Description
Test Description
What is it: Vitamin D is a fat soluble vitamin that is often believed to be a pro-hormone due to the many functions it has.
It is produced in the skin when skin is exposed to sunlight.
25- Hydroxycalciferol is the principle circulating reservoir of this hormone in plasma and is generally the best indicator of overall vitamin D status.
The majority of 25-OH vitamin D (25-D) in the circulation is derived from the conversion of 7-dehydrocholesterol in the skin that is irradiated with ultraviolet radiation in the UVB range.
The extent of vitamin D formation depends primarily on the duration and intensity of the UV irradiation.
Levels produced typically reach a plateau within 30 minutes of exposure. Unfortunately, use of a sunscreen with SPF as low as 15 reduces the rate of vitamin D production by 99.9%.
There are mechanisms in the skin also protect from overproduction of vitamin D.
Vitamin D is not very water-soluble, and is carried in the blood with a vitamin D-binding protein. In the circulation, vitamin D is metabolized to 25-hydroxy vitamin D(25-D) by the liver. 25-D is further metabolized by the kidney to produce the biologically-active form of vitamin D, 1,25-dihydroxy vitamin D (1,25-D).
Function: The hormonally-active form of vitamin D,1,25-D plays an integral role in calcium homeostasis and in the maintenance of healthy bone.
1,25-D stimulates the absorption of calcium at the level of the intestine and may also serve to increase calcium and phosphate reabsorption at the kidney level.
Renal production of 1,25-D is tightly controlled by parathyroid hormone and is important in the regulation of serum calcium homeostasis.
25-D levels have been shown to have an inverse relationship to serum parathyroid hormone levels.
Secondary hyperparathyroidism can be corrected when 25-D levels are increased to >32 ng/mL. Serum concentrations
Tested for: This test is used to rule out vitamin D deficiency as cause of bone disease, and in the differential diagnosis of hypocalcaemia.
Increased in: N/A
Decreased in: Vitamin D deficiency leads to the mobilization of calcium from bone. Individuals with more severe vitamin D deficiency can develop osteomalacia and/or osteoporosis. Osteomalacia in children, also referred to as rickets, results in well described skeletal malformations since their bones are actively growing. Recent studies suggest that vitamin D deficiency may play a role in several conditions unrelated to bone including prostate cancer, breast cancer, colon cancer, heart disease, hypertension, type 1 diabetes, seasonal affective disorder, fibromyalgia, low back pain, multiple sclerosis, and other autoimmune disorders. Numerous of studies have shown that vitamin D deficiency is very common, and certain populations are at high risk. This situation has occurred partly because the typical American diet is very low in vitamin D. Fatty fish, such as mackerel and salmon and fish liver oils, are natural dietary sources of vitamin D. A low vitamin D diet coupled with low sun exposure and the use of sun screens contributes to the increased frequency inadequate vitamin D levels.
Info: In the United States, vitamin D is added to milk in order to prevent the occurrence of rickets in the pediatric population. Human milk contains very little vitamin D because many mothers are also deficient, so children of mothers who choose to breastfeed are at risk of developing rickets if they are not given supplemental vitamin D. The American Academy of Pediatrics recommends that infants who are exclusively breastfeeding should be given a supplement of vitamin D.
• Individuals with malabsorption syndromes: Patients with pancreatic deficiency, Crohn disease, celiac disease, and surgical resection of stomach are at risk.
• Individuals with severe liver disease: Hepatic disease can reduce the conversion of vitamin D to 25-D and can lead to malabsorption of vitamin D.
• Individuals with kidney disease: Nephrotic syndrome can increase the urinary loss of vitamin D.
• Individuals taking certain drugs: Several medications, including phenytoin, phenobarbital, and rifampin accelerate the breakdown of vitamin D by the liver.
• Individuals who live at higher latitudes: Individuals who live in northern climates, especially in winter months are at increased risk of deficiency.
• Individuals who spend little time outside: Individuals who are homebound or simply choose to remain inside are at increased risk.
• Older adults: The skin becomes less efficient at producing vitamin D with age because of diminished levels of vitamin D precursors in the skin.
• Individuals with decreased sun exposure: Women in some societies are required to cover themselves with heavy clothing, reducing exposure to the sun's rays.
• Races with high melanin levels: Increased skin pigmentation can reduce the efficiency of vitamin D conversion in the skin as much as 50-fold.
Further studies suggest that Vitamin D sufficiency falls in the range of 40 to 100 ng/ml. (1), (50)
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