Vitamin D deficiency Vitamin DDefciency .

Mondo Health Updated on 2024-01-30

Vitamin D is an essential nutrient for human life and one of the most important biological regulators of calcium homeostasis, which is a group of sterols with the same physiological activity. For **, what direct effect can it play?Let's learn together today.

and pathogenesis

Vitamin D is mainly found in milk, cream, eggs, vegetable oil, beef, cod liver oil and liver and other foods, vitamin D in food is absorbed by the small intestine, under the action of bile to form chylomicrons, through the lymphatic vessels into the bloodstream, and the self-synthesized vitamin D3 is hydroxylated into 25 (OH) 2D3 in the liver, and the latter is further hydroxylated into 1,25 (OH) 2D3 in the kidney, It is the active metabolite of vitamin D, which then enters the human blood circulation and fat-rich tissues, and is distributed to related organs to play physiological functions. 7-dehydrocholesterol existing in the human body** can be synthesized by photolysis to synthesize vitamin D, so if there is enough ultraviolet radiation, the human body has the ability to synthesize the vitamin D it needs.

The cause of vitamin D deficiency is insufficient;Not enough sunshine;Dysdigestion and absorption (gastrointestinal diseases and surgery, bile deficiency, suffering from steatorrhoea, malabsorption syndromes, etc.);Increased physiological and pathological needs (infants, pregnant women, lactating women, fractures, trauma or orthopedic surgery);Poor liver and kidney function or lesions, vitamin D cannot be converted into active products, affecting its storage and reabsorption;True and pseudoparathyroid hormone levels are too low, affecting vitamin D3 productionFamilial hypophosphatemia and long-term use of phenytoin and phenobarbital cause hepatic destruction of vitamin D and its metabolites, or interference with 25-position hydroxylationLong-term use of glucocorticoids** in patients can cause defects in vitamin D metabolism and obstruct intestinal calcium absorption.

Vitamin D can promote the absorption of calcium and phosphorus by the intestinal mucosa, increase the reabsorption of calcium by the kidney, maintain serum calcium and phosphorus levels, promote the deposition of calcium salts in bone and cartilage, and make bone formation. At the same time, it also plays an important role in many aspects of some tissues, such as the hematopoietic system. It has an effect on cell differentiation and proliferation, such as the efficacy of UVB irradiation ** psoriasis, part of the effect is related to UVB-mediated synthesis of vitamin D Animal experiments have proved that vitamin D has the effect of preventing and inhibiting autoimmune diseases (including SLE), and is involved in the secretion of parathyroid hormone and insulin. When vitamin D is deficient, the absorption of calcium and phosphorus decreases, the serum level decreases, low blood calcium can stimulate the parathyroid glands, the secretion of the parathyroid glands increases, the intraosseous calcium is transferred to the blood, the osteois is more loose, the chondroblasts compensate to produce cartilage, the bone matrix and cartilage lack calcium deposits, the osteoclasts exceed osteogenesis, and the clinical appearance of rickets or osteomalacia. Decreased blood calcium causes symptoms such as increased nerve excitability and muscle and ligament relaxation and weakness.

Clinical presentation

Vitamin D deficiency and rickets in infants and young children. The child is irritable, sweating, night terrors, loss of appetite, easy diarrhea and stool, anemia, frailty, susceptible to respiratory tract infections, hepatosplenomegaly, abdominal distention, and the constant shaking of the head makes the neck and occipital hair thin or completely fall out, which is the only manifestation. Bone path changes include skull malacia, skull bulge, delayed teething and anterior flesh closure, bead-like protrusion at the junction of bone and costochondral cartilage, sternal lordosis or invagination, inward or external curvature of the inferior skin, scoliosis or hunchback, and obtuse and rounded protrusion of the wrist.

*The patient had hypochondriasis and clinical bone pain in the waist and legs, which affected walking. Severe decalcification can lead to osteoporosis, deformity of the lower limbs and pelvis, or spontaneous fractures, and vitamin D deficiency can be diagnosed in the absence of significant changes.

Prevention & **

Vitamin D deficiency should be removed first, sunbathed or given artificial ultraviolet light, vitamin D3 concentrate preparations, or cod liver oil concentrated, and vitamin D3 injected intramuscularly if necessary. Vitamin D intake is 5 g daily for infants and children and under 50 years of age**, 10 g daily for 50 and 70 years of age** and 15 g daily for those over 70 years of age.

To sum up, vitamin D deficiency is indispensable for the human body, although it will only lead to occipital baldness in infancy.

Occipital baldness in infants

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