An Overview of Rickets in Children

Abstract

Rickets is a common bone disease worldwide that is associated with disturbances in calcium and phosphate homeostasis and can lead to short stature and joint deformities. Rickets can be diagnosed based on history and physical examination, radiological features, and biochemical tests. It can be classified into 2 major groups based on phosphate or calcium levels: phosphopenic and calcipenic. Knowledge of categorization of the type of rickets is essential for prompt diagnosis and proper management. Nutritional rickets is a preventable disease through adequate intake of vitamin D through both dietary and sunlight exposure. There are other subtypes of rickets, such as vitamin D–dependent type 1 rickets and vitamin D–dependent type 2 rickets (due to defects in vitamin D metabolism), renal rickets (due to poor kidney function), and hypophosphatemic rickets (vitamin D–resistant rickets secondary to renal phosphate wasting wherein fibroblast growth factor-23 (FGF-23) often plays a major role), which requires closer monitoring and supplementation with activated vitamin D with or without phosphate supplements. An important development has been the introduction of burosumab, a human monoclonal antibody to FGF-23, which is approved for the treatment of X-linked hypophosphatemia among children 1 year and older. Rickets is a common bone disease worldwide that is associated with disturbances in calcium and phosphate homeostasis and can lead to short stature and joint deformities. Rickets can be diagnosed based on history and physical examination, radiological features, and biochemical tests. It can be classified into 2 major groups based on phosphate or calcium levels: phosphopenic and calcipenic. Knowledge of categorization of the type of rickets is essential for prompt diagnosis and proper management. Nutritional rickets is a preventable disease through adequate intake of vitamin D through both dietary and sunlight exposure. There are other subtypes of rickets, such as vitamin D–dependent type 1 rickets and vitamin D–dependent type 2 rickets (due to defects in vitamin D metabolism), renal rickets (due to poor kidney function), and hypophosphatemic rickets (vitamin D–resistant rickets secondary to renal phosphate wasting wherein fibroblast growth factor-23 (FGF-23) often plays a major role), which requires closer monitoring and supplementation with activated vitamin D with or without phosphate supplements. An important development has been the introduction of burosumab, a human monoclonal antibody to FGF-23, which is approved for the treatment of X-linked hypophosphatemia among children 1 year and older. Rickets, a common disease worldwide,1Craviari T. Pettifor J.M. Thacher T.D. et al.Rickets: an overview and future directions, with special reference to Bangladesh. A summary of the Rickets Convergence Group meeting, Dhaka, 26–27 January, 2006.J Health Popul Nutr. 2008; 26: 112-121PubMed Google Scholar,2Carpenter T.O. Shaw N.J. Portale A.A. et al.Rickets.Nat Rev Dis Primers. 2017; 3: 17101Crossref PubMed Scopus (57) Google Scholar substantially affects the health, growth, and development of children and adolescents. It results from abnormalities of the growth plate cartilage predominantly affecting longer bones and leads to poor bone growth, defective mineralization, and bony deformities, such as bow-legs and knock-knees.3Jagtap V.S. Sarathi V. Lila A.R. et al.Hypophosphatemic rickets.Indian J Endocrinol Metab. 2012; 16: 177-182Crossref PubMed Google Scholar This is usually secondary to deficiencies of calcium or phosphorus because they are essential for normal bone growth and mineralization.4Sahay M. Sahay R. Rickets-vitamin D deficiency and dependency.Indian J Endocrinol Metab. 2012; 16: 164-176Crossref PubMed Google Scholar,5Pitt M.J. Rickets and osteomalacia are still around.Radiol Clin North Am. 1991; 29: 97-118PubMed Google Scholar This review article delves and analyzes different types of rickets and their appropriate management plan. Bones consist of cells that have various specific roles during the bone formation process. Osteoblasts are bone-forming cells that secrete the extracellular matrix and mineralize the osteoid, whereas osteoclasts break down the bone matrix during the stage of remodeling, disease conditions, or aging. For bone maturation, the organic component of the bone matrix, the osteoid, must be mineralized by calcium salts. In rickets, this process is hampered and results in amassing of osteoid beneath the growth plate leading to softness in the bone over a gradual period of time.4Sahay M. Sahay R. Rickets-vitamin D deficiency and dependency.Indian J Endocrinol Metab. 2012; 16: 164-176Crossref PubMed Google Scholar Rickets can be classified into 2 major groups: phosphopenic and calcipenic3Jagtap V.S. Sarathi V. Lila A.R. et al.Hypophosphatemic rickets.Indian J Endocrinol Metab. 2012; 16: 177-182Crossref PubMed Google Scholar,6Tiosano D. Hochberg Z. Hypophosphatemia:the common denominator of all rickets.J Bone Miner Metab. 2009; 27: 392-401Crossref PubMed Scopus (108) Google Scholar (Figure 1). Abundant in all tissues of the body, phosphorus is a vital structural component for mineralization of bone. Both calcium and phosphorus keep the bone in a healthy, functional state.7Goldsweig B.K. Carpenter T.O. Hypophosphatemic rickets: lessons from disrupted FGF23 control of phosphorus homeostasis.Curr Osteoporos Rep. 2015; 13: 88-97Crossref PubMed Scopus (34) Google Scholar In phosphopenic/hypophosphatemic rickets, the defect usually results from increased renal excretion of phosphate.3Jagtap V.S. Sarathi V. Lila A.R. et al.Hypophosphatemic rickets.Indian J Endocrinol Metab. 2012; 16: 177-182Crossref PubMed Google Scholar Urinary loss of phosphate can be either as a part of generalized tubular dysfunction as seen in Fanconi syndrome, or secondary to either increased synthesis/ reduced catabolism of the FGF-23, or inactivating mutations in genes encoding for sodium-dependent phosphate transporters in the proximal renal tubule (Figure 1).8Mughal M.Z. Rickets.Curr Osteoporos Rep. 2011; 9: 291-299Crossref PubMed Scopus (28) Google Scholar Calcipenic rickets, as the name suggests, happens primarily because of a lack of calcium, which is most commonly due to a low availability or defective functioning of vitamin D in the body (Figure 1). Hence, calcipenic rickets can occur due to severe vitamin D deficiency (nutritional), inability to form either 25-hydroxyvitamin D (as in liver failure/drug intoxication; e.g., phenytoin) or 1,25-dihydroxy vitamin D (as in chronic kidney disease), or due to end-organ resistance to 1,25-dihydroxy vitamin D3Jagtap V.S. Sarathi V. Lila A.R. et al.Hypophosphatemic rickets.Indian J Endocrinol Metab. 2012; 16: 177-182Crossref PubMed Google Scholar. As a result, calcium absorption in the gut is decreased, which in turn increases parathyroid hormone (PTH) secretion by the parathyroid gland. PTH aims to preserve blood calcium levels by (i) activating bone resorption mediated by increasing RANKL by osteoblasts, (ii) decreasing renal calcium loss, and (iii) increasing renal phosphate loss by internalization and subsequent degradation of sodium-dependent phosphate cotransporter protein (NaPi-2a and NaPi-2c), which decreases tubular phosphate reabsorption.8Mughal M.Z. Rickets.Curr Osteoporos Rep. 2011; 9: 291-299Crossref PubMed Scopus (28) Google Scholar The common pathway in the development of rickets in both calcipenic and phosphopenic forms is reduced phosphate concentration.2Carpenter T.O. Shaw N.J. Portale A.A. et al.Rickets.Nat Rev Dis Primers. 2017; 3: 17101Crossref PubMed Scopus (57) Google Scholar,9Sabbagh Y. Carpenter T.O. Demay M.B. Hypophosphatemia leads to rickets by impairing caspase-mediated of PubMed Scopus Google Scholar D plays an essential in by normal blood levels of calcium and phosphorus (Figure et D in J PubMed Scopus Google for the on and management of Google Scholar There are 2 forms of vitamin vitamin and vitamin is primarily from In to in such as and liver the of vitamin through the of to in the by sunlight in the D to the vitamin D protein and is to the liver for and by by 2 into as which is in the proximal tubule of the kidney through the and R. M. et of and in the of vitamin 2011; PubMed Scopus Google Scholar and by the 1 by to form the of vitamin as 1,25-dihydroxy vitamin vitamin D deficiency and 2015; PubMed Scopus Google Scholar 1,25-dihydroxy vitamin D on the vitamin D in cells to the gut absorption of calcium by the calcium et PubMed Scopus Google Scholar As in is a the by the vitamin bone and is essential for proper management of and PTH the of 1,25-dihydroxy vitamin D. FGF-23, a hormone by plays an important in bone It the of 1,25-dihydroxy vitamin D and with the with the of a and increases the renal excretion of phosphate by the of the renal phosphate sodium-dependent phosphate and on the of proximal renal tubular V. and of the 2012; PubMed Scopus Google Scholar is by 2 major in and matrix 1 Both of which are primarily in by of results in that a in the of Nutritional rickets is the most common form of bone primarily affecting and primarily by vitamin D calcium and phosphate deficiencies a D calcium and phosphorus in the blood and deficiency of vitamin D in mineralization of osteoid by PubMed Scopus Google Scholar The of vitamin D deficiency usually of and lack of sunlight with by and et 1,25-dihydroxy vitamin D is associated with body J Nutr. 2008; PubMed Scopus Google Scholar 1 the of the of vitamin D Shaw M. et on and management of rickets.J Clin Endocrinol Metab. PubMed Scopus Google Scholar There is on the of normal vitamin D in children and in their levels for vitamin D R. M. et for vitamin D in children with chronic kidney disease and on 2017; PubMed Scopus Google Scholar The on the and management of rickets deficiency as vitamin D Shaw M. et on and management of rickets.J Clin Endocrinol Metab. PubMed Scopus Google Scholar Both and are in with and and bone M.Z. Rickets.Curr Osteoporos Rep. 2011; 9: 291-299Crossref PubMed Scopus (28) Google PubMed Scopus Google Scholar the other and M. Sahay R. Rickets-vitamin D deficiency and dependency.Indian J Endocrinol Metab. 2012; 16: 164-176Crossref PubMed Google Shaw M. et on and management of rickets.J Clin Endocrinol Metab. PubMed Scopus Google Scholar biochemical and are to with low of vitamin are in diagnosis as as in from other of rickets M. Sahay R. Rickets-vitamin D deficiency and dependency.Indian J Endocrinol Metab. 2012; 16: 164-176Crossref PubMed Google Shaw M. et on and management of rickets.J Clin Endocrinol Metab. PubMed Scopus Google of to for The by of for and D. of R. 2017; Google Scholar vitamin vitamin normal parathyroid increased The treatment of vitamin D deficiency with of an by a The in the and of in the by to in the et vitamin D PubMed Scopus (108) Google Scholar The for for all groups in the by to in the et and of vitamin D an Clin Endocrinol Metab. 2011; PubMed Scopus Google Scholar of calcium intake of the is The dietary of calcium is for to for to for children 1 to for to and for children to management in kidney an and Scopus Google Scholar normal of calcium and phosphorus in for bone and disease in children with chronic kidney J PubMed Google Scholar In children in calcium deficiency is the of rickets, calcium is T.O. Shaw N.J. Portale A.A. et al.Rickets.Nat Rev Dis Primers. 2017; 3: 17101Crossref PubMed Scopus (57) Google Scholar calcium 1 phosphorus 1 with vitamin D deficiency can be by a of among substantially vitamin D to children in the diagnosed with rickets, of children classified as rickets (vitamin D the substantially low in to to of the a et rickets in a 2017; PubMed Scopus Google Scholar A among the and the of both and the the 25-hydroxyvitamin in the which to in the In the a in vitamin D levels from a of during the to in the R. et to vitamin D levels in with the J PubMed Scopus Google Scholar from an important As is essential for the of vitamin M. Sahay R. Rickets-vitamin D deficiency and dependency.Indian J Endocrinol Metab. 2012; 16: 164-176Crossref PubMed Google and have the as to vitamin D in to J Clin Nutr. PubMed Scopus (108) Google Scholar sunlight and of of from vitamin D In a of the all low vitamin D levels with a of D among J Health 2012; Google Scholar This be secondary to the of in to be from to exposure. is the important for vitamin D of sunlight vitamin D deficiency has been in the of to in the which be due to the of a M. Sahay R. Rickets-vitamin D deficiency and dependency.Indian J Endocrinol Metab. 2012; 16: 164-176Crossref PubMed Google Y. D deficiency and in type 2 of 2017; PubMed Scopus Google Scholar is to vitamin D is a of vitamin D the and and the has low vitamin D the Pettifor J.M. vitamin D for the development of Clin North Am. of PubMed Scopus Google Scholar the vitamin D is a of of vitamin D of the the other of vitamin D because of the of the Hence, vitamin D deficiency is in A in with a of of vitamin D whereas a of M. Sahay R. Rickets-vitamin D deficiency and dependency.Indian J Endocrinol Metab. 2012; 16: 164-176Crossref PubMed Google M.Z. et D of and and in North a Nutr. PubMed Scopus Google Scholar with are a for rickets primarily because of calcium and phosphate T.O. Shaw N.J. Portale A.A. et al.Rickets.Nat Rev Dis Primers. 2017; 3: 17101Crossref PubMed Scopus (57) Google Scholar of vitamin D deficiency can be through adequate vitamin D of dietary and the normal calcium vitamin D supplementation is for from of For of vitamin D through or supplementation is M. Sahay R. Rickets-vitamin D deficiency and dependency.Indian J Endocrinol Metab. 2012; 16: 164-176Crossref PubMed Google for the on and management of Google Shaw M. et on and management of rickets.J Clin Endocrinol Metab. PubMed Scopus Google M. Sahay R. J Endocrinol Metab. PubMed Google et of rickets: a of from Dis PubMed Scopus Google Nutritional rickets the PubMed Scopus Google of rickets and vitamin D for vitamin D PubMed Scopus Google Scholar during the year of vitamin D–dependent type 1 rickets is a disease of vitamin D that due to inactivating mutations in the leading to of the 1 which in turn leads to low levels of the Y. et rickets type and type PubMed Scopus Google of vitamin D deficiency and rickets.J Clin PubMed Scopus Google rickets with sunlight to J Google Scholar of rickets, such as growth and increased to the vitamin D Y. et rickets type and type PubMed Scopus Google Scholar The low calcium, low and in to rickets they have normal or 25-hydroxyvitamin levels and low Y. et rickets type and type PubMed Scopus Google of vitamin D deficiency and rickets.J Clin PubMed Scopus Google Scholar As children to of to of or D intake of dietary calcium of be M. Sahay R. J Endocrinol Metab. PubMed Google Scholar radiological to of children be for of and secondary to M. Sahay R. J Endocrinol Metab. PubMed Google Scholar blood and calcium, for calcium and and kidney be during type 2 or vitamin D–resistant rickets, is a disease by a defect in the vitamin D of vitamin D deficiency and rickets.J Clin PubMed Scopus Google Scholar The defect the body to be to of vitamin D deficiency and rickets.J Clin PubMed Scopus Google Scholar with in and have rickets, growth and in of due to a lack of vitamin D and is a of disease M. Sahay R. J Endocrinol Metab. PubMed Google et of rickets with from the in the vitamin D Endocrinol Metab. PubMed Scopus Google Scholar The levels of levels of and PTH Y. et rickets type and type PubMed Scopus Google et vitamin D rickets: end-organ resistance to J Endocrinol Metab. PubMed Google Scholar levels of vitamin D from among which the levels are usually is a disease to treatment is of vitamin D deficiency and rickets.J Clin PubMed Scopus Google D. forms of vitamin rickets X-linked hypophosphatemia and vitamin D J Clin Nutr. 29: PubMed Scopus Google Scholar the most is to the normal through of and the leads to severe and most by Y. et rickets type and type PubMed Scopus Google Scholar of of low which be increased to with calcium and phosphate calcium for Y. et rickets type and type PubMed Scopus Google et vitamin D rickets: end-organ resistance to J Endocrinol Metab. PubMed Google Scholar The renal rickets is usually to with chronic kidney kidney disease results in the deficiency of the 1 which decreases the of vitamin D M. Sahay R. J Endocrinol Metab. PubMed Google Scholar A history of renal be that the from other bone usually low 25-hydroxyvitamin D levels be The most is the phosphate secondary to poor renal of chronic kidney PubMed Scopus Google Scholar with chronic kidney disease the into the form vitamin D supplementation is for renal a dietary phosphate and of 1 or is with normal 25-hydroxyvitamin D M. Sahay R. J Endocrinol Metab. PubMed Google to renal tubular in J Clin 2011; PubMed Scopus Google et by and to PubMed Scopus Google Scholar The defect in forms of rickets is the increased loss of phosphate through the occur due to mutations or matrix 1 or in X-linked or hypophosphatemic rickets, et is a common of renal to FGF23 and is by in 2012; PubMed Scopus Google Scholar Hypophosphatemic rickets be with which is a of due to the dysfunction of the an 2017; PubMed Scopus Google Scholar has of and and can as rickets, reduced and poor an 2017; PubMed Scopus Google Scholar It is by low which is because other forms of rickets are associated with an 2017; PubMed Scopus Google Scholar It is the most common form of with an of et of fibroblast growth hypophosphatemic in biochemical and 2015; PubMed Scopus Google Scholar The disease results from mutations of the on the which the of by an M.J. to the hypophosphatemic Clin Endocrinol Metab. 2012; PubMed Scopus Google Scholar results in renal wasting of phosphorus the proximal tubule which results in M. D. et D deficiency in children and review of and 2008; PubMed Scopus Google et with a and kidney of a in 2008; PubMed Scopus Google Scholar results in low vitamin D and are of the is which as as of As the leading to short stature with are leading to or abnormalities are common and often be the V. R. et hypophosphatemic rickets.J PubMed Scopus Google Scholar abnormalities and mineralization results in that of leading to and severe from in V. et management and treatment Bone PubMed Scopus Google Scholar In have of and of the and type 1 Y. et of and in children with hypophosphatemic rickets Bone Miner PubMed Scopus Google Scholar A of and children with X-linked hypophosphatemic rickets of or of the to be and of children type 1 Y. et of and in children with hypophosphatemic rickets Bone Miner PubMed Scopus Google Scholar to be associated with a history of Y. et of and in children with hypophosphatemic rickets Bone Miner PubMed Scopus Google Scholar in 2 children and of of children Y. et of and in children with hypophosphatemic rickets Bone Miner PubMed Scopus Google Scholar hypophosphatemic rickets has a of and an The defect an activating in leading to et hypophosphatemic rickets mutations PubMed Scopus Google Scholar In have that deficiency increases of the Z. M. et fibroblast growth in with hypophosphatemic rickets.J Bone Miner PubMed Scopus Google Scholar levels of and hypophosphatemia with deficiency in and with hypophosphatemic rickets Z. M. et fibroblast growth in with hypophosphatemic rickets.J Bone Miner PubMed Scopus Google Scholar on the of are 2 during and X-linked hypophosphatemic The other during or with bone and type 1 due to loss of mutations in a bone matrix protein in and et is a common of renal to FGF23 and is by in 2012; PubMed Scopus Google et of rickets and osteomalacia and a for in PubMed Scopus Google Scholar has a in and in the of and loss of renal phosphate loss and form of has been It due to loss of mutations in which is an that from and is a mineralization V. et hypophosphatemic rickets is associated with an in the J PubMed Scopus Google Scholar of mutations in this protein can lead to generalized of and biochemical of with are to with X-linked hypophosphatemic This of hypophosphatemic rickets results from a defect wherein is loss of in the that cotransporter in phosphate M. et mutations in with hypophosphatemic rickets with a for the cotransporter in phosphate J PubMed Scopus Google et hypophosphatemic rickets with is by mutations in the cotransporter J PubMed Scopus Google et in the hypophosphatemic rickets with Clin Endocrinol Metab. PubMed Scopus Google Scholar Bone and are the common abnormalities are usually In to other of rickets, is normal and 1,25-dihydroxy vitamin D levels are for low phosphorus which to et with a and kidney of a in 2008; PubMed Scopus Google Scholar hypophosphatemic rickets has been in children are with an et hypophosphatemia and bone disease associated with in and 2017; PubMed Scopus Google Scholar A of children for or rickets to have et hypophosphatemia and bone disease associated with in and 2017; PubMed Scopus Google Scholar of the children from and the common that they with et hypophosphatemia and bone disease associated with in and 2017; PubMed Scopus Google Scholar with renal phosphate et hypophosphatemia and bone disease associated with in and 2017; PubMed Scopus Google Scholar In of to dietary deficiency or severe phosphate et hypophosphatemia and bone disease associated with in and 2017; PubMed Scopus Google Scholar in with in abnormalities to a different of phosphorus in et hypophosphatemia and bone disease associated with in and 2017; PubMed Scopus Google Scholar monitoring of in children with is and prompt phosphate supplementation or to is hypophosphatemia is et hypophosphatemia and bone disease associated with in and 2017; PubMed Scopus Google Scholar common of secondary hypophosphatemia is of phosphate such as that results in reduced absorption of et hypophosphatemia and bone disease associated with in and 2017; PubMed Scopus Google Scholar due to such as calcium and phosphate in et hypophosphatemia and bone disease associated with in and 2017; PubMed Scopus Google Scholar of phosphate levels be without et hypophosphatemia and bone disease associated with in and 2017; PubMed Scopus Google Scholar an to a with As for the diagnosis and diagnosis of X-linked hypophosphatemic rickets is based on of rickets osteomalacia with hypophosphatemia and renal phosphate loss without deficiency of vitamin D or D. et for the diagnosis and management of X-linked Rev PubMed Scopus Google Scholar The diagnosis of X-linked rickets be by or levels D. et for the diagnosis and management of X-linked Rev PubMed Scopus Google Scholar supplementation phosphorus in to of to the of management. of from supplementation or to as the formation of B.K. Carpenter T.O. Hypophosphatemic rickets: lessons from disrupted FGF23 control of phosphorus homeostasis.Curr Osteoporos Rep. 2015; 13: 88-97Crossref PubMed Scopus (34) Google M.J. to the hypophosphatemic Clin Endocrinol Metab. 2012; PubMed Scopus Google D. et for the diagnosis and management of X-linked Rev PubMed Scopus Google X-linked of Scholar by calcium be to D. et for the diagnosis and management of X-linked Rev PubMed Scopus Google Scholar the management of with hypophosphatemic rickets with because the which and increases the for with phosphate forms the of Hypophosphatemic Endocrinol 2012; PubMed Scopus Google V. et al.Hypophosphatemic rickets: and J 2015; PubMed Scopus Google Scholar In to the and treatment of deficiency is important in children with hypophosphatemic rickets, as deficiency increased of the Z. M. et fibroblast growth in with hypophosphatemic rickets.J Bone Miner PubMed Scopus Google Scholar In a with hypophosphatemic rickets with supplementation and phosphorus Z. M. et fibroblast growth in with hypophosphatemic rickets.J Bone Miner PubMed Scopus Google Scholar with of and and phosphate Z. M. et fibroblast growth in with hypophosphatemic rickets.J Bone Miner PubMed Scopus Google Scholar In the management of X-linked secondary results from the of parathyroid cells by and phosphate and from the of vitamin D by in children with vitamin D. et for the diagnosis and management of X-linked Rev PubMed Scopus Google Scholar This secondary leads to increased and bone D. et for the diagnosis and management of X-linked Rev PubMed Scopus Google Scholar In vitamin D treatment phosphate intake PTH levels and results in reduced bone the process of rickets and D. et for the diagnosis and management of X-linked Rev PubMed Scopus Google Scholar This the of and monitoring of PTH levels to keep normal D. et for the diagnosis and management of X-linked Rev PubMed Scopus Google Scholar treatment with such as for secondary of vitamin D of phosphate to PTH D. et for the diagnosis and management of X-linked Rev PubMed Scopus Google Scholar be because of severe such as and D. et for the diagnosis and management of X-linked Rev PubMed Scopus Google Scholar for vitamin D and D. et for the diagnosis and management of X-linked Rev PubMed Scopus Google Scholar a by a bone disease is the of the D. et for the diagnosis and management of X-linked Rev PubMed Scopus Google Scholar An important development is the introduction of a human monoclonal antibody that has been to be in children with X-linked T.O. et in children with X-linked J PubMed Scopus Google Scholar A children with X-linked hypophosphatemia from the and of treatment with phosphate and vitamin D et in children with X-linked PubMed Scopus Google Scholar This the in of rickets, growth, and with the et in children with X-linked PubMed Scopus Google Scholar In 2 children with X-linked hypophosphatemia in a to either 2 or and the to a low normal phosphorus T.O. et in children with X-linked J PubMed Scopus Google Scholar with 2 a in the phosphorus levels and of rickets with the The that in the renal tubular phosphate phosphorus growth, and physical and reduced and the of rickets in children with X-linked T.O. et in children with X-linked J PubMed Scopus Google Scholar is and and are D. et for the diagnosis and management of X-linked Rev PubMed Scopus Google Scholar The most common of are and D. et for the diagnosis and management of X-linked Rev PubMed Scopus Google Scholar It approved by the and for in 1 year and in for form of rickets, Scholar the to in D. et for the diagnosis and management of X-linked Rev PubMed Scopus Google Scholar The a of 2 in X-linked hypophosphatemic children 1 year or with and of bone disease on or or or to D. et for the diagnosis and management of X-linked Rev PubMed Scopus Google Scholar The of be often and are in of to a of 2 to phosphate levels the of normal for the D. et for the diagnosis and management of X-linked Rev PubMed Scopus Google Scholar Fanconi syndrome, in which proximal results in proximal renal tubular and generalized can have phosphate loss in hypophosphatemic It be or secondary to syndrome, syndrome, or specific for the with phosphate supplementation and et J 2012; PubMed Scopus Google Scholar the various of different types of et of rickets and osteomalacia and a for in PubMed Scopus Google et in the X-linked abnormalities in PubMed Scopus Google M. et of the vitamin D of vitamin rickets type with PubMed Scopus Google et of the 25-hydroxyvitamin an of PubMed Scopus Google T. M. Y. et of an essential of FGF23 in phosphate and vitamin D Clin PubMed Scopus Google et in the by a is for rickets in 2011; PubMed Scopus Google M. et in an PubMed Scopus Google R. in a with vitamin rickets, type Endocrinol PubMed Scopus Google et and resistance to vitamin D in for vitamin D Clin PubMed Scopus Google Scholar Rickets is a of children that from defective mineralization of the growth Nutritional rickets is a preventable disease by an adequate intake of vitamin D through both dietary and sunlight exposure. D supplementation in rickets secondary to vitamin D deficiency in most of the of an to a with rickets and 2 the major the various types of Knowledge of is essential for prompt diagnosis and proper management.

Topics & Concepts