Vitamin D Deficiency
Medicine Central™ is a quick-consult mobile and web resource that includes diagnosis, treatment, medications, and follow-up information on over 700 diseases and disorders, providing fast answers—anytime, anywhere. Explore these free sample topics:
-- The first section of this topic is shown below --
This topic covers the commonly acquired vitamin D deficiency and not type II vitamin D–resistant rickets/type I pseudovitamin D–resistant rickets (both rare autosomal recessive disorders).
- Vitamin D is a hormone and a vitamin.
- Cholecalciferol (D3) is synthesized in the skin by exposure to ultraviolet B (UV-B) radiation. Ergocalciferol (D2) and D3 are present in foods.
- D2 and D3 are hydroxylated in the liver to 25 vitamin D (calcidiol), the major circulating form.
- Calcidiol is further hydroxylated in the kidney to the active metabolite 1,25 vitamin D (calcitriol).
- Hypocalcemia stimulates parathyroid hormone (PTH) to be secreted, which prompts the increased conversion of 25 vitamin D to 1,25 vitamin D.
- 1,25 vitamin D decreases renal calcium and phosphorus excretion, increases intestinal calcium and phosphorus absorption, and increases osteoclast activity. The net result is an increase in serum calcium.
- A community cohort study of asymptomatic adolescents in Boston found 24% were deficient, with 5% severely deficient.
- A study of hospitalized patients in Massachusetts found 57% vitamin D–deficient (VDD).
- Women with history of osteoporosis/osteoporotic fracture have high prevalence of vitamin D deficiency.
- A cohort study in Arizona found >25% of adults were VDD; highest rates among African Americans and Hispanics
- A study of about 56,000 individuals across Europe found 13% to have vitamin D deficiency.
NHANES data suggest 70% of children do not have sufficient 25-OH vitamin D serum levels (9% deficient and 61% insufficient); associated with an increase in BP and decrease in high-density lipoprotein (HDL) cholesterol
Etiology and Pathophysiology
- Insufficient dietary intake of vitamin D and/or lack of UV-B exposure (in sunlight) results in low levels of vitamin D.
- This limits calcium absorption, causing excess PTH release.
- PTH stimulates osteoclast activity, which helps to normalize calcium and phosphorous, but results in osteomalacia.
- Dietary deficiency
- Inadequate vitamin D intake
- Inadequate sunlight exposure
- Institutionalized/hospitalized patients
- Chronic illness: liver/kidney disease
- Malabsorptive states
Vitamin D–dependant rickets type 1 occurs due to inactivating mutation of the 1α hydroxylase gene; as a result, calcidiol is not hydroxylated to calcitriol.
- Inadequate sun exposure
- Dark skin
- Immigrant populations
- Low socioeconomic status
- Latitudes higher than 38 degrees
- Medications (phenobarbital, phenytoin)
- Gastric bypass surgery/malabsorption syndromes
- Adequate exposure to sunlight and dietary sources of vitamin D (plants, fish); many foods are fortified with vitamin D2 and D3.
- Recommended minimum daily requirement is 600 IU/day from age 1 to 70 years and 800 IU/day for those >70 years. Up to 4,000 IU/day is safe in healthy adults without risk of toxicity.
- For ages 51 to 70 years, minimally recommended supplementation is 800 IU/day to prevent nonvertebral fractures.
- The American Academy of Pediatrics recommends all breastfed babies receive 400 IU/day of vitamin D beginning “within the first few days of life.”
- 2016 Global Consensus Recommendations suggest all infants, regardless of feeding method, begin vitamin D 400 IU within a few days of birth (1).
U.S. Preventive Services Task Force recommends at least 800 IU/day vitamin D plus exercise or physical therapy to reduce risk of falls in community-dwelling older adults (3)[A].
Commonly Associated Conditions
- Osteomalacia, osteoporosis
- Premenstrual syndrome
- Celiac disease
- Gastric bypass
- Chronic renal disease
- Bacterial vaginosis in pregnant women