Vitamin D deficiency: Difference between revisions

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==Background==
==Background==
*AKA: Hypovitaminosis D
*AKA: Hypovitaminosis D
*Vitamin D
*Vitamin D deficiency leads to impaired bone mineralization and diseases such as:
**Lipid soluble
**Acts as a hormone which:
***Stimulates intestinal calcium absorption
***Maintains adequate phosphate levels for bone development
***Regulates cell growth proliferation and apoptosis
***Modulates immune function and inflammation reduction
*Deficiency leads to impaired bone mineralization and disease such as:  
**[[Rickets]] in children
**[[Rickets]] in children
**[[Osteomalacia]] and [[Osteoporosis]] in adults
**[[Osteomalacia]] and [[Osteoporosis]] in adults
 
===Metabolism and Physiology of Vitamin D===
==Metabolism and Physiology of Vitamin D==
*Gained from diet, supplements, or sunlight exposure
*Vitamin D gained from diet, supplements, or sunlight exposure
**Fortified foods (mainstay), supplements, fatty fish, egg yolks, fish liver oil, and some mushrooms  
*Vitamin D undergoes hydroxylation in the liver producing 25-hydroxyvitamin D
*A second hydroxylation occurs in the kidney producing 1,25-dihydroxyvitamin D which is the active form of vitamin D
**This step can occur extrarenally
**Regulated by PTH, serum calcium, and phosphorus levels
 
==Etiology of Vitamin D Deficiency==
*Inadequate intake
**Dietary sources such as fortified foods and supplements are the mainstay of vitamin D intake
**Foods rich in vitamin D include fatty fish, egg yolks, fish liver oil, and some mushrooms  
*Inadequate sunlight exposure
**Synthesis of vitamin D occurs in the skin through exposure to ultraviolet B radiation from sunlight
**Synthesis of vitamin D occurs in the skin through exposure to ultraviolet B radiation from sunlight
**Factors associated with vitamin D deficiency include darker skin pigmentation, prolonged winter season, and skin coverage
*Hydroxylated in liver--> 25-hydroxyvitamin D, which is further hydroxylated in kidney or extrarenally--> 1,25-dihydroxyvitamin D (active form)
*Disorders limiting vitamin D absorption
**Second hydroxylation regulated by PTH, serum calcium, and phosphorus levels
**[[Crohn's disease]]
*Vitamin D acts to:
**[[Cystic fibrosis]]
**Stimulate intestinal calcium absorption
*Conditions preventing vitamin D conversion into active metabolites
**Maintain adequate phosphate levels for bone development
**[[Renal Failure]]
**Regulate cell growth proliferation and apoptosis
**[[Liver failure]]
**Modulate immune function and inflammation reduction
===Etiology of Vitamin D Deficiency===
*Inadequate dietary intake, inadequate sunlight exposure
*Impaired vitamin D absorption
**[[Crohn's disease]], [[cystic fibrosis]]
*Impairment in conversion of vitamin D into active metabolites
**[[Renal Failure]], [[Liver failure]]


==Clinical Features==
==Clinical Features==
*Bone pain and muscle weakness
*Bone pain
*Muscle [[weakness]]
*Brittle bones
*Brittle bones
**[[Rickets]] in children
**[[Rickets]] in children
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***Craniotabe: abnormal softening or thinning of the skull  
***Craniotabe: abnormal softening or thinning of the skull  
**[[Osteomalacia]] and [[Osteoporosis]] in adults leading to increased risk of fractures
**[[Osteomalacia]] and [[Osteoporosis]] in adults leading to increased risk of fractures
*Associated with advancement of cancers
*Associated with advancement of cancers, particularly of breast, colon, ovarian, and prostate
**Breast, colon, ovarian, and prostate


==Differential Diagnosis==
==Differential Diagnosis==
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==Evaluation==
==Evaluation==
*Diagnosed by measuring the concentration of 25-hydroxyvitamin D
*Assess for fractures, if indicated
**This is the pre hormone, calcidiol, which is a precursor to the active form 1,25-dihydroxyvitamin D
*BMP, Mg/Phos, serum calcium
*Insufficient vitamin D defined as a 25-hydroxyvitamin level 25-75 nmol/L (normal range 75-250 nmol/L)
*Vitamin D assessed by measuring serum concentration of 25-hydroxyvitamin D (precursor to hormonally active 1,25-dihydroxyvitamin D)
*Vitamin D deficiency defined as a 25-hydroxyvitamin level <20-25 nmol/L
**Normal range: 75-250 nmol/L
*Screening adults not at risk and without symptoms not recommended
**Insufficiency: 25-75 nmol/L
**Deficiency: <25 nmol/L
**Screening adults not at risk and without symptoms not recommended


==Management==
==Management==
*Treat complications (e.g. fractures, pain)
*Supplemental vitamin D
*Supplemental vitamin D
**Initial high-dosage treatment phase
**Initial high-dosage treatment phase: 1,000 IU cholecalciferol per 10 nmol/L required serum increase given daily for 2-3 months
***1,000 IU cholecalciferol per 10 nmol/L required serum increase given daily for 2-3 months
**Maintenance: 400 IU daily
**Followed by maintenance dosage
***Double dosage for premature infants, infants/children with dark pigmentation, children with limited sun exposure, and obese patients
***400 IU daily for all age groups
**Some populations may require higher dosing (i.e. parathyroid disease, chronic liver disease, renal failure, and malabsorption disorders)
***Double dosage for premature infants, dark pigmented infants/children, children with limited sun exposure, and obese patients
**Special populations may require higher dosing (i.e. parathyroid disease, chronic liver disease, renal failure, and malabsorption disorders


==See Also==
==See Also==
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*2. <Holick MF, Binkley NC, Bischoff-Ferrari HA, Gordon CM, Hanley DA, Heaney RP, Murad H, and Weaver CM. Evaluation, treatment, and prevention of vitamin D deficiency: an Endocrine Society Clinical Practice Guideline. "J Clin Endocrinol Metab". Jul 2011; 96(7): 1911–1930.>
*2. <Holick MF, Binkley NC, Bischoff-Ferrari HA, Gordon CM, Hanley DA, Heaney RP, Murad H, and Weaver CM. Evaluation, treatment, and prevention of vitamin D deficiency: an Endocrine Society Clinical Practice Guideline. "J Clin Endocrinol Metab". Jul 2011; 96(7): 1911–1930.>


[[Category:Misc/General]]
[[Category:Misc/General]] [[Category:FEN]]

Revision as of 22:26, 15 January 2017

Background

  • AKA: Hypovitaminosis D
  • Vitamin D deficiency leads to impaired bone mineralization and diseases such as:

Metabolism and Physiology of Vitamin D

  • Gained from diet, supplements, or sunlight exposure
    • Fortified foods (mainstay), supplements, fatty fish, egg yolks, fish liver oil, and some mushrooms
    • Synthesis of vitamin D occurs in the skin through exposure to ultraviolet B radiation from sunlight
  • Hydroxylated in liver--> 25-hydroxyvitamin D, which is further hydroxylated in kidney or extrarenally--> 1,25-dihydroxyvitamin D (active form)
    • Second hydroxylation regulated by PTH, serum calcium, and phosphorus levels
  • Vitamin D acts to:
    • Stimulate intestinal calcium absorption
    • Maintain adequate phosphate levels for bone development
    • Regulate cell growth proliferation and apoptosis
    • Modulate immune function and inflammation reduction

Etiology of Vitamin D Deficiency

Clinical Features

  • Bone pain
  • Muscle weakness
  • Brittle bones
    • Rickets in children
      • Soft bones, skeletal deformities
      • Craniotabe: abnormal softening or thinning of the skull
    • Osteomalacia and Osteoporosis in adults leading to increased risk of fractures
  • Associated with advancement of cancers, particularly of breast, colon, ovarian, and prostate

Differential Diagnosis

Evaluation

  • Assess for fractures, if indicated
  • BMP, Mg/Phos, serum calcium
  • Vitamin D assessed by measuring serum concentration of 25-hydroxyvitamin D (precursor to hormonally active 1,25-dihydroxyvitamin D)
    • Normal range: 75-250 nmol/L
    • Insufficiency: 25-75 nmol/L
    • Deficiency: <25 nmol/L
    • Screening adults not at risk and without symptoms not recommended

Management

  • Treat complications (e.g. fractures, pain)
  • Supplemental vitamin D
    • Initial high-dosage treatment phase: 1,000 IU cholecalciferol per 10 nmol/L required serum increase given daily for 2-3 months
    • Maintenance: 400 IU daily
      • Double dosage for premature infants, infants/children with dark pigmentation, children with limited sun exposure, and obese patients
    • Some populations may require higher dosing (i.e. parathyroid disease, chronic liver disease, renal failure, and malabsorption disorders)

See Also

External Links

References

  • 1. <Health Quality Ontario. Clinical utility of vitamin d testing: an evidence-based analysis. Ont Health Technol Assess Ser. 2010;10(2): 1–93.>
  • 2. <Holick MF, Binkley NC, Bischoff-Ferrari HA, Gordon CM, Hanley DA, Heaney RP, Murad H, and Weaver CM. Evaluation, treatment, and prevention of vitamin D deficiency: an Endocrine Society Clinical Practice Guideline. "J Clin Endocrinol Metab". Jul 2011; 96(7): 1911–1930.>
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