Nutritional Rickets and Osteomalacia in the Twenty-first Century: Revised Concepts, Public Health, and Prevention Strategies.

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Term Occurence Count Dictionary
hypocalcaemia 3 endocrinologydiseases
rickets 36 endocrinologydiseases
secondary hyperparathyroidism 3 endocrinologydiseases
tetany 5 endocrinologydiseases
calcitriol 8 endocrinologydiseasesdrugs
cortisol 1 endocrinologydiseasesdrugs
folate deficiency 1 endocrinologydiseases
hyperparathyroidism 4 endocrinologydiseases

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Select Drug Character Offset Drug Term Instance
calcitriol 4775 (25OHD, calcidiol) and finally in the kidney and also the gut [[]] to the active hormone 1,25(OH)2D ( calcitriol or ‘active vitamin D’). Sadly, this terminology has confused generations of healthcare professionals.
calcitriol 4961 generations of healthcare professionals. Even today, conference presenters refer to calciferol, calcidiol and calcitriol as ‘vitamin D’. To add to the confusion, all three steroids exist either in their D2 (ergo-) or
calcitriol 5218 explored secosteroid versions of this vitamin. Vitamin D and 25OHD are biologically inert, whereas calcitriol is the active, potent hormone with its main function to increase intestinal absorption of calcium and
calcitriol 5720 is not a ‘cholesterol receptor’. Vitamin D does not bind to the ‘vitamin D receptor’, only calcitriol does and hence the appropriate term for this receptor is ‘calcitriol receptor’. This is not a semantic
calcitriol 5791 ‘vitamin D receptor’, only calcitriol does and hence the appropriate term for this receptor is ‘ calcitriol receptor’. This is not a semantic discussion. Even in the twenty-first century, there are reports
calcitriol 5908 receptor’. This is not a semantic discussion. Even in the twenty-first century, there are reports where calcitriol is used incorrectly to replace severe vitamin D deficiency, which not only leaves the individual vitamin
calcitriol 21432 modified by the human body to form active steroid hormones, vitamin D is modified to form the hormone calcitriol . Calcitriol acts on the calcitriol receptor (VDR), whilst vitamin D and 25OHD are biologically inert.Calcium
calcitriol 21467 active steroid hormones, vitamin D is modified to form the hormone calcitriol. Calcitriol acts on the calcitriol receptor (VDR), whilst vitamin D and 25OHD are biologically inert.Calcium deprivation and its complicationsCalcium
cortisol 5545 hydroxylation steps, and the concept of inert and active metabolites. In analogy to other steroid pathways, cortisol is not ‘active cholesterol’, or the mineralocorticoid receptor is not a ‘cholesterol receptor’.
Select Disease Character Offset Disease Term Instance
folate deficiency 23295 vitamin D deficiency often occurs combined with other micronutrient deficiencies, in particular iron and folate deficiency .Identifying Successful and Sustainable Implementation StrategiesAlthough most developed countries have
hyperparathyroidism 3125 primary spongiosa in the metaphysis (new bone) [[]]. In NR, hypophosphataemia is created by secondary hyperparathyroidism (see below). Osteomalacia constitutes defective mineralisation of existing (old) bone during the remodelling
hyperparathyroidism 7089 parathyroid’s chief cells, leading to increased release of parathyroid hormone (PTH) [[]]. This secondary hyperparathyroidism stimulates osteoclastic bone resorption with the aim to release stored bone minerals. This compensation
hyperparathyroidism 7289 minerals. This compensation mechanism works well to maintain normal serum calcium levels, but sustained hyperparathyroidism has two main complications: (1) structural damage to bone and (2) decreased renal reabsorption of phosphate.
hyperparathyroidism 8099 deprivation and its evolution into rickets and osteomalacia is depicted in Fig. 1. Because secondary hyperparathyroidism maintains normal serum calcium levels until compensation fails, serum calcium is a poor marker of calcium
hypocalcaemia 10120 skeleton at birth, referred to as congenital rickets [[]]. If undiagnosed, there is a concern that hypocalcaemia , cardiomyopathy and rickets will contribute to or cause infant mortality. A retrospective analysis post-mortem
hypocalcaemia 10256 rickets will contribute to or cause infant mortality. A retrospective analysis post-mortem identified hypocalcaemia contributing to death in 3 of 52 children; two had cardiomyopathy and one had hypocalcaemic seizures.
hypocalcaemia 30061 Unexpected Death in infancy and childhood [[]•, []]. Prolonged severe vitamin D deficiency leads to hypocalcaemia which can cause sudden death in infants [[]•]. The prevalence of insufficient 25OHD levels in undiagnosed
rickets 320 6/2017Publication date (pmc-release): 6/2017Publication date (ppub): /2017AbstractPurpose of ReviewNutritional rickets and osteomalacia are common in dark-skinned and migrant populations. Their global incidence is rising
rickets 663 spectrum has hypocalcaemic (seizures, tetany and dilated cardiomyopathy) and late hypophosphataemic ( rickets , osteomalacia and muscle weakness) complications. This article reviews sustainable prevention strategies
rickets 843 sustainable prevention strategies and identifies areas for future research.Recent FindingsThe global rickets consensus recognises the equal contribution of vitamin D and dietary calcium in the causation of calcium
rickets 1061 deprivation and provides a three stage categorisation for sufficiency, insufficiency and deficiency. For rickets prevention, 400 IU daily is recommended for all infants from birth and 600 IU in pregnancy, alongside
rickets 1405 food fortification with vitamin D or calcium. Future research should identify the true prevalence of rickets and osteomalacia, their role in bone fragility and infant mortality, and best screening and public health
rickets 1577 mortality, and best screening and public health prevention tools.IntroductionThe incidence of nutritional rickets (NR) is rising globally [[]], and hospitalisation is increasing even in high income countries [[]••,
rickets 1793 []]. The underlying calcium deprivation [[]•] does not just manifest as reduced bone mineralisation ( rickets and osteomalacia) but also as hypocalcaemic seizures, tetany and dilated cardiomyopathy including cardiac
rickets 2225 Therefore, clinically evident NR is only the tip of the iceberg, and the true burden of subclinical rickets and osteomalacia remains unidentified. Calcium deprivation is caused by two factors, low dietary calcium
rickets 2882 defective mineralisation of growth plates [[]••, [], []]. The underlying mechanism of all forms of rickets is low serum phosphate resulting in reduced apoptosis of hypertrophic chondrocytes in the growth plate
rickets 3299 mineralisation of existing (old) bone during the remodelling process and therefore always goes along with rickets in growing children (open growth plates) and occurs ubiquitously in bones of adults or adolescents (closed
rickets 3571 disease of adults, but the main reason for long bone bowing deformities and fractures in children with rickets , as poor mineralisation reduces bone stiffness. Low calcium intake and/or low vitamin D (from lack of
rickets 3999 traditional diets low in calcium, dark skin and cultural full body clothing, as the predominant causes of rickets and osteomalacia in sunny parts of the world such as the Indian subcontinent [[]•, []], the Middle
rickets 7648 complications (seizures, tetany and cardiomyopathy) and late hypophosphataemic complications (nutritional rickets , osteomalacia and muscle weakness) unless more calcium is made available to restore eucalcemia and normalise
rickets 7966 alongside a rise in serum alkaline phosphatase (ALP) and causes the growth plate abnormality known as rickets . The concept of calcium deprivation and its evolution into rickets and osteomalacia is depicted in Fig.
rickets 8033 growth plate abnormality known as rickets. The concept of calcium deprivation and its evolution into rickets and osteomalacia is depicted in Fig. 1. Because secondary hyperparathyroidism maintains normal serum
rickets 8706 deficient or the dietary calcium deficient state.Fig. 1Stages of calcium deprivation leading to nutritional rickets and osteomalaciaThe Clinical Spectrum of Calcium Deprivation from Conception to Old AgeThe role of vitamin
rickets 9321 start at birth to protect the neonate from developing complications from calcium deprivation, including rickets , during the rapid infantile growth [[]•]. Depending on the duration and severity of maternal vitamin
rickets 10066 deprivation during pregnancy will manifest in the newborn skeleton at birth, referred to as congenital rickets [[]]. If undiagnosed, there is a concern that hypocalcaemia, cardiomyopathy and rickets will contribute
rickets 10154 congenital rickets [[]]. If undiagnosed, there is a concern that hypocalcaemia, cardiomyopathy and rickets will contribute to or cause infant mortality. A retrospective analysis post-mortem identified hypocalcaemia
rickets 10474 All three patients were of Black ethnic origin and also had histological and radiological evidence of rickets [[]•]. Another UK post-mortem study highlighted that a significant proportion (76%) of children with
rickets 10692 unexplained sudden death (n = 25) had suboptimal vitamin D levels, of whom 69% had histological signs of rickets [[]]. In infants and young children, rickets remains a radiological diagnosis that needs to be confirmed
rickets 10737 vitamin D levels, of whom 69% had histological signs of rickets [[]]. In infants and young children, rickets remains a radiological diagnosis that needs to be confirmed by taking a knee X-ray.Older children can
rickets 11279 costochondral junctions), typical biochemical abnormalities (increased ALP and PTH) and radiological changes of rickets (cupping, splaying and fraying of metaphyses, widened growth plates and low bone mass). In older children
rickets 11503 specifically adolescents with less rapid growth, the radiological changes of the growth plate typical for rickets may not be visible, and equally, osteomalacia cannot be diagnosed on X-rays.Osteomalacia in girls can
rickets 12759 vitamin D enthusiasts towards the role of dietary calcium intake and PTH in the pathophysiology of rickets and osteomalacia. To provide clarification on this issue, representatives from 11 international scientific
rickets 18546 supplementation contribute to high prevalence of vitamin D deficiency in pregnancy [[]]. Congenital rickets and postnatal hypocalcaemic seizures are reported in risk groups in both developed and developing countries
rickets 21771 Calcium deprivation has hypocalcaemic (seizures, tetany and cardiomyopathy) and late hypophosphataemic ( rickets , osteomalacia and muscle weakness) complications.What to measure and how to make a diagnosis25OHD is
rickets 22026 calcium is a poor marker of calcium status. Consistent and early biochemical markers for diagnosis of rickets and osteomalacia are elevations in serum ALP and PTH. The diagnosis of rickets requires radiological
rickets 22105 markers for diagnosis of rickets and osteomalacia are elevations in serum ALP and PTH. The diagnosis of rickets requires radiological confirmation.High prevalence in risk groupsNR/osteomalacia is less common in the
rickets 23647 and New Zealand reported that none of the individuals with NR had received vitamin D supplements for rickets prevention despite the presence of national recommendations [[], []]. Similarly, 85% of British parents
rickets 27847 signs, biochemical markers (raised ALP and PTH, low calcium, low 25OHD) and radiological signs to define rickets , either in isolation or in combination [[]]. Further studies are warranted to identify the most appropriate
rickets 28226 histology relates to levels of calcium deprivation, elevations of ALP and PTH, radiological signs of rickets and fracture risk (Fig. 1). Until a reliable screening tool is available, NR should be considered a
rickets 28901 Deficiency and Non-accidental InjuriesThe role of vitamin D deficiency (with absent radiological signs of rickets ) in bone fragility is much debated in the context of non-accidental injuries [[], []]. The state of
rickets 29013 bone fragility is much debated in the context of non-accidental injuries [[], []]. The state of pre- rickets /osteomalacia (Fig. 1) is only identified on bone histology. It has been demonstrated that the pickup
rickets 29144 is only identified on bone histology. It has been demonstrated that the pickup rate of biopsy proven rickets by radiologists is poor [[]•, [], []]. NR and osteomalacia, as hypophosphataemic complications, occur
rickets 31687 recommendations [[]••, []] provide guidance both for clinicians and policy makers on the prevention of rickets , and infants, pregnant women and dark-skinned individuals should be at the core of any policies. In
secondary hyperparathyroidism 3115 mineralisation of primary spongiosa in the metaphysis (new bone) [[]]. In NR, hypophosphataemia is created by secondary hyperparathyroidism (see below). Osteomalacia constitutes defective mineralisation of existing (old) bone during the remodelling
secondary hyperparathyroidism 7079 the parathyroid’s chief cells, leading to increased release of parathyroid hormone (PTH) [[]]. This secondary hyperparathyroidism stimulates osteoclastic bone resorption with the aim to release stored bone minerals. This compensation
secondary hyperparathyroidism 8089 calcium deprivation and its evolution into rickets and osteomalacia is depicted in Fig. 1. Because secondary hyperparathyroidism maintains normal serum calcium levels until compensation fails, serum calcium is a poor marker of calcium
tetany 600 and missing implementation strategies. The calcium deprivation spectrum has hypocalcaemic (seizures, tetany and dilated cardiomyopathy) and late hypophosphataemic (rickets, osteomalacia and muscle weakness) complications.
tetany 1855 manifest as reduced bone mineralisation (rickets and osteomalacia) but also as hypocalcaemic seizures, tetany and dilated cardiomyopathy including cardiac failure and death [[], [], []•]. Undiagnosed NR has also
tetany 7567 calcium stored in bone will ultimately be depleted, leading to hypocalcaemic complications (seizures, tetany and cardiomyopathy) and late hypophosphataemic complications (nutritional rickets, osteomalacia and
tetany 9600 presenting in the first few days or months of life with hypocalcaemic complications. These include seizures, tetany [[]•, [], []] and dilated cardiomyopathy which may result in cardiac failure and death [[], [], []].
tetany 21716 secondary to low dietary calcium and/or low vitamin D. Calcium deprivation has hypocalcaemic (seizures, tetany and cardiomyopathy) and late hypophosphataemic (rickets, osteomalacia and muscle weakness) complications.What

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