Vitamin D

Vitamin D is a derivative of steroids and can be divided into vitamin D2 and vitamin D3. Vitamin D2 is mostly contained in plant foods. It is synthesized from the ergosterol of plants by sunlight. Vitamin D3 can be synthesized from human skin and adipose tissue by 7-dehydrocholesterol. Vitamin D is a fat-soluble vitamin. Vitamin D from food is absorbed through the small intestine together with fat. It forms chylomicrons with the help of bile. It enters the bloodstream from the lymphatic vessels and is transported into the liver along with its own synthesized vitamin D3. In the liver, through the action of the monooxygenase system (25-hydroxylase) in hepatocyte microsomes, 25(OH)D3.25(OH)D3 is formed in the mitochondrial α-hydroxylase system of renal proximal tubular epithelial cells. It is converted to 1,25(OH)2D3, which is the largest biological action form of vitamin D. It can promote the synthesis of intestinal calcium-binding protein and promote the calcium in the intestinal tract by increasing the serum calcium and phosphorus levels in the following three aspects. The absorption and operation of phosphorus increases the retention in the body. 2 Improve the reabsorption of calcium and phosphorus ions by the renal tubules, and reduce the discharge of urinary calcium and phosphorus. 3 When the calcium deficiency in the hypocalcemia diet, the absorption of calcium and phosphorus is promoted by the action of parathyroid hormone (PTH), and the release of calcium and phosphorus in the bone is mobilized. Therefore, in the initial stage of vitamin D deficiency, blood calcium is normal and blood phosphorus is slightly lower. When the vitamin D is further lowered, even if the secretion of PTH is increased, the amount of calcium absorbed back is small due to the decrease in the calcium content in the original urine, and the blood calcium is also lowered at this time. Basic Information Specialist classification: growth and development examination classification: blood examination Applicable gender: whether men and women apply fasting: fasting Analysis results: Below normal: Reduction of 25-(OH)2D is seen in VD deficiency (rickets, rickets), severe liver disease, nephrotic syndrome, and reduction in sun exposure. Normal value: 1,25-hydroxyvitamin D3: 26-65 ng / L Above normal: An increase in 25-(OH)2D is seen in VD poisoning. 1,25-(OH)2D elevation is seen in VD-dependent type II, late pregnancy, VD deficiency, and neoplastic hypercalcemia. negative: Positive: Tips: Dispose of preparations containing vitamin D3 before blood draw. Normal value The reference value of serum 25-hydroxyvitamin D3 is 26-65 ng/L. Clinical significance Abnormal result Vitamin D deficiency (vitaminDdeficiency) is also known as vitamin D deficiency rickets. Common in infants and young children, more common in the lack of vitamin D in the diet, or the lack of sunlight in the human body. Calcium and phosphorus metabolism disorders caused by insufficient vitamin D in the body, calcium salts can not be normally deposited in the growth part of the bone, so that a chronic nutritional disease characterized by growth of bone formation lesions, called rickets, if When the disease occurs in an adult, there is a calcification of the mature bone, called osteomalacia. The cause of vitamin D deficiency rickets is pediatric growth, vitamin D deficiency or insufficient direct sunlight or disease factors (such as gastrointestinal dysfunction, chronic liver and kidney disease). The incidence rate of the disease in the north is higher than that in the south, and there are more winter and spring seasons than in summer and autumn. The early symptoms of rickets are sweating, night terrors, irritability, and irritability. Signs with bone changes are most obvious, such as softening of the skull, square skull, ribbed beads, rib valgus, wrist and ankle bulging as "bangle" and "ankle bracelet"; in severe cases, the lower limbs are "X" or "O" Legs, the spine is curved. The disease can be prevented by oral vitamin D, and the content of vitamin D in cod liver oil, egg yolk and liver is relatively abundant. Need to check the population of abnormal bone development. Low results may be diseases: pediatric vitamin D deficiency hand and foot rickets, pediatric vitamin D deficiency rickets, pediatric familial hypophosphatemic rickets, neonatal rickets, postmenopausal osteoporosis, pediatric Crohn's disease, infant hand and foot sputum Symptoms, rickets, toxic diffuse goiter, high results of achondroplasia may be diseases: multiple renal tubular dysfunction syndrome in children Contraindications before examination: Dispose of preparations containing vitamin D3 before blood draw. Requirements for examination: When you take blood, you should relax your mind and check with your doctor. Inspection process Routine blood draw, check, test. Evaluation of laboratory diagnostic methods: (1) Determination of serum 25-hydroxyvitamin D3: 25-hydroxyvitamin D3 is the main metabolite of vitamin D3, and its value is determined by early diagnosis. Since the change of 25-hydroxyvitamin D3 precedes the change of bone, and with the season Fluctuations, which reflect a person's exposure to sunlight, have more important clinical implications for early diagnosis of rickets and osteoporosis syndrome. This test can also be used for follow-up after treatment for vitamin D deficiency, but it is more expensive and is not currently widely available. (2) Blood biochemical examination: its change is earlier than the bone change indicated by the X-ray image. The rise of blood alkaline phosphatase is earlier than the change of blood calcium and blood phosphorus. The recovery of blood alkaline phosphatase content during the recovery period of the disease precedes the recovery of blood calcium and blood phosphorus. Not suitable for the crowd A healthy group without vitamin D deficiency or excess. Adverse reactions and risks Discomfort: There may be pain, swelling, tenderness, and visible subcutaneous ecchymosis at the puncture site.

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