How is vitamin D metabolized?
Vitamin D is a fat-soluble ring-opening sterol, including animal-derived vitamin D3 and plant-derived vitamin D2. Vitamins D2 and D3 are inactive forms, and the two cannot be transformed into each other, collectively referred to as vitamin D. Vitamin D requires two hydroxylations to convert to 1,25(OH)2D and become a biologically active D hormone. The first step of hydroxylation is done primarily in the liver, and the second step of hydroxylation is done primarily in the kidneys.

What is the source of vitamin D in the human body? The human vitamin D is mainly derived from 7-dehydrocholesterol in the epidermis. After the epidermis is irradiated with ultraviolet rays in the sunlight, it is converted into a vitamin D3 precursor, which is converted into vitamin D3 by a warming action. Another source of vitamin D is food, including plant foods and animal foods. There are very few foods containing vitamin D2 or D3. Plant foods (such as mushrooms after sun exposure) contain richer vitamin D2, while animal foods (such as wild multi-fat marine fish) are rich in vitamin D3.

What are the physiological effects of vitamin D?
The main physiological role of vitamin D and its metabolites is to promote the absorption of calcium and phosphorus in the intestine, inhibit the release of parathyroid hormone (PTH), maintain normal blood calcium and phosphorus levels, and thus ensure bone health and normal neuromuscular function. The extra-skeletal effects of vitamin D include effects on muscle, cardiovascular, metabolic, immune, oncogenesis, pregnancy, and fetal development.

What are the risk factors for vitamin D deficiency?
There are many factors that affect vitamin D levels, including age, skin color, season, geographic latitude, altitude, sunshine time, dressing habits, sun protection measures, eating habits, air pollution, obesity, and drugs that affect vitamin D metabolism. It is not recommended to screen blood 25OHD levels in the population, but it is recommended to screen blood 25OHD levels in people with a risk of vitamin D deficiency and a need to maintain a reasonable vitamin D nutritional status.

What are the precautions for the clinical application of vitamin D?
Vitamin D is associated with a variety of diseases, as follows:

Application of vitamin D in rickets/osteosis
Vitamin D deficiency, abnormal vitamin D metabolism and abnormal action are important causes of rickets and osteomalacia. Prevention of rickets/osteomalacia caused by nutritional deficiencies need to ensure adequate vitamin D and calcium nutrition. Pseudovitamin D deficiency rickets Type I is currently treated with Alfacalcidol 0.5~1.5μg/d or calcitriol 0.5~1.0μg/d, and supplemented with appropriate amount of calcium. The treatment of fibroblast growth factor 23 associated with hypophosphatemic rickets/osteomatosis requires supplementation with phosphorus and the use of active vitamin D.

Application of vitamin D in osteoporosis
It is recommended that patients with osteoporosis receive adequate sun exposure to promote the synthesis of endogenous vitamin D in the skin. Insufficient sunshine can be supplemented with 600~1000 IU of ordinary vitamin D every day. It is recommended to regularly monitor the serum 25OHD and parathyroid hormone levels to guide the adjustment of the supplemental dose of common vitamin D. It is recommended to adjust the serum 25OHD concentration to at least 20μg/L (50nmol/L), preferably 30μg/L (75nmol/L). L).

Active vitamin D and its analogues are hydroxylated vitamin D analogs and are therapeutic agents for osteoporosis. They are recommended for those over 65 years of age or with serum creatinine clearance of less than 60 ml/min. Active vitamin D and its analogs for clinical applications include calcitriol and alfacalcidol.

Safety of vitamin D
Ordinary vitamin D has a wide range of safe doses, and there is very little long-term use of vitamin D that exceeds the maximum tolerated dose in the population. There are few reports of poisoning due to excessive intake of common vitamin D. It is usually possible to determine the presence of vitamin D poisoning by measuring the serum 25OHD concentration. Although the difference between different studies is very large, the blood 25OHD level of vitamin D poisoning is often above 224μg/L (560nmol/L), and the corresponding vitamin D supplement dose is more than 30,000IU per day, and the application time is longer. For healthy people, the 25OHD level should not exceed 150μg/L (375nmol/L), otherwise the risk of poisoning increases.

Active vitamin D and its analogues (calcitriol, alfacalcidol and paricalcitol) cause a higher risk of high urinary calcium than normal vitamin D, once high urinary calcium or hypercalcemia is found during administration, the drug should be immediately reduced or stopped. For patients who need long-term use of active vitamin D treatment, it is recommended to monitor urinary calcium, phosphorus and serum calcium and phosphorus levels at 1, 3 and 6 months after initiation of treatment. It is recommended to monitor blood calcium phosphate, urinary calcium phosphate and kidney twice a year thereafter.

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