Initial treatment of clinically significant vitamin D deficiency in adults

Cholecalciferol (vitamin D3) is synthesized in the skin from 7-dehydrocholesterol under the action of UV light and is converted into a biologically active form (1,25-dihydroxycholecalciferol).

Vitamin D3 in its active form promotes the absorption of calcium in the intestines, incorporation of calcium into ossein, and release of calcium from the bone tissue. In the small intestine it promotes rapid and delayed calcium absorption. It also stimulates the passive and active transport of phosphates. In the kidneys it inhibits the excretion of calcium and phosphates by promoting tubular absorption. The production of parathormone (PTH) in the parathyroid glands is directly inhibited by the biologically active form of cholecalciferol. Absorption of PTH is further inhibited by increasing the absorption of calcium in the small intestine under the action of the biologically active vitamin D3.
Due to its production method, physiological regulation and mechanism of action, the so called vitamin D3 is considered the precursor of steroid hormones.

Occurrence in natural conditions and demand:
The demand for vitamin D in adults is 20 μg, which corresponds to 800 IU daily. Healthy adults may cover their demand in the process of endogenous synthesis when exposure to sunlight is sufficient. Intake with food is of only secondary importance, but may play an important role in certain critical conditions (climate, lifestyle).
Fish liver oil and fish are especially rich in vitamin D. Small amounts can also be found in meat, egg yolks, milk, dairy products, and avocado.
Symptoms of vitamin D deficiency may appear for example in premature babies, infants fed only breast milk for longer than six months without any calcium supplementation, or children on a strict vegetarian diet. The causes of rarely occurring vitamin D deficiency in adults may include inappropriate diet, insufficient exposure to UV radiation, malabsorption and poor digestion, cirrhosis, and renal failure.
Common findings in vitamin D deficiency include bone calcification disorders (rickets) and permanent loss of calcium from bones (osteomalacia). Calcium and/or vitamin D deficiency causes a reversible, increased excretion of parathormone. This secondary hyperparathyroidism causes an increased rebuilding of the bone tissue, which may lead to fragile and broken bones