{
"topic": "Vitamin D Deficiency",
"slug": "vitamin-d-deficiency",
"category_id": 15039,
"passage_count": 14,
"source_chars": 12930,
"enough_material": true,
"references": [
{
"title": "Cover",
"author": "Vitalsource Download",
"pages": [
8230
]
},
{
"title": "Pediatric Nutrition (Ronald E. Kleinman, Frank R. Greer)",
"author": null,
"pages": [
656,
1187
]
},
{
"title": "Kliegman R. Nelson Textbook of Pediatrics 2-Volume Set 22ed 2024",
"author": null,
"pages": [
18,
443,
521,
522
]
},
{
"title": "Pediatric Decision-Making Strategies",
"author": "Pomeranz, Albert J.",
"pages": [
351
]
},
{
"title": "Pediatric Board Study Guide",
"author": null,
"pages": [
426,
732
]
},
{
"title": "Netters Pediatrics (Florin \u0422., Ludwig St.)",
"author": null,
"pages": [
123,
124,
453
]
}
],
"passages": [
{
"source": "Cover, p. 8230",
"text": "Infants and children with risk factors are screened for vitamin D deficiency or insufficiency by measuring the serum level of 25-hydroxyvitamin D (25OHD, also known as calcidiol). Vitamin D insufficiency is defined when the level is between 15 and 20 ng/mL, and vitamin D deficiency is defined as when it is less than 15 ng/mL. Vitamin D deficiency is more common in malnourished populations and in children with chronic illnesses (disorders of intestinal absorption, children on anticonvulsant medications such as phenytoin), but it is also found in children with insufficient intake of vitamin D in the developed world. It is primarily seen in dark-skinned infants and children with diets low in vitamin D without supplemental vitamin D and with limited exposure to sunlight and in premature infants or exclusively breastfed infants not receiving supplemental vitamin D. In patients with vitamin D\u2013deficient rickets, serum total calcium values are low-normal or low, phosphate levels are low, and alkaline phosphatase"
},
{
"source": "Pediatric Nutrition (Ronald E. Kleinman, Frank R. Greer), p. 656",
"text": "## _Deficiency_ The primary manifestations of vitamin D deficiency are related to the effects on calcium metabolism. Hypocalcemia, hypophosphatemia, tetany, osteomalacia, and rickets are the most common clinical features. Children at higher risk of deficiency include preterm infants, exclusively breastfed infants, children with dark skin pigmentation, and children with dietary fat malabsorption such as those with cholestatic liver disease, cystic fibrosis, and Crohn disease. More recently, obese children have also been identified as being at risk of vitamin D deficiency.[24,27]"
},
{
"source": "Kliegman R. Nelson Textbook of Pediatrics 2-Volume Set 22ed 2024, p. 521",
"text": "## Etiology Vitamin D deficiency most frequently occurs in infancy because of a combination of poor intake and inadequate cutaneous synthesis. Transplacental transport of vitamin D, mostly 25- D, typically provides enough vitamin D for the first or second months of life unless there is severe maternal vitamin D deficiency. Infants who receive formula receive adequate vitamin D, even without cutaneous synthesis. Because of the low vitamin D content of breast milk, breastfed infants rely on cutaneous synthesis or vitamin supplements. Cutaneous synthesis can be limited because of the ineffectiveness of the winter sun in stimulating vitamin D synthesis; avoidance of sunlight because of concerns about cancer, neighborhood safety, or cultural practices; and decreased cutaneous synthesis because of increased skin pigmentation."
},
{
"source": "Pediatric Decision-Making Strategies, p. 351",
"text": "|**Hypoalbuminemic**
**conditions2**
PTH = Parathyroid|||**Endotoxic shock3**
hormone|||**Aplasia/hypoplasia4**
**(DiGeorge syndrome)**
**Familial**
**Surgical5**
**Infiltrative lesions**
**(hemosiderosis, Wilson's**
**disease)**
**Autoimmune6**
**Idiopathic**
**Maternal hyperparathyroidism**
**(during pregnancy)7**|||||**Vitamin D deficiency8**
**Deficient sunlight**
**Nutritional/dietary deficiency**
**Malabsorption**
**Liver disease (biliary cirrhosis)**
**Renal disease**
**Anticonvulsants**
**Vitamin D dependent**
**rickets (Type I)9**
**Pseudohypoparathyroidism10**
**Hyperphosphatemia11**
**Tumor-lysis syndrome**
**Rhabdornyolysis**
**Laxatives/enemas**
**Acute pancreatitis12**
**Hungry bone syndrome13**
**Drugs (colchicine, estrogen,**
**calcitonin)**
**Large amounts of citrated blood**
**Vitamin D dependent rickets**
**(Type II)14**|||||**Alkalosis15**
**Rapid correction**
**of"
},
{
"source": "Pediatric Board Study Guide, p. 732",
"text": "- **Vitamin D Deficiency** : - Rickets, inadequate skeletal mineralization, characterized by widening of the end of long bones, rachitic rosary (rib beading), bowing of the legs, craniotabes, and\u2014in adults\u2014osteomalacia - UV light is important in the synthesis of vitamin D in the skin. Sunlight, however, is a risk of skin cancer. Decreased skin synthesis of vitamin D is associated with the use of sunscreens, increased levels of skin melanin and the distance one is from the Equator, time of day and the season of the year. - Naturally present in few foods: - Available in fortified dairy, eggs, some beverages, liver from any mammal, fatty fish and supplements - All breastfed infants should be supplemented with vitamin D, 400 IU, starting at birth and continuing until they consume 1 quart of formula daily. - Vitamin D insufficiency/deficiency is often seen in children and should be corrected: - Myopathies - Dysarthria - Impaired immune response"
},
{
"source": "Netters Pediatrics (Florin \u0422., Ludwig St.), p. 453",
"text": "Nutritional rickets secondary to vitamin D deficiency is common throughout the world and reflects inadequate exposure to sunlight and poor intake of dietary vitamin D. Vitamin D deficiency is easily prevented, and the prevalence of this condition can be reduced by adequate nutritional intake of vitamin D or vitamin D\u2013fortified foods (Figure 69-4). This form of rickets has a peak incidence between 3 and 18 months of age. Additional risk factors for vitamin D deficiency include dark skin, protracted exclusive breastfeeding, use of sunscreens or conservative clothing, fat malabsorption, use of anticonvulsants that induce hepatic P450 enzymes, marked prematurity, and lack of biliary secretions that may impair absorption of vitamin D and calcium. Mild to moderate vitamin D deficiency may be present for months before rickets is obvious on physical examination, and severe vitamin D deficiency may manifest as hypocalcemic seizures, growth failure, lethargy, irritability, and a predisposition to respiratory"
},
{
"source": "Pediatric Nutrition (Ronald E. Kleinman, Frank R. Greer), p. 1187",
"text": "Vitamin D is known to play important role in calcium and phosphate regulation and bone mineralization but is also thought to have an expanding role in immune regulation and, perhaps, in IBD course and response to treatment. Serum concentrations of 25-OH-D >20 ng/mL are considered sufficient for healthy children in the United States, although this cutoff was set mostly to help prevent rickets in early childhood. and the true level of sufficiency in IBD is not known. Vitamin D deficiency (25-OH-D \u226415 ng/mL) is common in children and young adults with IBD, with a prevalence as high as 35%.[28] Reduced dietary intake, decreased sun exposure, and reduced absorption attributable to intestinal inflammation may contribute to higher rates of vitamin D deficiency in children with IBD. Consistent risk factors for vitamin D deficiency include winter season, darker skin, and upper gastrointestinal tract involvement. Disease activity has not been consistently shown to correlate with vitamin D status in pediatric"
},
{
"source": "Netters Pediatrics (Florin \u0422., Ludwig St.), p. 123",
"text": "with vitamin D. After vitamin D is produced in the skin or consumed in food, it is converted in the liver and kidney to 1,25 dihydroxyvitamin D (1,25(OH)2D), the physiologically active form of vitamin D known as calcitriol. Vitamin D deficiency may result from a lack of exposure to UVB radiation; inadequate intake; fat malabsorption; liver or kidney disease, which can impair its conversion to active metabolites; and rarely, genetic disorders. Deficiency is most commonly seen in breastfed infants with inadequate vitamin D supplementation. Dark-skinned children are at increased risk of vitamin D deficiency because increased amounts of melanin in the skin reduce the body\u2019s ability to produce endogenous vitamin D in response to sunlight exposure. American Academy of Pediatrics (AAP) guidelines published in 2008 recommend supplementation of 400 IU/day vitamin D for all infants. The AAP also recommends that older children and adolescents who do not obtain 400 IU/d through diet should take a 400-IU vitamin D"
},
{
"source": "Netters Pediatrics (Florin \u0422., Ludwig St.), p. 124",
"text": " **----- Start of picture text -----**
Treatment includes taking supplements
of calcium, phosphorus, and vitamin D
and eating foods rich in these substances.
Insufficient vitamin D in the diet can
cause rickets. Children with darkly
pigmented skin and nonsupplemented
breast-fed babies are at a greater risk
for vitamin D\u2013deficient rickets.
Children with vitamin D deficiency may
have failure to thrive, bone fragility,
and bone pain in addition to the classic
physical findings of rickets.
with E. Hatton
**----- End of picture text -----**
   **Figure 16-4** _Vitamin D deficiency._ ## **FUTURE DIRECTIONS** Research is continuing on the various roles of vitamin D, recommendations for vitamin D and calcium requirements, and prevention of deficiencies."
},
{
"source": "Kliegman R. Nelson Textbook of Pediatrics 2-Volume Set 22ed 2024, p. 522",
"text": "Chapter 69 u Vitamin D Deficiency (Rickets) and Excess 475 have the same risk factors, decreased maternal vitamin D can also contribute, both by leading to reduced vitamin D content in breast milk and by lessening transplacental delivery of vitamin D. Rickets caused by vitamin D deficiency can also be secondary to dietary practices, such as vegan diets that use unfortified soy milk or rice milk. Children with restrictive food habits (autism) or food elimination diets (fear of allergies) may be at risk for vitamin D deficiency. ## Clinical Manifestations The clinical features are typical of rickets (see Table 69.3), with a significant minority presenting with symptoms of hypocalcemia. Prolonged laryngospasm is occasionally fatal. These children have an increased risk of pneumonia and muscle weakness leading to a delay in motor development. ## Laboratory Findings"
},
{
"source": "Kliegman R. Nelson Textbook of Pediatrics 2-Volume Set 22ed 2024, p. 522",
"text": "## Prognosis Most children with nutritional vitamin D deficiency have an excellent response to treatment, with radiologic healing occurring within a few months. Laboratory test results should also normalize rapidly. Many of the bone malformations improve dramatically, but children with severe disease can have permanent deformities and short stature. Rarely, patients benefit from orthopedic intervention for leg deformities, although this is generally not done until the metabolic bone disease has healed, there is clear evidence that the deformity will not self- resolve, and the deformity is causing functional problems. ## Prevention Most cases of nutritional rickets can be prevented by universal administration of 400 IU of vitamin D to infants <1 year old. Older children with risk factors for inadequate intake should receive 600 IU/day. Vitamin D may be administered as a component of a multivitamin or as a vitamin D supplement. ## **Congenital Vitamin D Deficiency**"
},
{
"source": "Pediatric Board Study Guide, p. 426",
"text": "- Vegan diets, especially lacto-vegans - Genetic defects ## **Diagnosis (Table 12.10)** - Low to normal calcium ## **Clinical presentation (Fig. 12.10)** - At very young ages, vitamin D deficiency is more likely to present as hypocalcemia than as rickets - Muscular hypotonia - Craniotabes (areas of thinning and softening of the bones of the skull) - Low phosphorus - High alkaline phosphatase - High PTH - Low 25(OH)D - Low to high 1,25-dihydroxyvitamin D - Normal HCO3 [Figure OCR, page 426, figure 1] Sun Skin wu 7-dehydrocholesterol Oral intake Cholecalciferol (Vitamin D3) Vitamin D3 (meat, fish) Vitamin D2 (supplements) 25 hydroxyvitamin D (Calcidiol) <4 PTH Kidney A. Morsi 420 **Fig. 12.10** Skeletal manifestations of rickets  **Table 12.10** Types of rickets, differential diagnosis, and common laboratory findings "
},
{
"source": "Kliegman R. Nelson Textbook of Pediatrics 2-Volume Set 22ed 2024, p. 18",
"text": "_69. Vitamin D Deficiency (Rickets) and Excess_ _70. Vitamin E Deficiency_ _71. Vitamin K Deficiency_ _72. Micronutrient Mineral Deficiencies_ _73. Electrolyte and Acid- Base Disorders_ _74. Maintenance and Replacement Therapy 75. Deficit Therapy_ _**V. Jordan Greenbaum, MD**_ Medical Director International Centre for Missing and Exploited Children Alexandria, Virginia _16. Child Trafficking for Sex and Labor_ _**Mary V. Greiner, MD, MS**_ Associate Professor of Pediatrics University of Cincinnati College of Medicine Medical Director, CHECK Foster Care Center Cincinnati Children\u2019s Hospital Medical Center Cincinnati, Ohio ## _**Anne G. Griffiths, MD**_ Pediatric Pulmonologist Director, Primary Ciliary Dyskinesia Center Children\u2019s Minnesota Children\u2019s Respiratory & Critical Care Specialists Minneapolis, Minnesota _422. Chronic or Recurrent Respiratory Symptoms_"
},
{
"source": "Kliegman R. Nelson Textbook of Pediatrics 2-Volume Set 22ed 2024, p. 443",
"text": "## **Vitamin D** Vitamin D insufficiency is more common than previously thought in infants and children. Vitamin D is central to calcium and bone metabolism but is also an important determinant of various nonosseous health outcomes (see Chapter 69). Children of all ages with darker skin and those who do not consume fortified dairy products should be considered for screening for vitamin D deficiency. The DRI for vitamin D is based on its effects on calcium status and bone health. The goal is to achieve serum 25- hydroxyvitamin D levels >50 nmol/L (30 ng/dL). Breast milk is a poor source of vitamin D. The American Academy of Pediatrics (AAP) recommends total vitamin D intake of 400 IU/day for infants (0 to <12 months). A supplement is recommended for all breastfed infants to ensure sufficient intake. The RDA of vitamin D is currently 600 units daily for healthy children 1- 18 years of age. ## **Calcium**"
}
]
}