The measurement of 25-hydroxy vitamin D is used in the diagnosis of vitamin D deficiency, in the differential diagnosis of the causes of rickets and osteomalacia, in the monitoring of vitamin D therapy and in the diagnosis of hypervitamin D.
Vitamin D is a fat-soluble vitamin. The two main forms of vitamin D are vitamin D2 (or ergocalciferol) and vitamin D3 (or cholecalciferol).
Vitamin D2 is derived from dietary sources of vegetable origin.
Vitamin D3 is produced in the skin when exposed to sunlight and more specifically to UVB (UVB). In this way, 7-dehydrocholesterol reacts with UVB light at wavelengths between 270 and 300 nm to produce vitamin D3. These wavelengths exist on a daily basis in the tropics, during spring and summer in temperate regions and almost never in the Arctic Circle. Adequate amounts of Vitamin D3 can be produced on the skin after 10 to 15 minutes of sun, face, arm and back exposure without sunscreen at least 2 times a week. Part of the body's vitamin D3 comes from preservative sources of animal origin. As only fish are naturally rich in vitamin D, most of the vitamin D obtained in industrialized societies comes from enriched products such as milk, soy milk, and cereals for breakfast or dietary supplements.
After the production of vitamin D in the skin or its intake from food, it is converted in the liver into 25-hydroxy vitamin D and the kidneys into 1,25-dihydroxy vitamin D (1,25 [OH] 2 D), the active form of vitamin D. After this conversion, the active form of vitamin D is released into the bloodstream.
Vitamin D regulates calcium and phosphorus levels in the blood by promoting their absorption from food into the gut and promoting kidney calcium uptake. This allows the normal intake of calcium in the bones necessary for their growth and regeneration. Vitamin D inhibits the secretion of parathyroid hormone from parathyroid glands. Vitamin D promotes the functions of the immune system by increasing phagocytosis, anti-cancer activity and has other immunomodulatory functions.
Vitamin D deficiency can result from inadequate dietary intake, inadequate sunlight exposure, malabsorption syndromes, liver or kidney disorders or a number of hereditary metabolic disorders. Its deficiency causes reduced calcium deposition in the bones and leads to bone diseases (rickets in children and osteomalacia in adults). Vitamin D deficiency can also contribute to the development of osteoporosis. Recently, it has been observed that vitamin D deficiency is associated with cancers of the colon, breast and pancreas. Several studies have also shown the beneficial association between vitamin D intake and the prevention of various forms of cancer. Vitamin D deficiency is associated with increased blood pressure and risk for cardiovascular disease.
Vitamin D levels can be measured in the blood. The levels of 25-hydroxy vitamin D2 and D3 are usually measured and the total of 25-hydroxy vitamin D. is calculated. The treatment is based on measuring all levels of 25-hydroxy vitamin D. 1,25-dihydroxy vitamin D (the active vitamin D metabolite can be measured and is useful in patients who have symptoms of vitamin D deficiency even if they have normal levels of total vitamin D.
The body's requirements for vitamin D increase with age. However, the skin's ability to convert 7-dehydrocholesterol to vitamin D3 is diminished and, at the same time, the kidneys' ability to convert D2 to its active form also diminishes with age, thus creating the need for increased vitamin D supplementation in the elderly. Other groups particularly at risk for vitamin D deficiency include:
- Infants who breastfeed because human milk alone does not have adequate amounts of vitamin D
- People with limited sun exposure
- Women wearing long robes and headgear
- People with occupations that prevent sun exposure
- People with body mass index (BMI) ≥ 30 because vitamin D2 is trapped in the subcutaneous fat
- People with reduced ability to absorb dietary fat because vitamin D (as a fat-soluble vitamin) requires some amount of dietary fat in the gut to be absorbed
- Patients with liver or kidney disease because they cannot convert vitamin D into its active metabolic form
Corticosteroids can lower vitamin D levels by reducing calcium absorption. Orlistat for weight loss and cholestyramine for lowering cholesterol may lower vitamin D levels due to a decrease in its absorption (as with other fat-soluble vitamins). Barbiturates and phenytoin reduce vitamin D levels, increasing the hepatic metabolism of vitamin D in inactive metabolites.
While 1,25-dihydroxy vitamin D is the most potent metabolite of vitamin D, levels of 25-OH hydroxy vitamin D more accurately reflect the body's vitamin D reserves.
In contrast to the high incidence of 25-OH-vitamin D deficiency in the general population, hypervitamin D is rare and only observed after prolonged exposure to extremely high doses of vitamin D. When present, it can lead to severe hypercalcaemia.
Possible Interpretations of Pathological Values
- Increase: William's Syndrome, dietary supplements
- Decrease: Rachitis, osteomalacia, osteoporosis, gastrointestinal disorders with malabsorption, renal insufficiency, liver disease, familial hypophosphatidemia rheumatoid arthritis, hypophosphatidemia
Laboratory test results are the most important parameter for the diagnosis and monitoring of all pathological conditions. 70%-80% of diagnostic decisions are based on laboratory tests. Correct interpretation of laboratory results allows a doctor to distinguish "healthy" from "diseased".
Laboratory test results should not be interpreted from the numerical result of a single analysis. Test results should be interpreted in relation to each individual case and family history, clinical findings and the results of other laboratory tests and information. Your personal physician should explain the importance of your test results.
At Diagnostiki Athinon we answer any questions you may have about the test you perform in our laboratory and we contact your doctor to get the best possible medical care.