solving classification problems was performed. Based on the clinical signs of diseases, an algorithm was proposed to build a knowledge base to diagnose diseases in cattle. This algorithm serves to increase the reliability of informative features. Based on the proposed algorithm, a program for diagnosing diseases in cattle was developed. Afterward, a computational experiment was performed. The results of the computational experiment are additional tools for decision-making on the diagnosis of a disease in cattle. Using the developed program, a Sugeno fuzzy logic model was built for diagnosing diseases in cattle. The analysis of the adequacy of the results obtained from the Sugeno fuzzy logic model was performed. The processes of solving several existing (model) classification and evaluation problems and comparing the results with several existing algorithms are considered. The results obtained enable it to be possible to promptly diagnose and perform certain therapeutic measures as well as reduce the time of data analysis and increase the efficiency of diagnosing cattle. The scientific novelty of this study is the creation of an algorithm for building a knowledge base and improving the algorithm for constructing the Sugeno fuzzy logic model for diagnosing diseases in cattle. The findings of this study can be widely used in veterinary medicine in solving the problems of diagnosing diseases in cattle and substantiating decision-making in intelligent systems. [ABSTRACT FROM AUTHOR]

Intense changes in mineral and bone metabolism are frequent in chronic kidney disease (CKD) and represent an important cause of morbidity and reduced quality of life. These disorders have conventionally been defined as renal osteodystrophy and classified based on bone biopsy, but due to a lack of bone biopsy data and validated radiological methods to evaluate bone morphology in children, it has been challenging to effectively assess renal osteodystrophy in pediatric CKD; the consequence has been the suboptimal management of bone disorders in children. CKD–mineral and bone disorder (CKD-MBD) is a new expression used to describe a systemic disorder of mineral and bone metabolism as a result of CKD. CKD-MBD is a triad of biochemical imbalances in calcium, phosphate, parathyroid hormone, and vitamin D; bone deformities and soft tissue calcification. This literature review aims to explore the pathogenesis, diagnostic approach, and treatment of CKD-MBD in children and the effects of renal osteodystrophy on growing skeleton, with a specific focus on the biological basis of this peculiar condition.

25-hydroxyvitamin D [25(OH)D] may not optimally indicate vitamin D receptor activity. Higher concentrations of its catabolic product 24,25-dihydroxyvitmin D [24,25(OH)2D] and a higher ratio of 24,25(OH)2D to 25(OH)D (the vitamin D metabolite ratio [VMR]) may provide additional information on receptor activity. We compared the strength of associations of these markers with serum PTH concentrations, hip bone mineral density (BMD), and risk of incident hip fracture in community-living older participants in the Cardiovascular Health Study. Among 890 participants, the mean age was 78years, 60% were women, and the mean 25(OH)D was 28±11ng/ml. In cross-sectional analysis, the strength of association of each vitamin D measure with PTH was similar; a 1% higher 25(OH)D, 24,25(OH)2D, and VMR were associated with 0.32%, 0.25%, and 0.26% lower PTH, respectively (p

Patients with CKD have a 4–fivefold higher rate of fractures. The incidence of fractures increases with deterioration of kidney function. The process of skeletal changes in CKD patients is characterized by compromised bone strength because of deterioration of bone quantity and/or quality. The fractures lead to a deleterious effect on the quality of life and higher mortality in patients with CKD. The pathogenesis of bone loss and fracture is complex and multi-factorial. Renal osteodystrophy, uremic milieu, drugs, and systemic diseases that lead to renal failure all contribute to bone damage in CKD patients. There is no consensus on the optimal diagnostic method of compromised bone assessment in patients with CKD. Bone quantity and mass can be assessed by dual-energy x-ray absorptiometry (DXA) or quantitative computed tomography (QCT). Bone quality on the other side can be assessed by non-invasive methods such as trabecular bone score (TBS), high-resolution bone imaging methods, and invasive bone biopsy. Bone turnover markers can reflect bone remodeling, but some of them are retained by kidneys. Understanding the mechanism of bone loss is pivotal in preventing fracture in patients with CKD. Several non-pharmacological and therapeutic interventions have been reported to improve bone health. Controlling laboratory abnormalities of CKD-MBD is crucial. Anti-resorptive therapies are effective in improving BMD and reducing fracture risk, but there are uncertainties about safety and efficacy especially in advanced CKD patients. Accepting the prevalent of low bone turnover in patients with advanced CKD, the osteo-anabolics are possibly promising. Parathyroidectomy should be considered a last resort for intractable cases of renal hyperparathyroidism. There is a wide unacceptable gap in osteoporosis management in patients with CKD. This article is focusing on the updated management of CKD-MBD and osteoporosis in CKD patients. Chronic kidney disease deteriorates bone quality and quantity. The mechanism of bone loss mainly determines pharmacological treatment. DXA and QCT provide information about bone quantity, but assessing bone quality, by TBS, high-resolution bone imaging, invasive bone biopsy, and bone turnover markers, can guide us about the mechanism of bone loss. [ABSTRACT FROM AUTHOR]

Hormonal changes and hepatic osteodystrophy are less often studied complications of cirrhosis. This study describes the variance in hormones and osteodystrophy between Frail and Not frail patients with cirrhosis. 116 outpatients with cirrhosis were prospectively enrolled in this study. Frailty assessment was done using Liver Frailty Index (LFI). Sociodemographic assessment, anthropometry, nutritional assessment, hormone profile, and dual-energy X-ray absorptiometry scan were done in all patients. 116 patients, predominantly males (100 (86.2%) with mean age of 50.16 years (95% CI, 48.43–51.89) were included. Malnutrition was more common in Frail group as compared to Not frail group. Subjective global assessment (SGA) class-B patients were significantly more in Frail group (37 (74%) vs 3 (4.5%), P = 0.001). The prevalence of lower parathyroid hormone (PTH) (14 (28%) vs 2 (3%)), testosterone (33 (66%) vs 15 (22.7%)), vitamin D3 (44 (88%) vs 39 (59.1%)), and cortisol (37 (74%) vs 37 (56.1) levels was higher in Frail group (P < 0.05). The number of patients diagnosed with osteodystrophy (34 (68%) vs 21 (31.8%), P = 0.001) was significantly higher in Frail group. The marker of osteoclastic activity, β-cross laps, was significantly elevated in the Frail group both in males (736 (655–818) vs 380 (329–432), P = 0.001) and (females 619 (479–758) vs 313 (83–543), P = 0.02). Bone mineral density (BMD) at lumbar spine (LS) and neck of femur (NF) had significant correlation with LFI (ρ = 0.60, P = 0.001 for LS and ρ = 0.59, P = 0.001 for NF), serum testosterone (ρ = 0.58, P = 0.001 for LS and ρ = 0.53, P = 0.001 for NF), β-cross laps (ρ = 0.38, P = 0.001for LS and ρ = 0.35, P = 0.000 for NF), vitamin D3 (ρ = 0.23, P = 0.04 for LS and ρ = 0.25, P = 0.01 for NF), PTH (ρ = 0.52, P = 0.001 for LS and ρ = 0.48. P = 0.001 for NF), and cortisol (ρ = 0.50, P = 0.001 for LS and ρ = 0.45, P = 0.001 for NF) levels. This is the first study that highlights the high prevalence of hormonal changes and hepatic osteodystrophy in frail patients with cirrhosis and opens a new dimension for research and target of therapy in this field. [ABSTRACT FROM AUTHOR]

Background: The growth hormone-insulin-like growth factor (GH-IGF-1) axis and its impairment with sarcopenia, frailty, bone health, complications, and prognosis are not well characterized in cirrhosis., Methods: We investigated the adult decompensated cirrhosis out-patients at a tertiary care institute between 2021 and 2023 for serum GH and IGF-1 levels, and associated them with sarcopenia (CT-SMI in cm 2 /m 2 ), liver frailty index (LFI), osteodystrophy (DEXA), clinical decompensations (overall, ascites, encephalopathy, infection, and bleed), and survival up to 180 days., Results: One-hundred-seventy-two patients, 95% males, aged 46.5 years (median). log IGF-1 levels were negatively associated with sarcopenia, osteodystrophy, LFI, CTP, and MELD-Na score ( P  < 0.05 each). Patients with low IGF-1 levels had a higher incidence of complications (overall, ascites and encephalopathy) than those with intermediate, and high IGF-1 levels ( P  < 0.05 each). Both log IGF-1 (AUC: 0.686) and MELD (AUC: 0.690) could predict 180-day mortality ( P  < 0.05, each). Adding log IGF-1 with MELDNa further improved discriminative accuracy of MELDNa (AUC: 0.729) P  < 0.001. The increase in IGF-1 on follow-up was associated with better survival and fewer complications., Conclusion: Reduced IGF-1 levels reflect sarcopenia, frailty, and osteodystrophy in cirrhosis. Low IGF-1 are associated with severity, development of decompensations, and mortality., (© 2024 Indian National Association for Study of the Liver. Published by Elsevier B.V. All rights are reserved, including those for text and data mining, AI training, and similar technologies.)

Background: Opsismodysplasia (OPSMD) is an extremely rare and severe autosomal recessive skeletal dysplasia that is under the category of severe spondylodysplastic dysplasia. It is characterized by delayed bone maturation, and affected patients are identified by a peculiar craniofacioskeletal dysmorphism in the form of wide anterior fontanelle, depressed nasal bridge, anteverted nares, and short limbs and feet. Radiologically, they are characterized by severe platyspondyly, squared metacarpals, delayed skeletal ossification, and metaphyseal cupping. Case Presentation: We present the clinical and radiological features of a 14-month-old boy with a homozygous, likely pathogenic variant in INPPL1 gene c.2627dup (p.Pro977Thrfs*7) consistent with the diagnosis of OPSMD. He also has dilated cardiomyopathy. Conclusion: OPSMD is an uncommon form of skeletal dysplasia that should be suspected in the context of short stature with characteristic radiological features. Up to now, no definitive therapeutic measures are available, and hence preventive measures are essential in the management of families with affected members. [JBCGenetics 2020; 3(2.000): 100-103]

Background Neuromusculoskeletal anomalies generally in combination with severe clinical symptoms, comprise a heterogeneous group of fairly common and mostly fatal disorders in man and animals. Osteogenesis imperfecta (OI), also known as brittle bone disease, causes bone fragility and deformity. Prominent extra-skeletal accessory manifestations of OI comprise blue/gray sclerae, hearing impairment, lung abnormalities and hypercalciuria. Cases of OI in cattle have been reported. However, no causative mutations have been identified in cattle so far. Aim To report a possible oligogenic origin identified in a calf from clinically healthy parents suffering from OI. Materials and Methods A neonatal embryo transfer male Holstein calf developing multiple fractures with bone tissue showing marked osteopenia was used for whole genome re-sequencing as well as its parents. In addition, 2,612 randomly chosen healthy Holstein cattle were genotyped as well as controls. Results Sixteen candidate genes with potential protein-altering variants were selected revealing non-synonymous variants only within IFITM5 and CRTAP genes. However, in-depth gene analysis did not result in the identification of a single causative mutation in the OI calf. Conclusion The analysis of the OI case revealed a possible oligogenic origin of the disease attributable to additive effects of three candidate genes, i.e., ABCA13, QRFPR, and IFTIM5. Clinical relevance Most OI cases in humans and domestic animals reported so far are caused by distinct dominant or recessive monogenic mutations, therefore a potential oligogenic additive genetic effect is a novel finding. Furthermore, the case presented here demonstrates that cross-species genetic analyses might not always be straightforward.

The health and productivity of animals, as well as farmers’ financial well-being, can be significantly impacted by cattle illnesses. Accurate and timely diagnosis is therefore essential for effective disease management and control. In this study, we consider the development of models and algorithms for diagnosing diseases in cattle based on Sugeno’s fuzzy inference. To achieve this goal, an analytical review of mathematical methods for diagnosing animal diseases and soft computing methods for solving classification problems was performed. Based on the clinical signs of diseases, an algorithm was proposed to build a knowledge base to diagnose diseases in cattle. This algorithm serves to increase the reliability of informative features. Based on the proposed algorithm, a program for diagnosing diseases in cattle was developed. Afterward, a computational experiment was performed. The results of the computational experiment are additional tools for decision-making on the diagnosis of a disease in cattle. Using the developed program, a Sugeno fuzzy logic model was built for diagnosing diseases in cattle. The analysis of the adequacy of the results obtained from the Sugeno fuzzy logic model was performed. The processes of solving several existing (model) classification and evaluation problems and comparing the results with several existing algorithms are considered. The results obtained enable it to be possible to promptly diagnose and perform certain therapeutic measures as well as reduce the time of data analysis and increase the efficiency of diagnosing cattle. The scientific novelty of this study is the creation of an algorithm for building a knowledge base and improving the algorithm for constructing the Sugeno fuzzy logic model for diagnosing diseases in cattle. The findings of this study can be widely used in veterinary medicine in solving the problems of diagnosing diseases in cattle and substantiating decision-making in intelligent systems.

Chronic kidney disease (CKD) and end-stage renal disease (ESRD) are often complicated by high-turnover renal osteodystrophy (HTRO) and secondary hyperparathyroidism (SHPT), characterized by disturbances in mineral metabolism and skeletal abnormalities. Genetic variations within the vitamin D receptor (VDR) gene, known as VDR gene polymorphisms, have been implicated in modulating the susceptibility to HTRO and SHPT. This systematic review aims to evaluate the existing literature on the association between VDR gene polymorphisms and the development of these complications in ESRD and hemodialysis patients. A comprehensive literature search across multiple databases was conducted, and studies investigating VDR gene polymorphisms and HTRO or SHPT in ESRD or hemodialysis patients were included. The included studies examined various VDR gene polymorphisms, such as BsmI, ApaI, TaqI, and FokI, and their associations with clinical outcomes like parathyroid hormone (PTH) levels, bone mineral density, and the development of SHPT or HTRO. The findings suggest that certain VDR gene polymorphisms, notably the ApaI "aa" genotype, BsmI "bb" genotype, TaqI "tt" genotype, and FokI variant, may contribute to the pathogenesis of SHPT and HTRO by affecting PTH levels, bone turnover markers, and vitamin D sensitivity. However, the studies had relatively small sample sizes and were conducted in different populations, limiting generalizability. Further larger-scale studies, functional investigations, and exploration of gene-environment interactions are warranted to elucidate the underlying mechanisms and facilitate personalized treatment approaches for CKD and ESRD patients with mineral and bone disorders., Competing Interests: Conflicts of interest: In compliance with the ICMJE uniform disclosure form, all authors declare the following: Payment/services info: All authors have declared that no financial support was received from any organization for the submitted work. Financial relationships: All authors have declared that they have no financial relationships at present or within the previous three years with any organizations that might have an interest in the submitted work. Other relationships: All authors have declared that there are no other relationships or activities that could appear to have influenced the submitted work., (Copyright © 2024, Sinha et al.)

Hyperphosphatemia is common in chronic kidney disease (CKD). Often seen as the "silent killer" because of its dramatic effect on vascular calcifications, hyperphosphatemia explains, at least partly, the onset of the complex mineral and bone disorders associated with CKD (CKD-MBD), together with hypocalcemia and decreased 1-25(OH)2 vitamin D levels. The impact of CKD-MBD may be immediate with abnormalities of bone and mineral metabolism with secondary hyperparathyroidism and increased FGF23 levels, or delayed with poor growth, bone deformities, fractures, and vascular calcifications, leading to increased morbidity and mortality. The global management of CKD-MBD has been detailed in international guidelines for adults and children, however, with difficulties to obtain an agreement on the ideal PTH targets. The clinical management of hyperphosphatemia is a daily challenge for nephrologists and pediatric nephrologists, notably because of the phosphate overload in occidental diets that is mainly due to the phosphate "hidden" in food additives. The management begins with a dietary restriction of phosphate intake, and is followed by the use of calcium-based and non-calcium-based phosphate binders, and/or the intensification of dialysis. The objective of this review is to provide an overview of the pathophysiology of hyperphosphatemia in CKD, with a focus on its deleterious effects and a description of the clinical management of hyperphosphatemia in a more global setting of CKD-MBD. [ABSTRACT FROM AUTHOR]

The endocrine system plays a key role in the pathogenesis of the non-infectious pathology of dairy cows. However, the role of a number of hormones in pathology is not clear. These hormones include insulin-like growth factors and leptin. The insulin-like growth factor is synthesized predominantly in the liver in response to an increase in the level of somatotropic hormone in the blood. According to its physiological properties, it is close to insulin, structurally similar, has common receptors that trigger the same chain of reactions: stimulates transport of amino acids and glucose in the muscles, increases the sensitivity of cells to insulin, in adipose tissue, transport glucose, oxidation of glucose to carbon dioxide, the inclusion of glucose in lipids. Leptin is synthesized by adipocytes, and its main physiological function is to reduce the synthesis of macroergic compounds and increase energy expenditure. Circulating in the blood, it helps to maintain an optimal level of glucose, which is necessary for the energy needs of the body. The purpose of this study was to investigate the concentration of insulin-like growth factor, leptin, glucose, pyruvate and lactate in the blood of cows under secondary osteodystrophy, ketosis and hepatodistrophy. This will give an opportunity to better understand the pathogenesis and create theoretical preconditions for the development of informative diagnostic tests and effective means of treatment. The experiment was conducted on dairy cows, analogues by age, breed, productivity and physiological state. According to clinical features, urine analysis and values of biochemical parameters of blood of experimental cows were divided into four groups: 1 – clinically healthy cows, 2 – patients with osteodystrophy, 3 – patients with ketosis, 4 – patients with hepatodistrophy. The obtained results of research indicate that the internal non-contagious pathology in dairy cows deficiency of exchange energy is recorded, which induces an increase in the activity of gluconeogenesis and is expressed by lowering the concentration of glucose and increasing the content of pyruvate and lactate. At the same time, a decrease in the level of insulin-like growth factor and leptin was found. The lowest level of insulin-like growth factor and leptin was determined by ketosis. The decrease in the level of tissue hormones in the blood plasma of cows under osteodystrophy was within the statistical error.

Hyperparathyroidism is one of the most common endocrinopathies. This disease leads to a violation of phosphorus-calcium metabolism and the washing out of calcium from bone tissue. Breach of the skeleton’s structure in hyperparathyroidism is often mistaken for metastatic bone damage, which leads to incorrect treatment tactics. In this work we present the clinical observation of a patient with an adenoma of the parathyroid gland and a severe bone form of hyperparathyroidism. Multiple lesions of bones with destruction of the cortical layer and the presence of the softtissue component were initially regarded as metastases in the bone. However, the morphological pattern of bone foci, as well as an elevated level of calcium and parathyroid hormone, made it possible to diagnose the bony form of hyperparathyroidism. The search for the cause of hyperparathyroidism revealed a tumor in the projection of the right lower parathyroid gland. Surgical removal of parathyroid adenoma led to the normalization of the level of calcium and parathyroid hormone. The article presents data of laboratory-instrumental methods of research and the results of surgical treatment of a patient.

Chronic kidney disease affects patients of all ages and, as it progresses, it greatly affects their lives, especially with the complications it causes. One major complication is renal osteodystrophy (ROD) which starts to develop from the early stages of the disease, but becomes most apparent in patients in need of renal replacement therapy. Diagnosing ROD in the early stages remains a challenge, which brings up the need to find novel biomarkers. Studies are focusing on the role of fibroblast growth factor 23 and Klotho in the bone and mineral homeostasis, but the results are conflicting. ROD remains a major complication in CKD patients, therefore we need to gain a better understanding from the pathophysiological point of view, in order to be able to adjust the medical therapy. [ABSTRACT FROM AUTHOR]

Background: From 1980s to the new millennium, the number of patients surviving with end stage renal disease (ESRD) has increased by 3 fold. This is driven by early detection of primordial and primary risk factors, state of the art renal replacement therapy and ease of public access to healthcare. Renal osteodystrophy (RO) is a metabolic bone disease causing significant morbidity in patients with ESRD, in particular fragility fractures. In this case series, we present the surgical management of 3 ESRD patients with pathological fractures of the neck of femur (NOF) and surgical treatment (parathyroidectomy) of tertiary hyperparathyroidism of ESRD patients in the same surgical setting. Up to date there has been no reports on bipolar hemiarthroplasty and total parathyroidectomy implemented in the same operative setting. Methods: We present 3 cases, 2 males and a female with an average age of 48 years. All patients presented with no trauma or minimal trauma. With high index of suspicion and after confirming the diagnosis with advanced imaging, the patients underwent cemented modular hemiarthroplasty with posterior approach. Parathyroidectomy was sequentially performed to address the tertiary hyperparathyroidism at the same setting. We followed them for 48 months. Results: At 48-month follow up, all the patients were at their pre-morbid ambulatory status and there were no major complications. They did not need any revision surgery or re-operation either for the hemiarthroplasty surgery or the parathyroidectomy during the follow up period. Conclusion: To avoid diagnostic pitfalls in this group of patients we recommend MRIs of both hips in patients complaining of unilateral hip pain even when the roentgenograms are clear of fractures. Total parathyroidectomy at the same setting with the bipolar hemi-arthroplasty is a safe combination. This reduces the anaesthesia risk, the recovery time as well as the equilibrium time for calcium homeostasis. [ABSTRACT FROM AUTHOR]

A female German Shepherd dog aged 10 years was presented to the Referral Veterinary Polyclinic, Indian Veterinary Research Institute, Bareilly, with the chief complaint of facial swelling for the last 7 days. Physical examination revealed a painless, soft swelling of the maxilla and mandible. Radiographic examination showed fibrous osteodystrophy. Serum biochemistry revealed hypocalcemia, hyperphosphatemia and azotemia. Based on the clinical, laboratory and imaging studies, the case was diagnosed as renal osteodystrophy. [ABSTRACT FROM AUTHOR]

Pseudopseudohypoparathyroidism is a rare clinical entity of autosomal dominant inheritance, which shows phenotypic similarity to pseudohypoparathyroidism. However, the main difference lies in their biochemical profiles. The former disease is characterized by normal serum calcium, phosphorus, vitamin D, and parathyroid hormone (PTH) level, whereas the latter shows features suggestive of PTH resistance. Our patient presented after post blunt trauma of head with diabetes insipidus and short stature. Investigations revealed multiple pituitary hormone deficiency. Further examination was conducted for pseudohypoparathyroidism, keeping in mind short metacarpals, knuckle knuckle dimple dimple sign, and short stature, but normal calcium, phosphorus, vitamin D and PTH value led to the diagnosis of pseudopseudohypoparathyroidism. GNAS mutation analysis is necessary to confirm the diagnosis, which could not be performed in this patient due to the high cost. This case shows that pseudopseudohypoparathyroidism, although a rare disease, should be appropriately investigated in such patients if they present with peculiar skeletal features of pseudohypoparathyroidism. [ABSTRACT FROM AUTHOR]

L'ostéodystrophie hépatique peut compliquer les hépatites virales chroniques. En Tunisie, l'étude des anomalies du métabolisme osseux dans ces cas est rare. Les objectifs de ce travail étaient d'évaluer l'atteinte osseuse et l'intérêt des marqueurs biologiques de remodelage osseux dans l'ostéodystrophie des hépatopathies chroniques virales B et C. Il s'agit d'une étude rétrospective, descriptive et analytique. Nous avons inclus des patients atteints d'hépatopathies virales chroniques B et C compensées indemnes d'autres pathologies affectant le métabolisme osseux. Le bilan biologique a comporté la calcémie, la phosphorémie, les phosphatases alcalines, la parathormone, la vitamine D, l'ostéocalcine et le CTX urinaire. La densitométrie était mesurée au niveau du rachis et du fémur. L'étude statistique a été faite par SPSS 20.0. Quarante et un patients et 33 témoins ont été colligés (âge médian respectif : 51 et 44 ans). Une vitamine D basse était trouvée chez 97,6 % des patients (médiane = 8,6 ng/mL). Une hyperparathyroïdie a été notée chez neuf patients (22 %). L'ostéocalcine était basse chez 21 % des patients (médiane = 21,7 ng/mL). Le taux médian de CTX urinaire était de 204 μg/mmol de créatinine. Une masse osseuse basse était notée dans 70,7 % des cas (ostéoporose = 9,7 %, ostéopénie = 61 %). Aucune corrélation n'a été trouvée entre les paramètres de remodelage osseux et la densitométrie osseuse ainsi que l'activité de l'hépatopathie ou la fibrose. L'ostéodystrophie est très fréquente et doit être dépistée au cours des hépatopathies virales chroniques compensées indépendamment de l'activité ou de la fibrose. Le seul examen qui serait recommandé dans ce cas est l'ostéodensitométrie. Hepatic osteodystrophy may be a complication of chronic viral hepatitis. In Tunisia, there is a scarcity of studies that focused on bone metabolism abnormalities in these populations. The aim of this work was to evaluate the bone status and the usefulness of bone turn over markers in osteodystrophy associated to chronic viral hepatitis B and C. It is a retrospective, descriptive and analytic study. We included patients suffering from chronic viral hepatitis B and C, non cirrhotic. Any disease which could interfere with bone metabolism was an exclusion criteria. The biological tests performed were: calcémia, phosphorémia, alcalin phosphatases, parathormon, vitamine D, osteocalcin and urinary CTX. Bone mineral density was measured at the rachis and the femoral bone. Statistical analysis was done by SPSS 20.0. Forty-one patients and 33 controls were enrolled. The median ages were respectively 51 and 44 years. Vitamine D was low in 97.6% of the patients (median = 8.6 ng/mL). hyperparathyroïdism was noted in nine patients (22%). Osteocalcin was low in 21% of cases (median = 21.7 ng/mL). The median rate of urinary CTX was 204 μg/mmol of creatinine. Low bone mineral density was observed based on 70.7% of cases (osteoporosis = 9.7%, osteopenia = 61%). We did not found any correlation between bone turn over markers and mineral density neither activity nor fibrosis. Hepatic osteodystrophy is very frequent independently of activity or fibrosis and patients with chronic viral hepatitis should be screened for. The only investigation recommended in these patients is measurement of bone mineral density. [ABSTRACT FROM AUTHOR]

Bone is a dense, semi rigid, porous, calcified connective tissue forming the major portion of the skeleton of most vertebrates. It consists of a dense organic matrix and an inorganic mineral component. Bone remodelling is a complex process by which old bone is continuously replaced by new tissue, which requires interaction between different cell phenotypes and is regulated by a variety of biochemical and mechanical factors. In a homeostatic equilibrium, the process of resorption and formation are balanced so that old bone is continuously replaced by new tissue and it adapts to mechanical load and strain. Several local and systematic factors which cause disturbances in bone resorption and deposition leads to abnormal or defective development of bone commonly termed as osteodystrophy - A defective ossification of bone usually is associated with disturbed calcium and phosphorus metabolism. The better understanding of molecular cellular biology and pathogenic mechanism aids to define the abnormalities in osteoblastic and osteoclastic lineages and to develop new therapeutic approaches. [ABSTRACT FROM AUTHOR]

The control of secondary hyperparathyroidism (SHPT) in pediatric chronic kidney disease is of utmost importance. Even though parathyroid hormone (PTH) is an important biomarker of mineral and bone disorders associated to CKD (CKD-MBD), calcium, phosphate, alkaline phosphatase, and vitamin D are also crucial and should be assessed together. In pediatric dialysis, high PTH levels have been associated with impaired longitudinal growth, bone disease, cardiovascular comorbidities, left ventricular hypertrophy, anemia, and even mortality (when PTH levels were above 500 pg/mL, i.e., 8.3-fold the upper normal limit (UNL)). As such, high PTH levels are for sure deleterious, but too low PTH levels have also been shown to impair growth and to promote vascular calcifications because of the underlying adynamic bone. This manuscript is part of a pros and cons debate for keeping PTH levels within the normal range in pediatric CKD, focusing on the pros. High bone turnover lesions can occur at lower PTH levels than "current" guidelines would suggest; thus, PTH alone is not a good predictor of the underlying osteodystrophy. PTH results can vary locally depending on the assay. Existing guidelines for PTH targets are conflicting and based on a very little evidence. However, the 120–180 pg/mL (2- to 3-fold the UNL) range is common to most of the guidelines; it seems to be a reasonable target in children undergoing dialysis, even though it does not correspond to "normal" PTH levels. As always, the philosophy of PTH levels in pediatric dialysis may be balanced, i.e., "not too low, not too high, and keep phosphate under control." [ABSTRACT FROM AUTHOR]

We recently studied a patient who meets criteria for autistic disorder and has a 2q37 deletion. Molecular cytogenetic studies were carried out using DNA isolated from 22 different 2q37 mapped BACs to more precisely define the extent of the chromosome deletion. We also analyzed 2q37 mapped polymorphic markers. In addition DNA sequences of BACs in the deletion region were scanned to identify microsatellite repeats. We describe four new polymorphic microsatellite repeat markers in the 2q37.3 region. These markers enabled us to determine the parental origin of the deletion in our patient. DNA from 8-13 unrelated individuals was used to determine heterozygosity estimates for these markers. We review four genes deleted in our patient - genes whose known functions and sites of expression in the brain and/or bone make them candidates for involvement in autism and/or the osteodystrophy observed in patients with 2q37.3 deletions.

Background: Disordered metabolism of bone and minerals is a problem frequently encountered in patients with chronic kidney disease. Early biochemical changes include altered calcium and phosphate balance, while advanced disease produces reduced bone strength and extraskeletal calcification. The syndrome describing this constellation of findings is termed chronic kidney disease mineral and bone disorder. Case Report: This report details a rare and extrememanifestation of chronic kidney disease mineral and bone disorder in a patient on long-term hemodialysis for end-stage renal failure. Progressive abnormalities of the thoracic skeleton were ultimately severe enough to produce restrictive lung physiology and symptomatic respiratory failure. Conclusion: Cases of chronic kidney disease mineral and bone disorder with pronounced clinical sequelae occur uncommonly in contemporary practice because of early detection and effective therapies. To our knowledge, this report is the first case in the literature of severe thoracic involvement manifesting as respiratory failure. [ABSTRACT FROM AUTHOR]

The risk of mineral and bone disorders among patients with chronic kidney disease is substantially elevated, owing largely to alterations in calcium, phosphorus, vitamin D, parathyroid hormone, and fibroblast growth factor 23. The interwoven relationship among these minerals and hormones results in maladaptive responses that are differentially affected by the process of kidney transplantation. Interpretation of conventional labs, imaging, and other fracture risk assessment tools are not standardized in the post-transplant setting. Post-transplant bone disease is not uniformly improved and considerable variation exists in monitoring and treatment practices. A spectrum of abnormalities such as hypophosphatemia, hypercalcemia, hyperparathyroidism, osteomalacia, osteopenia, and osteoporosis are commonly encountered in the post-transplant period. Thus, reducing fracture risk and other bone-related complications requires recognition of these abnormalities along with the risk incurred by concomitant immunosuppression use. As kidney transplant recipients continue to age, the drivers of bone disease vary throughout the post-transplant period among persistent hyperparathyroidism, de novo hyperparathyroidism, and osteoporosis. The use of anti-resorptive therapies require understanding of different options and the clinical scenarios that warrant their use. With limited studies underscoring clinical events such as fractures, expert understanding of MBD physiology, and surrogate marker interpretation is needed to determine ideal and individualized therapy.

Renal osteodystrophy develops as a result of phosphocalcium metabolism imbalance in patients with advanced chronic kidney disease. The aspects of renal osteodystrophy pathomechanism are still incompletely elucidated; however, recent findings regarding the importance and action of fibroblast growth factor 23 have led to changes in recommendations for monitoring disease activity. Despite the availability of international monitoring guidelines and the recent findings on the pathomechanism of this condition, the therapeutic options remain limited and the prognosis is discouraging. [ABSTRACT FROM AUTHOR]

Primary hyperparathyroidism (PHPT) is currently the most common endocrine disorder in Czech Republic after diabetes and thyroid diseases particularly in postmenopausal women. Over the past 40 years PHPT has changed from a rare severe disease of the bones and kidneys to common disease with hypertension, peptic ulcer, pancreatitis, easy fatigue and proximal muscle weakness. During 43 years we have examined one of the greatest groups of patients with PHPT. In the early 1970 the estimated incidence of PHPT in former Czechoslovakia was approximately 8 cases per 100 000 persons per year. Our data showed that the incidence of PHPT increased sharply to 24 cases per 100 000 persons per year in same community with the introduction of automated serum calcium and iPTH measurement. The disease is four times more frequent in women as in man. The ratio women to men did not changed since 1981. However the incidence of PHPT changed in Czech Republic from previous years, it develops around the fifth decade of life and is increasingly discovered with advancing age. The incidence of hypertension, diabetes mellitus, cholelithiasis, pancreatitis and peptic ulcer among patients with PHPT is higher as compared with the incidence of these diseases in the general population. However there are still patients suffering from bone and renal complication of PHPT. Removing the adenoma by an experienced surgeon is the first choice of treatment of patients with PHPT. The study offers valuable data on the actual state of hyperparathyroid patients in the Czech Republic.

Renal osteodystrophy is a skeletal pathology characterized by bone mineralization deficiency, which is a direct result of endocrine and electrolyte derangements that accompany chronic kidney disease. We hereby present a case of a 60-year-old man with chronic renal failure showing classical osseous changes of osteomalacia and osteosclerosis.

Background Nutritional fibrous osteodystrophy may be developed due to dietary deficiency of calcium or dietary excess of phosphorus. Fibrous osteodystrophy (FOD) provokes hyperostotic distortion of cancellous bones, connective tissue proliferation, and poor mineralization of bone. The objectives of this study were to report the clinical characteristics and therapeutic management of FOD in goats. Materials and methods Four out of 8 Jamnapari goats developed fibrous osteodystrophy in a small scale intensive household farm in Chittagong. The age range of the affected goats was 4-5 months. The feeding history of goats was primarily wheat bran, gram and pea husk. Blood sample from all affected and non-affected animals and feed sample from household farm were collected for laboratory analysis. Fibrous osteodystrophy was primarily diagnosed by observing clinical signs of mandibular and maxillary enlargement, pain on pressure at the enlarged bone, protruded tongue and dyspnea, which was then confirmed by high level of phosphorus in serum evaluation. Results The calcium and phosphorus contents in the sampled gram, pea husk and bran were 0.5%, 0.3% and 0.5%, and 0.71%, 0.49% and 0.61%, respectively. Most of the affected animals had increased serum levels of phosphorus, glucose and alkaline phosphatase and decreased level of calcium. Based on the clinical findings and the laboratory report, the cases were diagnosed as fibrous osteodystrophy due to nutritional imbalance in diet. The owner was advised strictly to stop providing any bran to animals (affected and healthy). Affected animals were additionally treated with calcium preparation, vitamin ADE, ketoprofen, protein, and penicillin-streptomycin combination. Conclusion Treatment of fibrous osteodystrophy required a long time recovery along with balanced ration. A combined therapy of calcium and vitamin D and protein preparation is effective for treatment along with adequate green grass and balanced rations. [ABSTRACT FROM AUTHOR]

The aim of this study was to establish the indicators of protein and lipid metabolism in Saanen goats in different physiological periods and with osteodystrophy. Fifteen goats were studied in the spring (postpartum period), in summer (lactation period), in autumn (initial fetal period of gestation), in winter (ending fetal period of gestation) for determine the influence of the physiological state of animals on the level of biochemical parameters in the blood serum. Two groups of goats were formed for 10 head in each: the first group - clinically healthy, the second - with clinical signs of osteodystrophy for establish the biochemical parameters of osteodystrophy. The content of total protein, protein fractions, β-lipoproteins, cholesterol, triglycerides and activity of the enzymes AlAT and AsAT were determined in the blood serum of goat's. It was established that the level of biochemical parameters varied in goats of the Saanen breed in different physiological periods. In goats with osteodystrophy there were significant changes in the parameters of protein and lipid metabolism: decrease levels of albumins; increase levels of β- and γ-globulin the activity of transaminases and concentration of ß-lipoproteins. [ABSTRACT FROM AUTHOR]

The purpose of this study was to research comparative analysis of data that have been obtained after clinical examination of goats and analysis of biochemical research of the level of metabolites of bone tissue metabolism in blood serum and urine for determination of criteria at diagnostics of osteodystrophy. The material of the study consisted of 20 adult goats. Diagnosis of was made according to physical examination of goats and analysis of biochemical research of the level of metabolites of bone tissue metabolism in blood serum and urine. Activity of aminotransferase (alanine aminotransferase, aspartate aminotransferase) and alkaline phosphatase and also concentration of glycoproteins (GP), chondroitin sulfate, fractional content of glucosaminoglycans, content of total and ionized calcium were assessed in blood serum. The content of hydroxyproline and total uronic acid were analyzed in urine. Comparative analysis of total clinical status of goats and level of biochemical components in blood serum and urine that characterize the state of connective tissue at diagnostics of osteodystrophy was conducted. The intergroup significant differences of some biochemical parameters (aspartate aminotransferase, alkaline phosphatase, chondroitin sulfate, fraction II mucopolysaccharides, sum of fractions glucosaminoglycans) were determined. Further investigation must be conducted to determine the biochemical parameters in goat with subclinical signs of osteodystrophy. [ABSTRACT FROM AUTHOR]