Books: 'Vitamin D; bone cells'

1

Maisonneuve, Caroline. The influence of vitamin D repletion on bone and dentin apposition in vitamin D deficient rats. [Toronto]: Faculty of Dentistry, University of Toronto, 1985.

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2

Wallington, Lisa Ann. Investigations of the influences of retinoids and vitamin D[inferior 3] on HL60 cells. Birmingham: University of Birmingham, 1997.

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3

International, Workshop on Calcified Tissues (6th 1984 Kiryat ʻAnavim Israel). Current advances in skeletogenesis: Induction, biomineralization, bone seeking hormones, congenital and metabolic bone diseases : proceedings of the Sixth International Workshop on Calcified Tissues, Kiryat-Anavim, Israel, 18-23 March 1984. Amsterdam: Excerpta Medica, 1985.

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4

Arie, Harell, Sela Jona, and Ornoy Asher, eds. Current advances in skeletogenesis: Induction, biomineralization, bone seeking hormones, congenital and metabolic bone diseases : proceedings of the Sixth International Workshop on Calcified Tissues, Kiryat-Anavim, Israel, 18-23 March 1984. Amsterdam: Excerpta Medica, 1985.

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5

V, Cohn David, Glorieux Francis H, Martin T. John, and American Society for Bone and Mineral Research. Meeting, eds. Calcium regulation and bone metabolism: Basic and clinical aspects : proceedings of the 10th International Conference on Calcium Regulating Hormones and Bone Metabolism, Montréal, September 9-14, 1989. Amsterdam: Excerpta Medica, 1990.

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6

V, Cohn David, Martin T. John, Meunier P. J, and International Conferences on Calcium Regulating Hormones, Inc., eds. Calcium regulation and bone metabolism: Basic clinical aspects : proceedings of the 9th International Conference on Calcium Regulating Hormones and Bone Metabolism, Nice, 25 October-1 November 1986. Amsterdam: Excerpta Medica, 1987.

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7

Ringe, Johann. Alfacalcidol in prevention and treatment of all major forms of osteoporosis and in renal osteopathy: Distinction to plain vitamin D, clinical evidence, and practical recommendations. Stuttgart: Thieme, 2006.

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8

International Congress on Calciotropic Hormones and Calcium Metabolism. (6th 1987 Abano Terme, Italy). Calciotropic hormones and calcium metabolism: Proceedings of the 6th International Congress on Calciotropic Hormones and Calcium Metabolism, Abano Terme, Centro Congressi Hotel Alexander, March 25-28, 1987. Verona: Bi & Gi Medical and Scientific Publishers, 1988.

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9

M, Cecchettin, and Segre Giorgio, eds. Calciotropic hormones and calcium metabolism: Proceedings of the 5th International Congress on Calciotropic Hormones and Calcium Metabolism, Venice, Italy, 28-30 April 1985. Amsterdam: Excerpta Medica, 1986.

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10

H, Morii, ed. Calcium-regulating hormones. Basel: Karger, 1991.

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11

Jonathan, Prince, ed. Survival of the Sickest: The Surprising Connections Between Disease and Longevity. London: Harper, 2008.

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12

Moalem, Sharon. Survival of the Sickest: A Medical Maverick Discovers the Surprising Connections Between Disease and Longevity. New York: HarperCollins e-books, 2007.

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13

Jonathan, Prince, ed. Survival of the Sickest: A Medical Maverick Discovers Why We Need Disease. New York: William Morrow, 2007.

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14

Moalem, Sharon, and Jonathan Prince. Survival of the Sickest: A Medical Maverick Discovers Why We Need Disease. Pymble, NSW, Australia: William Morrow, 2007.

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15

C, Farach-Carson Mary, and United States. National Aeronautics and Space Administration., eds. Round 1 progress report: Anabolic vitamin D analogs as countermeasures to bone loss. [Washington, DC: National Aeronautics and Space Administration, 1997.

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16

Petrovich, Patrick Martin. Vitamin A, vitamin D r, and epidermal growth factor: mechanisms of interaction in rat bone cells. 1986.

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17

Bender, David A. 7. Vitamins and minerals. Oxford University Press, 2014. http://dx.doi.org/10.1093/actrade/9780199681921.003.0007.

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Along with energy and protein, the body needs two further groups of nutrients in the diet, in relatively small amounts: mineral salts and vitamins. ‘Vitamins and minerals’ explains how these micro-nutrients are essential for maintenance of normal health, growth, and metabolic integrity. Vitamin D and niacin are the only vitamins that can be synthesized by the body; all other vitamins must be provided in the diet. The most important minerals are iron and calcium, but other trace elements are required in small amounts. Iron is needed for synthesis of the protein haemoglobin, which transports oxygen in red blood cells, and calcium is required for bone formation and regulating the activity of muscle.

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18

Butler, Gary, and Jeremy Kirk. Calcium, vitamin D, and bone disorders. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780199232222.003.0081.

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Physiology of calcium regulation 272Bone mineralization 274Causes of loss of bone mass 276Hypocalcaemia 278Hypercalcaemia 282Rickets 284Further reading 287The control of calcium metabolism is complex and depends on several systems—parathyroid hormone, calcitonin, and vitamin D3—which have an interdependence which is not yet fully understood (...

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19

Gutiérrez, Orlando M. Fibroblast growth factor 23, Klotho, and phosphorus metabolism in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0119.

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Fibroblast growth factor 23 (FGF23) and Klotho have emerged as major hormonal regulators of phosphorus (P) and vitamin D metabolism. FGF23 is secreted by bone cells and acts in the kidneys to increase urinary P excretion and inhibit the synthesis of 1,25 dihydroxyvitamin D (1,25(OH)2D) and in the parathyroid glands to inhibit the synthesis and secretion of parathyroid hormone. Phosphorus excess stimulates FGF23 secretion, likely as an appropriate physiological adaptation to maintain normal P homeostasis by enhancing urinary P excretion and diminishing intestinal P absorption via lower 1,25(OH)2D. The FGF23 concentrations are elevated early in the course of chronic kidney disease (CKD) and may be a primary initiating factor for the development of secondary hyperparathyroidism in this setting. Klotho exists in two forms: a transmembrane form and a secreted form, each with distinct functions. The transmembrane form acts as the key co-factor needed for FGF23 to bind to and activate its cognate receptor in the kidneys and the parathyroid glands. The secreted form of Klotho has FGF23-independent effects on renal P and calcium handling, insulin sensitivity, and endothelial function. Disturbances in the expression of Klotho may play a role in the development of altered bone and mineral metabolism in early CKD. In addition, abnormal circulating concentrations of both FGF23 and Klotho have been linked to excess cardiovascular disease, suggesting that both play an important role in maintaining cardiovascular health.

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20

Covic, Adrian, Mugurel Apetrii, Luminita Voroneanu, and David J. Goldsmith. Vascular calcification. Edited by David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0120_update_001.

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Vascular calcification (VC) is a common feature of patients with advanced CKD and it could be, at least in part, the cause of increased cardiovascular mortality in these patients. From a morphologic point of view, there are at least two types of pathologic calcium phosphate deposition in the arterial wall—namely, intima calcification (mostly associated with atherosclerotic plaques) and media calcification (associated with stiffening of the vasculature, resulting in significantly adverse cardiovascular outcomes). Although VC was viewed initially as a passive phenomenon, it appears to be a cell-mediated, dynamic, and actively regulated process that closely resembles the formation of normal bone tissue, as discovered recently. VC seems to be the result of the dysregulation of the equilibrium between promoters and inhibitors. The determinants are mostly represented by altered calcium and phosphorus metabolism, secondary hyperparathyroidism, vitamin D excess, high fibroblast growth factor 23, and high levels of indoxyl sulphate or leptin; meanwhile, the inhibitors are vitamin K, fetuin A, matrix G1a protein, osteoprotegerin, and pyrophosphate. A number of non-invasive imaging techniques are available to investigate cardiac and vascular calcification: plain X-rays, to identify macroscopic calcifications of the aorta and peripheral arteries; two-dimensional ultrasound for investigating the calcification of carotid arteries, femoral arteries, and aorta; echocardiography, for assessment of valvular calcification; and, of course, computed tomography technologies, which constitute the gold standard for quantification of coronary artery and aorta calcification. All these methods have a series of advantages and limitations. The treatment/ prevention of VC is currently mostly around calcium-mineral bone disease interventions, and unproven. There are interesting hypotheses around vitamin K, Magnesium, sodium thiosulphate and other potential agents.

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21

Kuhlencordt, Friedrich. Calcium Metabolism, Bone and Metabolic Bone Diseases. Springer, 2012.

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22

Aging, National Institute on, ed. Osteoporosis: The bone thief. [Gaithersburg, MD]: U.S. Dept. of Health and Human Services, Public Health Service, National Institutes of Health, National Institute on Aging, 2004.

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23

Herdes, Thomas Dieter. Effects of glucocorticoids and vitamin D on bone apposition in rats. 1985.

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24

Ann, Cranney, United States. Agency for Healthcare Research and Quality., and University of Ottawa Evidence-based Practice Center., eds. Effectiveness and safety of vitamin D in relation to bone health. Rockville, MD: U.S. Dept. of Health and Human Services, Public Health Service, Agency for Healthcare Research and Quality, 2007.

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25

Khavandi, Kaivan, Halima Amer, Sarah Withers, and Behdad Afzali. Pleiotropic effects of vitamin D. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0127.

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Vitamin D is a fat-soluble steroid pro-hormone integral to physiological health, fulfilling a central role in skeletal mineralization, bone metabolism, and immune biology. Although vitamin D is synthesized photochemically in the skin and some is absorbed from dietary sources, vitamin D insufficiency and deficiency are very common. Epidemiological studies have demonstrated a strong association between vitamin D and kidney and heart disease, and some supplementation studies have suggested that repletion may prevent and/or ameliorate cardiorenal injury. This chapter focuses on vitamin D biology and discusses the many associations of vitamin D perturbation with diseases of humans.

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26

Anderson, Paul. Physiological Basis of Metabolic Bone Disease. Taylor & Francis Group, 2017.

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27

Anderson, Paul. Physiological Basis of Metabolic Bone Disease. Taylor & Francis Group, 2014.

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28

Anderson, Paul, Borje Edgar Christopher Nordin, and Howard Arthur Morris. Physiological Basis of Metabolic Bone Disease. Taylor & Francis Group, 2014.

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29

Anderson, Paul, Borje Edgar Christopher Nordin, and Howard Arthur Morris. Physiological Basis of Metabolic Bone Disease. Taylor & Francis Group, 2014.

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30

Gluckman, Sir Peter, Mark Hanson, Chong Yap Seng, and Anne Bardsley. Vitamin D in pregnancy and breastfeeding. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198722700.003.0015.

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Vitamin D, which is synthesized in skin exposed to UV light, or is consumed in the diet, plays a key role in maintaining bone integrity via the regulation of calcium and phosphorus homeostasis. It also influences a number of extra-skeletal processes, including immune function and blood glucose homeostasis. Maternal vitamin D deficiency in pregnancy leads to poor fetal skeletal mineralization in utero that can manifest as rickets in newborns. In addition to skeletal effects, women with very low vitamin D status face increased risks of other adverse pregnancy outcomes and possible long-term effects on their own health and that of their offspring. However, controversy remains over definitions of vitamin D sufficiency and deficiency, complicating recommendations on maternal intakes. At a minimum, all pregnant women should take a supplement of 400 IU/day, in addition to sensible sun exposure and increasing their intake of food sources.

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31

Jadon, Deepak R., Tehseen Ahmed, and Ashok K. Bhalla. Disorders of bone mineralization—osteomalacia. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0146.

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Disorders of bone mineralization cause rickets in children and osteomalacia in adults. Both remain common in developing countries. Incidence in Western countries had declined since the fortification of foodstuffs, but appears to be increasing again. Calcium and inorganic phosphate are the key precursors for bone mineralization and growth. The commonest aetiology of osteomalacia is vitamin D deficiency, primarily due to low dietary intake and inadequate sun exposure. In the last decade gene mutations have been identified that are responsible for inherited rickets and osteomalacia, particularly those that result in phosphate deficiency, hypophosphatasia, and vitamin D receptor or metabolizing enzyme mutations. Additionally, the pathogenesis of tumour-induced osteomalacia is becoming better understood. Osteomalacia may present as bone pain and tenderness, muscle pain and weakness, and skeletal deformity or fracture. Key investigations include biochemical assessment and plain radiographs. Radioisotope bone scans and bone biopsy may be considered in selected cases. Differential diagnoses include osteoporosis, seronegative arthritides, and localized soft tissue disorders. Treatment, guided by the underlying aetiology, aims to reduce symptoms, fracture risk, bone deformity and sequelae. Vitamin D deficient patients require vitamin D and calcium replacement.

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32

Jadon, Deepak R., Tehseen Ahmed, and Ashok K. Bhalla. Disorders of bone mineralization—osteomalacia. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199642489.003.0146_update_001.

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Disorders of bone mineralization cause rickets in children and osteomalacia in adults. Both remain common in developing countries. Incidence in Western countries had declined since the fortification of foodstuffs, but appears to be increasing again. Calcium and inorganic phosphate are the key precursors for bone mineralization and growth. The commonest aetiology of osteomalacia is vitamin D deficiency, primarily due to low dietary intake and inadequate sun exposure. In the last decade gene mutations have been identified that are responsible for inherited rickets and osteomalacia, particularly those that result in phosphate deficiency, hypophosphatasia, and vitamin D receptor or metabolizing enzyme mutations. Additionally, the pathogenesis of tumour-induced osteomalacia is becoming better understood. Osteomalacia may present as bone pain and tenderness, muscle pain and weakness, and skeletal deformity or fracture. Key investigations include biochemical assessment and plain radiographs. Radioisotope bone scans and bone biopsy may be considered in selected cases. Differential diagnoses include osteoporosis, seronegative arthritides, and localized soft tissue disorders. Treatment, guided by the underlying aetiology, aims to reduce symptoms, fracture risk, bone deformity and sequelae. Vitamin D deficient patients require vitamin D and calcium replacement.

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33

J, Raitan Daniel, National Institute of Child Health and Human Development (U.S.), Office of Dietary Supplements, National Cancer Institute (U.S.), and Vitamin D and Health in the 21st Century. Conference (2003 : Bethesda, Md.), eds. Vitamin D and health in the 21st century: Bone and beyond : proceedings of a conference held in Bethesda, MD, October 9-10, 2003. American Journal of Clinical Nutrition, 2004.

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34

Voinescu, Alexandra, Nadia Wasi Iqbal, and Kevin J. Martin. Pathophysiology of chronic kidney disease-mineral and bone disorder. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0117.

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Chronic kidney disease is associated with the inability to control normal mineral homeostasis, resulting in abnormalities in serum levels of calcium, phosphorus, parathyroid hormone, fibroblast growth factor 23 (FGF23) and vitamin D metabolism. These disturbances lead to the development of secondary hyperparathyroidism, skeletal abnormalities, vascular calcifications, and other systemic manifestations. Traditionally, mineral and bone abnormalities seen in chronic kidney disease were included in the term ‘renal osteodystrophy’. More recently, the term chronic kidney disease-mineral and bone disorder was introduced to define the biochemical abnormalities of phosphorus, parathyroid hormone, FGF23, calcium, or vitamin D metabolism, abnormalities in bone remodelling and mineralization, and vascular or other soft tissue calcifications.

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35

Ralston, Stuart H. Paget’s disease of bone. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0144.

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Paget's disease of bone (PDB) affects up to 1% of people of European origin aged 55 years and above. It is characterized by focal abnormalities of bone remodelling which disrupt normal bone architecture, leading to expansion and reduced mechanical strength of affected bones. This can lead to various complications including deformity, fracture, nerve compression syndromes, and osteoarthritis, although many patients are asymptomatic. Genetic factors play a key role in the pathogenesis of PDB. This seems to be mediated by a combination of rare genetic variants which cause familial forms of the disease and common variants which increase susceptibility to environmental triggers. Environmental factors which have been suggested to predispose to PDB include viral infections, calcium and vitamin D deficiency, and excessive mechanical loading of affected bones. The diagnosis can be made by the characteristic changes seen on radiographs, but isotope bone scans are helpful in defining disease extent. Serum alkaline phosphatase levels can be used as a measure of disease activity. Inhibitors of bone resorption are the mainstay of medical management for PDB and bisphosphonates are regarded as the treatment of choice. Bisphosphonates are highly effective at reducing bone turnover in PDB and have been found to heal osteolytic lesions, and normalize bone histology. Although bisphosphonates can improving bone pain caused by elevated bone turnover, most patients require additional therapy to deal with symptoms associated with disease complications. It is currently unclear whether bisphosphonate therapy is effective at preventing complications of PDB.

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36

Ralston, Stuart H. Paget’s disease of bone. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199642489.003.0144_update_001.

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Paget’s disease of bone (PDB) affects up to 1% of people of European origin aged 55 years and above. It is characterized by focal abnormalities of bone remodelling which disrupt normal bone architecture, leading to expansion and reduced mechanical strength of affected bones. This can lead to various complications including deformity, fracture, nerve compression syndromes, and osteoarthritis, although many patients are asymptomatic. Genetic factors play a key role in the pathogenesis of PDB. This seems to be mediated by a combination of rare genetic variants which cause familial forms of the disease and common variants which increase susceptibility to environmental triggers. Environmental factors which have been suggested to predispose to PDB include viral infections, calcium and vitamin D deficiency, and excessive mechanical loading of affected bones. The diagnosis can be made by the characteristic changes seen on radiographs, but isotope bone scans are helpful in defining disease extent. Serum alkaline phosphatase levels can be used as a measure of disease activity. Inhibitors of bone resorption are the mainstay of medical management for PDB and bisphosphonates are regarded as the treatment of choice. Bisphosphonates are highly effective at reducing bone turnover in PDB and have been found to heal osteolytic lesions, and normalize bone histology. Although bisphosphonates can improving bone pain caused by elevated bone turnover, most patients require additional therapy to deal with symptoms associated with disease complications. It is currently unclear whether bisphosphonate therapy is effective at preventing complications of PDB.

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37

Voinescu, Alexandra, Nadia Wasi Iqbal, and Kevin J. Martin. Management of chronic kidney disease-mineral and bone disorder. Edited by David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0118_update_001.

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In all patients with chronic kidney disease (CKD) stages 3–5, regular monitoring of serum markers of CKD-mineral and bone disorder, including calcium (Ca), phosphorus (P), parathyroid hormone (PTH), 25-hydroxyvitamin D, and alkaline phosphatase, is recommended. Target ranges for these markers are endorsed by guidelines. The principles of therapy for secondary hyperparathyroidism include control of hyperphosphataemia, correction of hypocalcaemia, use of vitamin D sterols, use of calcimimetics, and parathyroidectomy. of hyperphosphataemia is crucial and may be achieved by means of dietary P restriction, use of P binders, and P removal by dialysis. Dietary P restriction requires caution, as it may be associated with protein malnutrition. Aluminium salts are effective P binders, but they are not recommended for long-term use, as Aluminium toxicity (though from contaminated dialysis water rather than oral intake) may cause cognitive impairment, osteomalacia, refractory microcytic anaemia, and myopathy. Ca-based P binders are also quite effective, but should be avoided in patients with hypercalcaemia, vascular calcifications, or persistently low PTH levels. Non-aluminium, non-Ca binders, like sevelamer and lanthanum carbonate, may be more adequate for such patients; however, they are expensive and may have several side effects. Furthermore, comparative trials have failed so far to provide conclusive evidence on the superiority of these newer P binders over Ca-based binders in terms of preventing vascular calcifications, bone abnormalities, and mortality. P removal is about 1800–2700 mg per week with conventional thrice-weekly haemodialysis, but may be increased by using haemodiafiltration or intensified regimens, such as short daily, extended daily or three times weekly nocturnal haemodialysis. Several vitamin D derivatives are currently used for the treatment of secondary hyperparathyroidism. In comparison with the natural form calcitriol, the vitamin D analogue paricalcitol seems to be more fast-acting and less prone to induce hypercalcaemia and hyperphosphataemia, but whether these advantages translate into better clinical outcomes is unknown. Calcimimetics such as cinacalcet can significantly reduce PTH, Ca, and P levels, but they have failed to definitively prove any benefits in terms of mortality and cardiovascular events in dialysis patients. Parathyroidectomy is often indicated in CKD patients with severe persistent hyperparathyroidism, refractory to aggressive medical treatment with vitamin D analogues and/or calcimimetics. This procedure usually leads to rapid improvements in biochemical markers (i.e. significant lowering of serum Ca, P, and PTH) and clinical manifestations (such as pruritus and bone pain); however, the long-term benefits are still unclear.

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38

Elder, Grahame J. Metabolic bone disease after renal transplantation. Edited by Jeremy R. Chapman. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0288.

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Patients who undergo kidney transplantation have laboratory, bone, and soft tissue abnormalities that characterize chronic kidney disease mineral and bone disorder (CKD-MBD). After successful transplantation, abnormal values of parathyroid hormone, fibroblast growth factor 23, calcium, phosphate, vitamin D sterols, and sex hormones generally improve, but abnormalities often persist. Cardiovascular risk remains high and is influenced by prevalent vascular calcification, and fracture risk increases due to a combination of abnormal bone ‘quality’, compounded by immunosuppressive drugs and reductions in bone mineral density. Patients with well managed CKD-MBD before transplantation generally have a smoother post-transplant course, and it is useful to assess patients soon after transplantation for risk factors relevant to the general population and to patients with CKD. Targeted laboratory assessment, bone densitometry, and X-ray of the spine are useful for guiding therapy to minimize post-transplant effects of CKD-MBD. To reduce fracture risk, general measures include glucocorticoid dose minimization, attaining adequate 25(OH)D levels, and maintaining calcium and phosphate values in the normal range. Calcitriol or its analogues and antiresorptive agents such as bisphosphonates may protect bone from glucocorticoid effects and ongoing hyperparathyroidism, but the efficacy of these therapies to reduce fractures is unproven. Alternate therapies with fewer data include denosumab, strontium ranelate, teriparatide, oestrogen or testosterone hormone replacement therapy, tibolone, selective oestrogen receptor modulators, and cinacalcet. Parathyroidectomy may be necessary, but is generally avoided within the first post-transplant year. A schema is presented in this chapter that aims to minimize harm when allocating therapy.

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39

Sprague, Stuart M., and Menaka Sarav. Chronic kidney disease-mineral and bone disorder. Edited by David J. Goldsmith. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199592548.003.0115_update_001.

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The kidneys play a critical role in maintaining normal serum calcium and phosphorus concentrations, under the regulation of three main hormones: parathyroid hormone, calcitriol, and fibroblast growth factor 23. With the progression of chronic kidney disease (CKD), most patients develop CKD–mineral and bone disorder (CKD-MBD), which is a systemic disorder involving derangement in mineral metabolism, renal osteodystrophy, and extraskeletal calcification. Disturbances in mineral metabolism develop early in CKD and include phosphate retention, hypocalcaemia, vitamin D deficiency, and hyperparathyroidism. Renal osteodystrophy involves pathologic changes of bone morphology related to progressive CKD and is quantifiable by histomorphometry, based on bone biopsy. CKD-MBD is associated with significant morbidity, including bone loss, fractures, cardiovascular disease, immune suppression, as well as increased mortality. As the disorder begins early in the course of CKD, a proactive approach with intervention is important. Therapeutic strategies could then be employed to prevent and correct these disturbances, aiming to improve cardiovascular outcomes and survival. Current practice guidelines for CKD-MBD are based on insufficient data and high-quality studies are required before specific treatment can be advocated strongly.

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40

Barry, Amelia, and Guy Trudel. Bone and Joint Disease Following Critical Illness. Oxford University Press, 2014. http://dx.doi.org/10.1093/med/9780199653461.003.0025.

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Bone and joint processes take second stage to life-threatening organ failure in the setting of critical illness. However, bone and joint disorders can cause significant impairment in survivors of critical illness. Return to pre-admission function is often limited by acquired complications such as joint contractures, heterotopic ossification, and altered bone metabolism. Critical care physicians should maintain a high index of suspicion for joint contractures, as they are often asymptomatic but the source of enduring disability once the critical illness had receded. Research is needed to document the effectiveness of alternate positioning, stretching, and bracing which are the current standard practice for prevention of contractures. Heterotopic ossification should be considered in the context of a swollen, warm, painful musculoskeletal site. Early detection with triple phase bone scan and, in some cases, prophylaxis with non-steroidal anti-inflammatory medication or radiation may be warranted. Bone hyperresorption in ICU patients can be caused by immobility, heightened inflammatory status, medication, hormonal changes, and vitamin D deficiency. Laboratory biomarkers can guide treatment, which is important to prevent long-term osteoporosis and stress fractures. Systematic physical examination and early patient mobilization may represent important steps to detect and prevent joint contractures and heterotopic ossification.

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41

C, Tsang Reginald, and Mimouni Francis, eds. Calcium nutriture for mothers and children. Glendale, Calif: Carnation Education, 1992.

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42

Sprague, Stuart M., and James M. Pullman. Spectrum of bone pathologies in chronic kidney disease. Edited by David J. Goldsmith. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0122.

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Histologic bone abnormalities begin very early in the course of chronic kidney disease. The KDIGO guidelines recommend that bone disease in patients with chronic kidney disease should be diagnosed on the basis of bone biopsy examination, with bone histomorphometry. They have also proposed a new classification system (TMV), using three key features of bone histology—turnover, mineralization, and volume—to describe bone disease in these patients. However, bone biopsy is still rarely performed today, as it involves an invasive procedure and highly specialized laboratory techniques. High-turnover bone disease (osteitis fibrosa cystica) is mainly related to secondary hyperparathyroidism and is characterized by increased rates of both bone formation and resorption, with extensive osteoclast and osteoblast activity, and a progressive increase in peritrabecular marrow space fibrosis. On the other hand, low-turnover (adynamic) bone disease involves a decline in osteoblast and osteoclast activities, reduced new bone formation and mineralization, and endosteal fibrosis. The pathophysiological mechanisms of adynamic bone include vitamin D deficiency, hyperphosphataemia, metabolic acidosis, inflammation, low oestrogen and testosterone levels, bone resistance to parathyroid hormone, and high serum fibroblast growth factor 23. Mixed uraemic osteodystrophy describes a combination of osteitis fibrosa and mineralization defect. In the past few decades, an increase in the prevalence of mixed uraemic osteodystrophy and adynamic bone disease has been observed.

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43

(Editor), M. Cecchettin, and G. Segre (Editor), eds. Calciotropic Hormones and Calcium Metabolism (International congress series). Elsevier, 1986.

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44

Javaid, Kassim. Osteomalacia. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0273.

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Osteomalacia is a disorder of bone mineralization and is due to a lack of vitamin D. Vitamin D is a prohormone formed by the action of UV radiation on the vitamin’s precursor (7-dehydrocholesterol) in the skin. It undergoes two hydroxylation steps to become an active hormone. The commonest cause of osteomalacia is vitamin D deficiency due to a lack of UVB skin exposure. Other causes include malabsorption (coeliac disease and pancreatic insufficiency), obesity, and chronic kidney disease. The typical symptoms of osteomalacia are non-specific bone pain, proximal myopathy, fatigue, and polyarthralgia. This chapter addresses the causes, diagnosis, and management of osteomalacia.

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45

O’Neal, M. Angela. Pain in the Back. Edited by Angela O’Neal. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190609917.003.0006.

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This case explores how bone health can be affected by antiepileptic drugs (AEDs), and why this is an important issue in women with epilepsy (WWE). AEDs affect bone health through activation of the cytochrome P450 system in the liver, leading to increased metabolism of vitamin D. The enzyme-inducing AEDs include phenytoin, carbamazepine, phenobarbital, and primidone. Risk factors for osteoporosis include female gender, low body mass, inadequate vitamin D intake, and smoking. The specific AEDs used and the length of treatment confer additional risks. Furthermore, in WWE, risks are magnified related to falls, either from seizures or related to medication toxicity. Screening with bone density and measures to promote bone health are extremely important in these at-risk women.

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46

Bell, Tanvir K. Musculoskeletal Complications of HIV. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780190493097.003.0043.

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Vitamin D levels have been observed to be low in HIV-infected patients. If replacement of low vitamin D is warranted, supplementation is done with vitamin D2 or D3. HIV-infected patients may be at higher risk for osteopenia, osteoporosis, and fragility fractures. Tenofovir alafenamide has been shown to produce less bone loss compared to tenofovir disoproxil fumarate. Muscle disorders can be debilitating in HIV-infected patients. Myopathies can have a range of presentation from myalgias to rhabdomyolysis. HIV myopathy is a rare proximal muscle disorder that can occur in HIV-infected patients. Antiretroviral drugs, including zidovudine and raltegravir, can cause myopathy and elevated creatine kinase.

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Bardin, Thomas, and Tilman Drüeke. Renal osteodystrophy. Oxford University Press, 2013. http://dx.doi.org/10.1093/med/9780199642489.003.0149.

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Renal osteodystrophy (ROD) is a term that encompasses the various consequences of chronic kidney disease (CKD) for the bone. It has been divided into several entities based on bone histomorphometry observations. ROD is accompanied by several abnormalities of mineral metabolism: abnormal levels of serum calcium, phosphorus, parathyroid hormone (PTH), vitamin D metabolites, alkaline phosphatases, fibroblast growth factor-23 (FGF-23) and klotho, which all have been identified as cardiovascular risk factors in patients with CKD. ROD can presently be schematically divided into three main types by histology: (1) osteitis fibrosa as the bony expression of secondary hyperparathyroidism (sHP), which is a high bone turnover disease developing early in CKD; (2) adynamic bone disease (ABD), the most frequent type of ROD in dialysis patients, which is at present most often observed in the absence of aluminium intoxication and develops mainly as a result of excessive PTH suppression; and (3) mixed ROD, a combination of osteitis fibrosa and osteomalacia whose prevalence has decreased in the last decade. Laboratory features include increased serum levels of PTH and bone turnover markers such as total and bone alkaline phosphatases, osteocalcin, and several products of type I collagen metabolism products. Serum phosphorus is increased only in CKD stages 4-5. Serum calcium levels are variable. They may be low initially, but hypercalcaemia develops in case of severe sHP. Serum 25-OH-vitamin D (25OHD) levels are generally below 30 ng/mL, indicating vitamin D insufficiency or deficiency. The international KDIGO guideline recommends serum PTH levels to be maintained in the range of approximately 2-9 times the upper normal normal limit of the assay and to intervene only in case of significant changes in PTH levels. It is generally recommended that calcium intake should be up to 2 g per day including intake with food and administration of calcium supplements or calcium-containing phosphate binders. Reduction of serum phosphorus towards the normal range in patients with endstage kidney failure is a major objective. Once sHP has developed, active vitamin D derivatives such as alfacalcidol or calcitriol are indicated in order to halt its progression.

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Chakera, Aron, William G. Herrington, and Christopher A. O’Callaghant. Disorders of plasma calcium. Edited by Patrick Davey and David Sprigings. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780199568741.003.0175.

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The extracellular calcium ion concentration is tightly regulated through the actions of parathyroid hormone (PTH) and vitamin D (1,25-dihydroxyvitamin D) on bone, kidney, and intestines. Abnormalities in these homeostatic mechanisms may lead to increased or decreased serum calcium concentrations, resulting in hypercalcaemia or hypocalcaemia, respectively. Hypercalcaemic disorders may be further divided into those associated with a high/high-normal serum PTH level, and those associated with a low serum PTH concentration. Hypocalcaemia occurs when abnormalities in the physiological regulation of PTH and vitamin D results in calcium levels lower than the desired normal range. Failure of release of calcium from bone, and increased binding of calcium in the circulation, are other factors causing hypocalcaemia. This chapter discusses hypercalcaemia and hypocalcaemia, exploring definitions of the diseases, their etiologies, typical and uncommon symptoms, demographics, natural history, complications, diagnostic approaches, other diagnoses that should be considered, prognosis, and treatment.

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Gluckman, Sir Peter, Mark Hanson, Chong Yap Seng, and Anne Bardsley. Effects of maternal age on pregnancy outcomes. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780198722700.003.0034.

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Maternal age on both ends of the reproductive spectrum (teenage and 35+) is associated with increased risk of adverse pregnancy outcomes, as compared with the age range from 20–34 years old. Some of the increase in pregnancy complications in older mothers is caused by underlying age-related health issues such as hypertension and diabetes, the prevalence of which increases linearly with age. The risks associated with young maternal age are more related to nutritional deficits and the fact that pregnant adolescents may still be growing themselves. Poor fetal growth often seen in adolescent pregnancies possibly results from competition for nutrients. Maternal bone loss is also a concern, as adolescent diets are commonly low in calcium and vitamin D. Pregnant adolescents may benefit from calcium supplementation to compensate for the increased need for their own bone growth and should at minimum receive vitamin D supplements, as recommended for all pregnant women.

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Linglart, Agnès, and Anne-Sophie Lambert. Approach to the patient with hypocalcaemia. Edited by Robert Unwin. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0038.

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Calcium homeostasis is maintained through a fine balance between calcium absorption, parathyroid hormone secretion and action, vitamin D production and action, cellular compartmentalization of calcium ions, and renal function. Although the extracellular calcium level does not vary with age, the maintenance of calcium faces the significant mineral requirement of skeletal growth and bone mass acquisition during childhood. Acquired or genetic defects in any determinants of blood calcium (i.e. vitamin D, parathyroid hormone, calcium absorption, etc.) may manifest as hypocalcaemia, especially during childhood/adolescence. The discovery of hypocalcaemia in a patient should trigger two clinical responses: (1) therapy to restore the calcium level to normal and (2) investigations to determine the cause of hypo/hypercalcaemia.

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