Chapter 23, Nutritional Rickets

Evidence Maternal vitamin D intake during lactation correlates with milk vitamin D activity. Causes and therapy of congenital rickets 4. Evidence Approximately 80 cases of congenital rickets, defined as babies presenting within the first 4 weeks of life with biochemical and radiographic signs of rickets, have been described in the medical literature. Assessment of disease burden 5. Recommendations The prevalence of rickets should be determined by population-based samples, by case reports from sentinel centers, or by mandatory reporting.

Evidence NR has been increasingly reported in high- and low-income countries 55 , , — Public health strategies for rickets prevention 5. Recommendation Universally supplement all infants with vitamin D from birth to 12 months of age, independent of their mode of feeding. Vitamin D supplementation Infants aged 0—12 months and adolescents are at increased risk of NR and osteomalacia from vitamin D deficiency due to rapid growth. Food fortification with vitamin D Food fortification of commonly consumed staple foods safely provides adequate intake to prevent deficiency at minimal cost.

Food fortification with calcium Inadequate dietary calcium intake is a risk factor for NR in children over the age of 12 months with low dairy product intake, a common situation in low-income countries. Health promotion Education of medical providers and organizations, health insurers, policy makers, governments, public health officials, and the general public is vital to address the public health issue of NR and vitamin D deficiency.

Recommendation The cost-effectiveness of supplementation and food fortification programs needs further study. Evidence Very weak evidence supports a policy of providing vitamin D supplementation to Asian children in the United Kingdom for the first 2 years of life Future economic models should include: Resources associated with different supplementation strategies. Health care costs of disease caused by both skeletal and extraskeletal effects of vitamin D deficiency.

Conclusion Vitamin D deficiency should be considered a major global public health priority. Acknowledgments Editorial support was provided by Sally Farrand. Vitamin D-deficiency rickets among children in Canada. Incidence of vitamin D deficiency rickets among Australian children: Incidence of symptomatic vitamin D deficiency. Nutritional rickets in Denmark: A comparison of calcium, vitamin D, or both for nutritional rickets in Nigerian children.

N Engl J Med. Balasubramanian K, Rajeswari J, Gulab, et al. Varying role of vitamin D deficiency in the etiology of rickets in young children vs. Relationship between serum hydroxyvitamin D and parathyroid hormone in the search for a biochemical definition of vitamin D deficiency in children. Vitamin D and health in pregnancy, infants, children and adolescents in Australia and New Zealand: Vitamin D deficiency and nutritional rickets in children.

Hypocalcaemia and vitamin D deficiency: Deaths in childbed from the eighteenth century to A case for clarity, consistency, and helpfulness: Tiosano D, Hochberg Z. J Bone Miner Metab. The National Academies Press; Accuracy of hydroxyvitamin D assays: State-of-the-art vitamin D assays: Development of a candidate reference measurement procedure for the determination of hydroxyvitamin D3 and hydroxyvitamin D2 in human serum using isotope-dilution liquid chromatography-tandem mass spectrometry. Candidate reference measurement procedures for serum hydroxyvitamin D3 and hydroxyvitamin D2 by using isotope-dilution liquid chromatography-tandem mass spectrometry.

Vitamin D status as an international issue: Assessing vitamin D status: Interlaboratory variation in hydroxyvitamin D2 and hydroxyvitamin D3 is significantly improved if common calibration material is used. Higher prevalence of vitamin D deficiency in mothers of rachitic than nonrachitic children. Prospective study of vitamin D supplementation and rickets in China. Risk factors for nutritional rickets among children in Kuwait.

Vitamin D status of mothers and their neonates in Kuwait. The report on dietary reference intakes for calcium and vitamin D from the Institute of Medicine: Vitamin D and multiple health outcomes: Role of calcium deficiency in development of nutritional rickets in Indian children: The natural history of vitamin D deficiency in African refugees living in Sydney.

Vitamin D supplementation and risk of toxicity in pediatrics: Twice single doses of , IU of vitamin D in winter is adequate and safe for prevention of vitamin D deficiency in healthy children from Ushuaia, Tierra Del Fuego, Argentina. J Steroid Biochem Mol Biol. Hypercalcemia due to hypervitaminosis D: Acute vitamin D intoxication in a child.

Bereket A, Erdogan T. Oral bisphosphonate therapy for vitamin D intoxication of the infant. Vitamin D intoxication due to an erroneously manufactured dietary supplement in seven children. Short- and long-term safety of weekly high-dose vitamin D3 supplementation in school children. Hypercalcemia in children receiving pharmacologic doses of vitamin D. Rickets in children of rural origin in South Africa: Rickets due to dietary calcium deficiency. Dietary calcium intake in rural black South African children. The relationship between calcium intake and calcium nutritional status.

Hum Nutr Clin Nutr. Rickets in Nigerian children: Fractures in infants and toddlers with rickets. Nutritional rickets in African American breast-fed infants. Saudi J Kidney Dis Transpl. Variable presentations of rickets in children in the emergency department. Fractures in undermonth-old exclusively breast-fed infants born to immigrant parents: Pathological fractures secondary to vitamin D deficiency rickets in undermonths-old, exclusively breast-fed infants, born to immigrant parents.

Rickets in the dairy state. Vitamin D deficiency rickets simulating child abuse. Vitamin D deficiency rickets and allegations of non-accidental injury. Vitamin D status in abused and nonabused children younger than 2 years old with fractures. Effect of different dosages of oral vitamin D supplementation on vitamin D status in healthy, breastfed infants: Beser E, Cakmakci T.

Factors affecting the morbidity of vitamin D deficiency rickets and primary prevention. East Afr Med J. Vitamin D prophylaxis during infancy: Am J Clin Nutr. Calcium and vitamin D metabolism in children in developing countries. Vitamin D deficiency in children with a chronic illness—seasonal and age-related variations in serum hydroxy vitamin D concentrations.

Prevention of rickets and vitamin D deficiency in infants, children, and adolescents. Vitamin D in the healthy European paediatric population. J Pediatr Gastroenterol Nutr. Evaluation, treatment, and prevention of vitamin D deficiency: Vitamin D fortification in the United States and Canada: Comparison of low and high dose of vitamin D treatment in nutritional vitamin D deficiency rickets. J Pediatr Endocrinol Metab. Plasma concentrations of vitamin D metabolites before and during treatment of vitamin D deficiency rickets in children.

Pathophysiology of calcium metabolism in children with vitamin D-deficiency rickets. Comparisons of oral calcium, high dose vitamin D and a combination of these in the treatment of nutritional rickets in children. Radiological and biochemical resolution of nutritional rickets with calcium. Long-term bioavailability after a single oral or intramuscular administration of , IU of ergocalciferol or cholecalciferol: Treatment of hypovitaminosis D with pharmacologic doses of cholecalciferol, oral vs intramuscular; an open labeled RCT. A randomized controlled trial on safety and efficacy of single intramuscular versus staggered oral dose of IU Vitamin D in treatment of nutritional rickets.

Comparison of vitamin D2 and vitamin D3 supplementation in raising serum hydroxyvitamin D status: Vitamin D deficiency in children and its management: Diagnosis and management of vitamin D deficiency. Vitamin D and child health: Prevention and treatment of infant and childhood vitamin D deficiency in Australia and New Zealand: Vitamin D deficiency in mothers of rachitic infants. Nutritional rickets presenting with myelofibrosis. Images in pediatric endocrinology: Sanyal D, Raychaudhuri M.

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Infants with dilated cardiomyopathy and hypocalcemia. Indian J Endocrinol Metab. Clinical, biochemical, and radiological manifestations of vitamin D deficiency in newborns presented with hypocalcemia. The re-emerging burden of rickets: Epidemiology of nutritional rickets in children. Severe vitamin D deficiency in 6 Canadian First Nation formula-fed infants.

Int J Circumpolar Health. Randomized controlled trial RCT of vitamin D supplementation in pregnancy in a population with endemic vitamin D deficiency. Hypocalcemic rickets and dilated cardiomyopathy: Vitamin D deficiency rickets in breast-fed infants presenting with hypocalcaemic seizures. An outbreak of vitamin D deficiency rickets in a susceptible population. Binet A, Kooh S. Persistence of vitamin D-deficiency rickets in Toronto in the s. Can J Public Health. Vitamin D deficiency rickets in infants presenting with hypocalcaemic convulsions.

West Indian Med J. Nutritional rickets with normal circulating hydroxyvitamin D: Vitamin-D-deficient rickets in Manitoba, — Prevalence and risk factors of vitamin D deficiency rickets in Hokkaido, Japan. A comparison of breastfed children with nutritional rickets who present during and after the first year of life. Hypocalcemic seizures in breastfed infants with rickets secondary to severe maternal vitamin D deficiency.

Pak J Biol Sci. Increasing incidence of nutritional rickets: J R Soc Promot Health. Nutritional vitamin D deficiency rickets in Sudanese children. Vitamin D deficiency rickets. A report on three cases. Clin Orthop Relat Res. Lesson of the week: Presentation and predisposing factors of nutritional rickets in children of Hazara Division. J Ayub Med Coll Abbottabad. Lerch C, Meissner T. Interventions for the prevention of nutritional rickets in term born children.

Cochrane Database Syst Rev. Prevalence of vitamin D deficiency rickets in the Eastern part of Turkey. Children with nutritional rickets referred to hospitals in Copenhagen during a year period. Survey of clinical rickets in the infant population in Cape Town, — S Afr Med J. Preventing rickets in locally appropriate ways: Int Q Community Health Educ. Early and severe presentation of vitamin D deficiency and nutritional rickets among hospitalized infants and the effective factors. Apparent efficacy of food-based calcium supplementation in preventing rickets in Bangladesh.

Biol Trace Elem Res. Combs GF, Hassan N. The Chakaria food system study: Eur J Clin Nutr. Two cases with faulty infant feeding practices. Am J Dis Child. Nutritional rickets in vegetarian children. Can Med Assoc J. Food allergy as a risk factor for nutritional rickets. Vitamin D deficiency rickets due to soybean milk. J Paediatr Child Health. Vitamin D deficiency rickets caused by improper lifestyle in Japanese children. Vitamin D—deficient rickets in a child with cow's milk allergy.

Environmental factors that influence the cutaneous production of vitamin D. Vitamin D production after UVB: Influence of season and latitude on the cutaneous synthesis of vitamin D3: The impact of atmospheric pollution on vitamin D status of infants and toddlers in Delhi, India. Seasonal changes in plasma hydroxyvitamin D concentrations of young American black and white women. Sun and ski holidays improve vitamin D status, but are associated with high levels of DNA damage. Influence of external, intrinsic and individual behaviour variables on serum 25 OH D in a German survey.

J Photochem Photobiol B. Estimated equivalency of vitamin D production from natural sun exposure versus oral vitamin D supplementation across seasons at two US latitudes. J Am Acad Dermatol. McCollum Award Lecture, UVR exposure and vitamin D in a rural population. A study of outdoor working farmers, their spouses and children. Interdependence between body surface area and ultraviolet B dose in vitamin D production: Lifestyle factors including less cutaneous sun exposure contribute to starkly lower vitamin D levels in U.

South Asians compared with the white population. UV radiation exposure related to age, sex, occupation, and sun behavior based on time-stamped personal dosimeter readings. Is casual exposure to summer sunlight effective at maintaining adequate vitamin D status? Recommended summer sunlight exposure amounts fail to produce sufficient vitamin D status in UK adults of South Asian origin. Efficacy of a dose range of simulated sunlight exposures in raising vitamin D status in South Asian adults: Aging decreases the capacity of human skin to produce vitamin D3. The role of sunlight exposure in determining the vitamin D status of the U.

Frequency of nutritional rickets in children admitted with severe pneumonia. J Pak Med Assoc. J Clin Res Pediatr Endocrinol. Indian J Med Res. Teotia SP, Teotia M. Nutritional bone disease in Indian population. Vitamin D supplements in pregnant Asian women: Effect of vitamin D supplementation during pregnancy on neonatal mineral homeostasis and anthropometry of the newborn and infant.

Effect of vitamin D supplementation during pregnancy on foetal growth. Maternal vitamin D intake and mineral metabolism in mothers and their newborn infants. Vitamin D supplementation during pregnancy: Effect on neonatal calcium homeostasis. Mineral content of the forearms of babies born to Asian and white mothers. Vitamin D supplementation in pregnancy: Intrauterine vitamin D nutrition and postnatal growth in Asian infants.

Vitamin D deficiency and supplementation during pregnancy. J Bone Miner Res. A randomized trial of vitamin D supplementation in 2 community health center networks in South Carolina. Am J Obstet Gynecol. Efficacy of daily and monthly high-dose calciferol in vitamin D-deficient nulliparous and lactating women. Maternal early pregnancy vitamin D status in relation to fetal and neonatal growth: Vitamin D deficiency and whole-body and femur bone mass relative to weight in healthy newborns.

Maternal vitamin D status determines bone variables in the newborn. Low maternal vitamin D status and fetal bone development: The effect of maternal vitamin D concentration on fetal bone. Maternal vitamin D status during pregnancy and childhood bone mass at age 9 years: Association of maternal vitamin D status during pregnancy with bone-mineral content in offspring: Sayers A, Tobias J. Estimated maternal ultraviolet B exposure levels in pregnancy influence skeletal development of the child. Randomized, placebo-controlled, calcium supplementation study in pregnant Gambian women: Maternal calcium supplementation and fetal bone mineralization.

World Health Organization randomized trial of calcium supplementation among low calcium intake pregnant women. Vitamin D requirements during lactation: High-dose vitamin D3 supplementation in a cohort of breastfeeding mothers and their infants: Effect of combined maternal and infant vitamin D supplementation on vitamin D status of exclusively breastfed infants.

Maternal vitamin D supplementation to improve the vitamin D status of breast-fed infants: The effect of high-dose vitamin D supplementation on serum vitamin D levels and milk calcium concentration in lactating women and their infants. Maternal-infant vitamin D relationships during breast-feeding. Maternal compared with infant vitamin D supplementation. Calcium levels in maternal milk: Calcium requirements of lactating Gambian mothers: The effect of calcium supplementation on bone density during lactation and after weaning.

Longitudinal changes in the mineral content of human milk.

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Influence of mineral intake and use of oral contraceptives before pregnancy on the mineral content of human colostrum and of more mature milk. Vitamin D status does not influence the breast-milk calcium concentration of lactating mothers accustomed to a low calcium intake. Maternal malabsorption presenting as congenital rickets. Moncrieff M, Fadahunsi TO. Congenital rickets due to maternal vitamin D deficiency. Zeidan S, Bamford M. Congenital rickets with maternal pre-eclampsia.

J R Soc Med. Osteomalacia of the mother—rickets of the newborn. Metabolic studies in congenital vitamin D deficiency rickets. Study of the evolution of secondary hyperparathyroidism. Vitamin D deficiency rickets at birth in Kuwait. Congenital rickets caused by maternal vitamin D deficiency. Severe congenital rickets secondary to maternal hypovitaminosis D: Hypocalcemic seizure due to congenital rickets in the first day of life. Congenital rickets presenting as refractory respiratory distress at birth. Congenital hyperparathyroidism and rickets: Isr J Med Sci.

Transient neonatal hyperparathyroidism secondary to maternal pseudohypoparathyroidism. Spectrum and natural history of congenital hyperparathyroidism secondary to maternal hypocalcemia. Hyperparathyroidism secondary to maternal hypoparathyroidism and vitamin D deficiency: Congenital rickets — a case report. Congenital rickets—a patient report. Congenital rickets secondary to untreated maternal renal failure. Skeletal dysplasias with osteopenia in the newborn: J Matern Fetal Neonatal Med. Connatal rickets following repeated administration of phosphate enemas in pregnancy: Congenital rickets associated with magnesium sulfate infusion for tocolysis.

Nutritional rickets around the world: Vitamin D deficiency in healthy children in a sunny country: Int J Food Sci Nutr. Nutritional and health status of Tibetan children living at high altitudes. Case-control study of the role of nutritional rickets in the risk of developing pneumonia in Ethiopian children. Prevention of nutritional rickets in Nigerian children with dietary calcium supplementation.

Nutritional rickets without vitamin D deficiency in Bangladesh. Radiographic scoring method for the assessment of the severity of nutritional rickets. Evaluation of children with nutritional rickets. Nutritional rickets among children in the United States: Prevalence of classic signs and symptoms of rickets and vitamin D deficiency in Mongolian children and women. Bener A, Hoffmann G.

Nutritional rickets among children in a sun rich country. Int J Pediatr Endocrinol. Prevalence of rickets in Mongolia. Asia Pac J Clin Nutr. Underwood P, Margetts B. High levels of childhood rickets in rural North Yemen. Hospitalisation for children with rickets in England: Treatment of hypovitaminosis D in infants and toddlers.

Diagnosis of rickets and reassessment of prevalence among rural children in northern China. Use of supplemental vitamin D among infants breastfed for prolonged periods. Case-control study of factors associated with nutritional rickets in Nigerian children. Guidelines on food fortification with micronutrients.

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World Health Organization; New approaches for designing and evaluating food fortification programs. Recommendations for a national policy on vitamin D supplementation for infants in Ireland. Food Safety Authority of Ireland; Consumption of potentially fortifiable foods by women and young children varies by ecological zone and socio-economic status in Cameroon. Modern India and the vitamin D dilemma: Mol Nutri Food Res. Kiely M, Black L. Dietary strategies to maintain adequacy of circulating hydroxyvitamin D concentrations.

Vitamin D - a systematic literature review for the 5th edition of the Nordic Nutrition Recommendations. An updated systematic review and meta-analysis of the efficacy of vitamin D food fortification. Prevention of vitamin-D deficiency in Asians. Impact of national fortification of fluid milks and margarines with vitamin D on dietary intake and serum hydroxyvitamin D concentration in 4-year-old children.

Impact of vitamin D fortified milk supplementation on vitamin D status of healthy school children aged 10—14 years. Prevalence and associations of hydroxyvitamin D deficiency in US children: Vitamin D treatment in calcium-deficiency rickets: A pilot randomized controlled trial of oral calcium and vitamin D supplementation using fortified laddoos in underprivileged Indian toddlers. Ingestion of micronutrient fortified breakfast cereal has no influence on immune function in healthy children: The selection and prevalence of natural and fortified calcium food sources in the diets of adolescent girls.

J Nutr Educ Behav. The importance of fortification of flour with calcium and the sources of Ca in the diet of English adolescents. Defining vitamin D deficiency in children: Support Center Support Center. Please review our privacy policy. Swelling wrists and ankles. Delayed fontanelle closure normally closed by age 2 y. Delayed tooth eruption no incisors by age 10 mo, no molars by age 18 mo.

Leg deformity genu varum, genu valgum, windswept deformity. Rachitic rosary enlarged costochondral joints—felt anteriorly, lateral to the nipple line. For children with phosphopenic rickets, the causes can be distinguished by measuring urinary amino acids, bicarbonate, glucose, and calcium concentrations. For children with calcipenic rickets, measurements of serum 25 OH D help to distinguish rickets caused by vitamin D deficiency the most common form from other causes of calcipenic rickets. Serum concentration of 25 OH D reflects the amount of vitamin D stored in the body and, consequently, is low in vitamin D deficiency, while it is normal or slightly increased in the other forms.

The best way to assess vitamin D status is to measure 25 OH D levels. As 25 OH D levels fall, intestinal absorption of calcium falls, leading to a decrease in serum calcium. The optimal 25 OH D concentration may also be defined clinically, such as level needed for fracture reduction. There is no consensus on the optimal 25 OH D concentration for skeletal health. A safe upper serum level has also not been determined. There is an increased risk for fractures and some cancers e. Currently accepted standards for defining vitamin D status in children and adolescents are: These cut-offs may need to be revised if future pediatric studies demonstrate efficacy of higher 25 OH D level.

The level of 25 OH D is the best indicator of vitamin D status and stores. Also, its concentration correlates more with kidney function than with vitamin D deficiency. Hence, it is not useful for assessment of vitamin D stores. There are many commercially available 25 OH D assays used for the determination of vitamin D status.

These include chemical assays [high-pressure liquid chromatography HPLC and mass spectrometry MS ] and binding assays — immunoassays [i. Variability among assays is an important problem. Immunoassays and protein-binding assays report total value. Chemical assays can report both vitamin D2 and d3. Overt vitamin D deficiency, characterized by hypocalcemia or hypophosphatemia and rickets or osteomalacia, is now uncommon in most developed countries. However, subclinical vitamin D deficiency is associated with osteoporosis, increased risk of falls, and possibly fractures.

This may be due to assay changes, changes in milk intake, use of sun protection, and changes in body mass index BMI. Estimates of vitamin D requirements vary and depend in part on sun exposure and the standards used to define a deficient state. The dietary reference intakes were based upon data examining the beneficial effects of calcium and vitamin D on skeletal health and not on extraskeletal health. This intervention sufficiently increases the vitamin D content of breast milk to allow sufficient vitamin D intake by the infant without causing hypervitaminosis d in the mother.

More moderate vitamin D doses e. However, these doses may not result in sufficient vitamin D in breast milk to meet the infant's needs, and supplementation may still be necessary for the infant. This target serum level was later considered inadequate because these levels are not sufficient for preventing all cases of florid rickets.

Children who are obese and those on anticonvulsants, glucocorticoids, and medications for HIV infection require higher doses. Intake of IU is recommended. However, some studies suggest that higher intakes may be necessary to maintain normal levels of 25 OH D during pregnancy and lactation. It is not necessary to perform universal screening of serum 25 OH D levels in the general population.

In individuals who are in the high-risk groups described above, it is appropriate to measure serum 25 OH D to supplement with the amount estimated to reach the target 25 OH D level, and then to measure again 3—4 months later to verify that the target has been achieved. Children with elevated levels of serum ALP e. Multiple preparations of vitamin D are available. The two common forms of vitamin D supplements are ergocalciferol and cholecalciferol. Vitamin D3 is available in , , , , , 10,, and 60, unit capsules. It is available in some countries as an intramuscular injection Arachital 6 lakhs units, which maintains vitamin D levels for 1 year.

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Vitamin D metabolites can be used to treat vitamin D deficiency, particularly when there is abnormal vitamin D metabolism renal or liver disease. The recommended preparation and dose vary with the clinical condition. Dosing of vitamin D depends upon the nature and severity of the deficiency. In patients with normal absorptive capacity, for every units of added vitamin D3, serum 25 OH D concentrations increase by approximately 1. Multiple dosing regimens have been shown to treat vitamin D deficiency effectively. In a 2-month trial of oral vitamin D3 repletion in elderly women with hip fracture, the same cumulative dose given daily units , weekly 10, units , or monthly 45, units resulted in similar increments in serum 25 OH D levels.

Although large annual doses of vitamin D3 increase serum 25 OH D levels, they are not recommended as undesirable effects of increasing falls and fractures in older adults are seen. Various regimes which can be used are as follows:. The above recommendations are in agreement with Endocrine Society practice guidelines on the treatment of vitamin D deficiency. All patients should consume total calcium of at least mg for ages 19—70 years to mg for women of ages 51 through 70 years and for all adults 71 years and older per day.

The upper level UL of intake for calcium in most adults is — mg daily. Repeat boluses may also be necessary. High doses of calcium are necessary early in the course of therapy, after which doses are reduced by half for the next 1—2 weeks. The most widely used treatment for vitamin D deficiency consists of vitamin D2 ergocalciferol or vitamin D3 cholecalciferol. Treatment is continued until there is radiographic evidence of healing; subsequently, the dose of vitamin D is reduced to IU daily.

This leads to resolution of the biochemical and radiological abnormalities within 3 months. Skeletal deformities regress completely after medical therapy. However, orthopedic intervention can be done if deformities do not improve even after radiologic appearance of the growth plates has normalized. High-dose vitamin D may need to be intermittently repeated usually every 3 months if poor compliance persists. Stoss therapy is useful when compliance is a problem. However, such high doses of vitamin D can lead to hypercalcemia. Doses of , or , IU are equally effective with lesser side effects.

Side effects of calcitriol therapy include hypercalcemia, hypercalciuria, nephrocalcinosis, and intraocular calcifications. There may be polyuria, pruritis, and azotemia. Many patients take vitamin and mineral supplements that contain vitamin D without being aware of these. It is important to inquire about additional dietary supplements that patients may be taking before prescribing extra vitamin D.

Within about 20 minutes of UV exposure in light-skinned individuals, the concentrations of vitamin D precursors produced in the skin reach an equilibrium and any further vitamin D that is produced is degraded. Some patients with vitamin D deficiency have coexisting primary hyperparathyroidism that is not recognized until vitamin D is repleted.

In contrast, in individuals with clinically significant vitamin D deficiency and SHPT, calcium concentrations are generally normal or at the lower end of normal rarely below normal and PTH concentrations are mildly elevated. The PTH level should return to normal upon vitamin D repletion. Urinary calcium is extremely low in patients with vitamin D deficiency and SHPT and takes months to normalize, whereas in primary hyperparathyroidism it normalizes very rapidly with vitamin D replacement.

The skeletal benefits of calcium and vitamin D supplementation have been demonstrated in prospective, randomized, placebo-controlled studies of calcium and vitamin D in community-dwelling older individuals. In addition to skeletal effects, vitamin D may have several other benefits, including beneficial effects on the immune and cardiovascular systems.

Healthy individuals on vitamin D supplementation do not require an initial or follow-up serum 25 OH D measurement after starting supplementation, but in patients being treated for deficiency, close supervision is needed during treatment. It includes physical examination and biochemical evaluation every 2 weeks. Radiographs should be taken at 4 weeks. Response is deemed if radiographs show clear improvement and serum calcium and phosphorus levels have normalized, and ALP has started to decrease toward the reference range.

Radiograph and biochemistry should be repeated after 3 months, when the growth plates should have regained a normal appearance and biochemistry should be normal and urine calcium should become detectable. Patients may be evaluated at 3-month intervals during maintenance therapy. PTH should be assayed in 6 months. Hand radiographs, renal ultrasound, and ophthalmologic consultation slit-lamp examination should be performed once per year. VDDR-I is an autosomal recessive disorder. VDDR-I is characterized by early onset of skeletal disease within the first year of life , severe hypocalcemia sometimes with tetany , and moderate hypophosphatemia.

Patients exhibit enamel hypoplasia, muscle weakness, hypotonia, motor retardation, and stunted growth. With progression, patients develop the classic radiographic signs of vitamin D deficiency rickets and bone biopsy evidence of osteomalacia. Biochemical evaluation shows hypocalcemia, increased PTH, and increase in urinary excretion of amino acids and phosphate.

The characteristic biochemical findings of VDDR-I are normal serum levels of calcidiol and low levels of calcitriol. The clinical and biochemical evidence of rickets can be corrected with 1,25 OH 2 D treatment.

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The dose depends upon the severity of disease and body weight. Treatment is continued at this dose until bones are healed. Thereafter, the maintenance dose varies between 0. The aims of the treatment are to achieve normocalcemia, to maintain PTH levels within normal limits, and to avoid hypercalciuria.

HVDRR is a very rare autosomal recessive form of rickets, with fewer than 50 known affected kindreds.

Global Consensus Recommendations on Prevention and Management of Nutritional Rickets

It is associated with end-organ resistance to calcitriol, usually caused by mutations in the gene encoding the vitamin D receptor. The defect in the receptor interferes with the function of the hormone—receptor complex, thereby preventing calcitriol action. The clinical spectrum of HVDRR varies with the type of mutation within the vitamin D receptor and residual vitamin D receptor activity. Affected children usually appear normal at birth, but develop rickets within the first 2 years of life.

A unique feature of the syndrome is alopecia, which is seen in approximately two-thirds of cases and is a marker of disease severity. Alopecia results from the lack of vitamin D receptor action within keratinocytes. Additional ectodermal anomalies may also be seen, including multiple milia, epidermal cysts, and oligodontia. The individual response varies with the severity of the receptor defect.

Therapy is started at daily doses of 2 mcg of calcitriol and mg of calcium. Long-term infusion of calcium into a central vein is an alternative for resistant patients and needs to be continued for many months. Oral calcium therapy may be sufficient once radiographic healing has been observed. During treatment, patients should initially be evaluated at least once per week. If the biochemical parameters do not respond, the dose of calcitriol should be gradually increased to reach serum concentrations of up to times the normal mean.

Failure of therapy should be considered if no biochemical response occurs after 3—5 months of treatment. Screening for vitamin D deficiency is recommended in individuals at risk. Proper treatment corrects the disturbed bone metabolism and deformities. In addition, vitamin D has multiple extraskeletal benefits and treatment of vitamin D deficiency improves the quality of life. VDDR is another form of bone disease related to vitamin D, but unlike vitamin D deficient rickets it is hereditary.

Though uncommon, recognition of VDDR is essential for treatment. National Center for Biotechnology Information , U. Indian J Endocrinol Metab. Manisha Sahay and Rakesh Sahay 1. Author information Copyright and License information Disclaimer. This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3. This article has been cited by other articles in PMC.

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6. Rickets–vitamin D deficiency and dependency!

Abstract Rickets is an important problem even in countries with adequate sun exposure. Calcipenic rickets Calcipenic hypocalcemic rickets is characterized by deficiency of calcium or more commonly vitamin D. Open in a separate window. Phosphopenic rickets Phosphopenic rickets is commonly caused by renal phosphate wasting.

Sun exposure Dietary vitamin D deficiency can also occur in children, with differences among ethnic groups depending on skin pigmentation and varied ingestion of supplements. Cold climates Vitamin D deficiency is also common at the end of the winter due to less sun exposure. Extensive burns In patients with a history of extensive burn injuries, vitamin D synthesis in skin is below normal, even with sun exposure.

Nutritional deficiency Vitamin D deficiency can occur even with adequate sun exposure. Elderly people Cutaneous vitamin D production and vitamin D stores decline with age. Maternal vitamin D deficiency Vitamin D is transferred from the mother to the fetus across the placenta, and reduced vitamin D stores in the mother are associated with lower vitamin D levels in the infant. Prematurity Vitamin D levels are low in premature infants, who have less time to accumulate vitamin D from the mother through transplacental transfer.

Obesity 25 OH D levels are low in obese individuals as vitamin D is sequestrated in fat. Hospitalized patients Inadequate intake and lack of sun exposure cause vitamin D deficiency in this group of patients. Women treated for osteoporosis Subclinical vitamin D deficiency is common in postmenopausal women on therapy for osteoporosis bisphosphonates, raloxifene, calcitonin, or PTH.

Rickets–vitamin D deficiency and dependency

Nephrotic syndrome Most of the calcidiol in serum is bound to DBP. Distal renal tubular acidosis Hypocalcemia can occur in dRTA, along with acidosis, which causes rickets. Gastric bypass Patients with short-limb bypass have secondary hyperparathyroidism SHPT in spite of normal 25 OH D concentrations, due to calcium malabsorption.

Skeletal findings The skeletal changes are similar in calcipenic and phosphopenic rickets. Extraskeletal findings The child may be asymptomatic or may present with pain, irritability, delay in motor milestones, and poor growth. Radiographic findings In children, the changes of rickets can be seen at the growth plate of rapidly growing bones.

Bone mineral density Several studies have demonstrated markedly reduced spine, hip, and forearm bone density [as measured by dual-energy X-ray absorptiometry DXA ] in patients with osteomalacia related to vitamin D deficiency. Pregnant and lactating mothers Intake of IU is recommended.

Vitamin D metabolites Vitamin D metabolites can be used to treat vitamin D deficiency, particularly when there is abnormal vitamin D metabolism renal or liver disease. It does not require hepatic hydroxylation, and is therefore most useful in patients with liver disease. The onset of action is more rapid and the half-life of 2—3 weeks is shorter than that of Vitamin D3 and similar to that of Vitamin D2. Calcitriol may be used in patients with severe liver disease who remain deficient after treatment with Vitamin D2 or Vitamin D3.

Calcitriol [1,25 OH 2 D] is available in capsules of 0. Calcitriol has a rapid onset of action and its half-life is only 6 hours, is expensive, and does not build up vitamin D stores. Hence, calcitriol is not preferred for stoss therapy or for nutritional deficiency. It is associated with a high incidence of hypercalcemia, so the serum calcium should be monitored carefully. While using calcitriol as a supplement, 25 OH D levels do not indicate clinical vitamin D status. Doxercalciferol is used in the treatment of SHPT due to chronic kidney disease. It is the first pro-Vitamin D2 to be available in India as 0.

DHT is a synthetic vitamin D analog activated in the liver, which does not require renal hydroxylation. It is functionally equivalent to 1a-hydroxy vitamin D. It requires hepatic hydroxylation prior to becoming therapeutically active. Various regimes which can be used are as follows: In pregnant women, weekly doses of 50, units for 6—8 weeks are not recommended and — units of vitamin D3 daily are thought to be safer.

Urinary calcium excretion increases in pregnancy, and it should be monitored when treating vitamin D deficiency, especially in women with a history of renal stones. In malabsorption or patients with gastrectomy, generally high doses of vitamin D of 10,—50, units daily are needed to correct the deficiency. Hydroxylated vitamin D metabolites are good options because they are more readily absorbed. Children The most widely used treatment for vitamin D deficiency consists of vitamin D2 ergocalciferol or vitamin D3 cholecalciferol.

Extraskeletal benefits In addition to skeletal effects, vitamin D may have several other benefits, including beneficial effects on the immune and cardiovascular systems. Footnotes Source of Support: Nil Conflict of Interest: Rickets and osteomalacia are still around. Radiol Clin North Am. Indian J Med Res. Carpenter Nutritional rickets with normal circulating hydroxyvitamin D: A call for reexamining the role of dietary calcium intake in North American infants.

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Clin J Am Soc Nephrol. Fibroblast growth factor 23 is a counter-regulatory phosphaturic hormone for vitamin D. J Am Soc Nephrol. Nonclassic actions of vitamin D. N Engl J Med. Low vitamin D status despite abundant sun exposure. A clinical research center study. Synthesis of vitamin D in skin after burns. Severe nutritional deficiencies in toddlers resulting from health food milk alternatives. High-dose maternal supplementation as therapy to prevent hypovitaminosis D for both the mother and the nursing infant.

Am J Clin Nutr. Thandrayen K, Pettifor JM. Maternal vitamin D status: Implications for the development of infantile nutritional rickets. Sunshine exposure and serum hydroxyvitamin D concentrations in exclusively breast-fed infants. Digital Education Publishing; Formula fed nutrition during infancy: Principles and Practice; p. The relationship between obesity and serum 1, dihydroxy vitamin D concentrations in healthy adults.