Vitamin D deficiency in children

Introduction

Introduction Vitamin D deficiency is mainly caused by vitamin D deficiency, decreased blood calcium and increased neuromuscular excitability, and symptoms such as convulsions, throat or hand and foot convulsions. More common in infants from 4 months to 3 years old. There is a history of vitamin D deficiency, such as a history of insufficient sun exposure; a history of inadequate intake of vitamin D in the diet, such as infants with low vitamin D content; there is a history of relative deficiency of vitamin D due to increased demand, such as growth Fast babies, premature babies; vitamin D malabsorption such as pancreatic and intestinal diseases, history of biliary tract and lymphatic obstruction.

Cause

Cause

1. Insufficient sunlight:

The vitamin D supplied by natural foods is far from satisfying the needs of the human body. The main source of vitamin D in the body is the endogenous synthesis of 7-dehydrocholesterol in the skin by ultraviolet irradiation. Under normal circumstances, the daily exposure to sunlight for more than two hours, the incidence of rickets is significantly reduced, but the ultraviolet rays in the sun are often blocked or absorbed by dust, soot, clothes or ordinary glass, affecting its role. Geographical environments (such as rain and fog, northern regions) and seasons (winter, spring) and ultraviolet radiation have a great impact on the ground. In areas with long cold seasons, short sunshine hours, and low outdoor activities, the incidence of rickets in children is significantly higher.

2. Insufficient intake of vitamin D and calcium and phosphorus:

The human body needs about 400-800 international units of vitamin D per day, but the vitamin D obtained by the baby every day from human milk, milk, egg yolk, liver and other foods is less than 100 IU, and the human milk contains vitamin D 0.4 to 10.0 UI/ D1, milk contains 0.3 ~ 4.0 IU / d1, the content of various types of fruits and vegetables is also very small, far from meeting normal needs, so it is necessary to add vitamin D in the second month after birth, if not added in time is easy Caused by insufficient. Starchy foods contain insufficient calcium and contain more phytic acid. The latter can combine with calcium and phosphorus to form a poorly soluble complex and hinder the absorption of calcium and phosphorus. The ratio of milk is 1.2:1, which is not conducive to absorption (optimal absorption). The ratio is 2:1), so the incidence of rickets in artificial feeding is higher.

3. Vitamin D and calcium and phosphorus absorption disorders:

In children with cholestasis, common bile duct dilatation, refractory diarrhea, steatorrhea, chronic respiratory infections, intestinal lipid absorption disorders can affect the absorption of vitamin D and calcium and phosphorus.

4. Other:

(1) Liver and kidney are the main organs that activate vitamin D. When it is sick, it can directly affect the normal metabolism of vitamin D, such as infant hepatitis syndrome, intrahepatic biliary atresia.

(2) Anti-epileptic drugs can shorten the half-life of vitamin D, stimulate the micro-stereo-oxidase system of hepatocytes, increase the metabolism of various steroid hormones, and increase the metabolism of 25-(OH)D3, leading to 1,25(OH). Insufficient 2D3 production, intestinal calcium absorption disorder and cause rickets.

(3) The growth rate of bone growth is directly proportional to the need of vitamins and calcium and phosphorus. The growth is fast, the amount is large, and the relative supply is insufficient. The vitamin D and the storage of calcium and phosphorus in the immature body are insufficient (the fetal calcium reserve is 70-80% in gestational age). After 28 weeks, it was obtained from the mother. Therefore, children under 2 years of age, especially in dry children, have more rickets than other children. Very small immature children due to the large amount of vitamin D, coupled with renal 1-hydroxylase activity disorder, the incidence of rickets can be as high as 59.2%, and often with the general dose of vitamin D3 can not achieve the purpose of prevention, need to give 1a-OH-D3 To prevent and treat.

Examine

an examination

Related inspection

Trace element detection in human body

Clinical manifestations: Non-specific neuropsychiatric symptoms often appear in the initial stage, and bone changes gradually appear in the future.

1. Non-specific symptoms: more than one year old baby, can occur 1 month after birth. The main symptoms are irritability, night terrors, nightingale and sweating, sweaty special, often wet pillows, occipital hair loss (occipital baldness). The disease develops, showing muscle and tendon relaxation, low muscle tone, abdominal bulging (frog frog), excessive joint extension, slow or retrograde motor function development. Also seen liver splenomegaly, anemia, susceptible to respiratory infections.

2. Signs of skeletal changes: The skull can be softened early (<3 months of babies can be physiological), the door is large, the cranial suture is widened, and the edges are soft. 7-8 months or more children can see teeth late, square skull, saddle-shaped skull or cruciform cranium; ribs are enlarged (beads), ribs are pulled by the diaphragm to form costal cartilage groove (Hao'ergou), and under the ribs The valgus is valgus; the wrist and the tread are enlarged at the end of the bone (Bracelet sign, ankle bracelet sign). Children over one year old may have a late closure of the door, a chicken breast, a funnel chest, a 0-leg, an x-shaped leg, a posterior process of the spine or a lateral process.

Diagnosis

Differential diagnosis

Vitamin D deficiency in children is often accompanied by skeletal deformities, anterior sacral enlargement and other symptoms, which need to be identified as follows:

1. cretinism (small ailments): caused by congenital thyroid insufficiency, with special face and posture: small eye cracks, wide eye distance, wide nose, flat tongue, often protruding out of the mouth, short limbs, relative torso Longer, thinning hair, dry and thick skin, may have myxedema. The expression is sluggish and the intelligence is significantly lower. X-ray shows that the bone age is obviously behind, but the blood calcium and phosphorus are normal, and the sputum phosphatase is reduced, which can be differentiated from rickets.

2. Hydrocephalus: Uniformity of the skull is enlarged, with progressive anterior cardia enlargement, bulging, separation of the skull joints, and the lower eye of both eyes is "falling shape". In severe cases, there are optic nerve head edema, vomiting, limb paralysis and other skulls. Increased pressure signs.

3. Cartilage dystrophic disorder: for the progenitor cartilage developmental disorder, there is a special face with large head, forehead and mandibular protruding nasal roots. The limbs and fingers are short and thick, and the five fingers are flush. The upper body volume is significantly disproportionate to the lower body. Lumbar lordosis, hip kyphosis. Blood calcium and phosphorus are normal. X-ray showed thick and short bones, widened dry ends, and no typical changes in rickets.

4. Hypophosphatemic anti-vitamin D rickets: a systemic joint dominant or autosomal dominant/recessive hereditary disease, also known as familial hypophosphatemia. It is a congenital tubular resorption of phosphorus and intestinal calcium, phosphorus absorption, and transport of primary defects. Characteristic

(1) There is often a family history.

(2) Symptoms and signs appear after 1 year of age, and there is still clinical manifestation of the duration of rickets after 3 years of age.

(3) Increased urinary phosphorus and decreased blood phosphorus.

(4) The conventional therapeutic dose of vitamin D is ineffective, and the oral phosphorus should be 1.5-2.0 g/day.

5, congenital osteogenesis imperfect: bones are brittle, easy to fold, often due to multiple fractures caused by limb deformity, X-ray see the cortical bones, fractures and deformities, the biggest feature is the combination of deafness and sclera blue.

6, congenital muscle relaxation: muscle ligament relaxation, excessive joint flexion, but blood biochemistry and bone X-ray examination is normal.

7, renal rickets: renal rickets (renalrickets) caused by congenital renal hypoplasia, chronic nephritis and other renal dysfunction, causing skeletal deformities. Although blood calcium is low, it rarely causes hand and foot spasms.

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