Vitamin D deficiency rickets in children
Introduction
Introduction to vitamin D deficiency rickets in children Vitamin Ddeficiency rickets are diseases characterized by vitamin D deficiency, which leads to disorders of calcium and phosphorus metabolism and clinical calcification disorders of bone. Vitamin D is an essential nutrient for maintaining the life of higher animals. It is one of the most important biological regulators of calcium metabolism. This disease is one of the four diseases prevention and treatment in childhood. Vitamin D has always been considered to be involved in the regulation of calcium and mineral balance in the body all the time. The deficiency of vitamin D is a chronic nutritional deficiency disease. It is slow to develop and is not easy to attract the attention of parents, affecting the growth and development of children. . Therefore, we must actively prevent it. basic knowledge Sickness ratio: 5% Susceptible people: children Mode of infection: non-infectious Complications: pneumonia, diarrhea, anemia
Cause
The cause of vitamin D deficiency rickets in children
Insufficient sunlight (20%):
Vitamin D can be produced by the sun through the skin, such as lack of sunshine, especially in the winter, it needs to be supplemented regularly by the meal. In addition, air pollution can also block the ultraviolet rays in the sun. People wear everyday clothes and live in high-rise areas. Indoors, the use of synthetic sun screens to block UV rays, living in areas with insufficient sunlight, etc. affect the skin biosynthesis of a sufficient amount of vitamin D. For infants and children, sunbathing is an important way to make the body synthesize vitamin D3.
Insufficient intake of vitamin D (20%):
Animal foods are the main source of natural vitamin D. Marine fish such as salmon, sardines, animal liver, cod liver oil are good sources of vitamin D2. Small amounts of vitamin D2 are also available from eggs, beef, butter and vegetable oils. Sexual foods contain less vitamin D. The vitamin D contained in natural foods can't meet the needs of infants and young children. It needs to be more sun-dried and supplemented with cod liver oil.
Calcium content is too low or the ratio of calcium to phosphorus is not good (15%):
Insufficient calcium content in food and improper ratio of calcium and phosphorus can affect the absorption of calcium and phosphorus. Although the content of calcium and phosphorus in human milk is low, the ratio (2:1) is suitable and easy to be absorbed, while the content of calcium and phosphorus in milk is higher. High, but the ratio of calcium to phosphorus (1.2:1) is improper, and the absorption rate of calcium is low.
Increase in demand (10%):
Premature infants are prone to rickets because of their fast growth rate and insufficient calcium storage in the body; infants grow fast, and the demand for vitamin D and calcium increases, which is easy to cause rickets; after 2 years of age, the growth rate slows down and outdoor activities increase. The incidence of rickets is gradually decreasing.
Disease and drug effects (10%):
Liver, kidney disease and gastrointestinal diseases affect the absorption and utilization of vitamin D, calcium and phosphorus, cholestasis in children, dilatation of common bile duct, congenital biliary stricture or atresia, steatorrhea, pancreatitis, refractory diarrhea, etc. It affects the absorption of vitamin D, calcium and phosphorus and suffers from rickets. Long-term use of phenytoin, phenobarbital sodium and other drugs can accelerate the decomposition and metabolism of vitamin D and cause rickets.
(two) pathogenesis
Vitamin D in the human body can be obtained from two ways, namely through intradermal transformation and oral intake, both endogenous and exogenous. Endogenous vitamin D is 7-dehydrocholesterol in human skin. Ultraviolet radiation in sunlight produces inactive vitamin D2; exogenous vitamin D comes from foods such as fish, liver, eggs, milk, etc., which are rich in vitamin D2. Vitamin D2 in the diet is assisted by bile. The chylomicrons formed in the small intestine are absorbed into the plasma, and are transported to the liver together with the endogenous vitamin D3 via vitamin D-binding protein (an alpha-globulin in plasma), which is oxidized in the liver by the catalysis of 25-hydroxylase. It becomes 25-hydroxy D3. At this time, although it has anti-caries activity, it is not strong, and after being transported to the kidney, it is further oxidized to have a strong anti-caries activity by the catalysis of 1-hydroxylase. , 25-(OH)2D3, finally exerts its physiological role by circulating blood to the relevant target organs.
1,25-(OH)2D3, which is transported to the small intestine, enters the intestinal epithelial cells first, forming a complex with specific receptors in the cytoplasm, acting on the nuclear chromatin, and inducing the synthesis of specific calcium-binding proteins. The role of the calcium channel transport on the surface of the intestine is brought into the mucosal cells, thereby entering the blood circulation to increase blood calcium and promote the deposition of calcium in the bone. In addition, 1,25-(OH)2D3 also has kidneys. Direct action promotes the reabsorption of calcium and phosphorus by the renal tubules to reduce the loss of calcium and phosphorus.
When vitamin D is deficient, calcium and phosphorus are reduced by intestinal absorption, hypocalcemia stimulates increased secretion of parathyroid hormone, parathyroid hormone promotes bone resorption, bone salt dissolves, and parathyroid hormone promotes kidney formation 1,25- (OH) 2D3, promotes the absorption of calcium in the small intestine, because parathyroid hormone inhibits the reabsorption of phosphorus by the renal tubules, relatively promotes the absorption of calcium, and causes the urinary phosphorus to be discharged in a large amount, and the urinary calcium tends to be normal or slightly lower, but Eventually, the bone-like tissue calcification process is impaired, even osteolysis, osteoblast compensatory hyperplasia, local bone-like tissue accumulation, and increased alkaline phosphatase secretion, resulting in a series of bone changes and biochemical changes in the clinic.
Prevention
Vitamin D deficiency rickets prevention in children
1. Sunbathing: The best prevention is to sunbathe. About 80% of the vitamin D needed by the human body is synthesized by itself. Some people measure it. After the sun is shining, every square centimeter of skin can synthesize vitamin D18U within 3 hours, in a sunny outdoor. Children should wear clothes without wearing caps. The time for sunbathing to prevent rickets is 2 hours per week. Children born in spring and summer can take out the outdoors after full moon. Children born in autumn and winter can also take out outdoors for 3 months. Every time you go out for 10 to 15 minutes, you can extend the time appropriately, such as opening a window indoors.
2. Correct feeding: correct feeding is also important for prevention. Breastfeeding is recommended. Breast-fed infants should be supplemented with vitamin D400U every day from 1 week after birth. Premature infants should be supplemented with 800U per day. Supplementary food should be added in time. A good diet should be cultivated after weaning. Habits, not picky eaters, partial eclipse, to ensure the needs of children with various nutrients.
3. Vitamin D supplementation: For preterm infants, double fetuses, artificial feeding, the use of vitamin D prevention is still an important method.
Complication
Pediatric vitamin D deficiency rickets complications Complications, pneumonia, diarrhea, anemia
Although the disease itself is rarely life-threatening, it is easy to be neglected due to slow onset. Once the obvious symptoms occur, the body's resistance is low, and it is easy to have pneumonia, diarrhea, anemia and various infectious diseases. The disease is harmful to children's health. Larger, is one of the "four diseases" in the prevention and treatment of children's health care. The growth and development disorders of children with rickets, skeletal deformities, the formation of square skull, thoracic X, O-shaped legs or X-shaped legs, and kyphosis, lateral processes, etc., affect Physiological function of children.
Symptom
Vitamin D deficiency rickets in children Symptoms Common symptoms Vitamin D deficiency, weakness, thoracic deformity, infant rib valgus, crying, restlessness, spine, knee valgus, valgus or hip palpebral closure, late neonatal tremor
Vitamin D deficiency rickets, clinically mainly skeletal changes, muscle relaxation, and non-specific mental, neurological symptoms, severe rickets can affect the digestive system, respiratory system, circulatory system and immune system, and also have an impact on children's mental development .
Vitamin D deficiency rickets are clinically divided into early stage, stimulating period, recovery period and sequelae period, initial stage, stimulating period and recovery period, collectively referred to as active period.
1. Initiation: Most of the disease started from about 3 months. In this period, the symptoms are mainly neuropsychiatric symptoms. The child has sleeplessness, crying, sweating, etc. After sweating, the scalp itch and shakes the head on the pillow. The pillow is bald.
2. Stimulating period: In addition to the initial symptoms, the child is mainly affected by skeletal changes and dysfunction of the motor function. With the fingers pressed on the occipital and parietal bones of the children for 3 to 6 months, the skull is invaginated and bounces back with ease. It is called table tennis sign. The head of the child is often square in 8~9 months. The front sac is large and the closure is delayed. In severe cases, the anterior iliac crest is not closed at 18 months, and the ribs and rib cartilage at both sides are swollen like beads. It is called ribbed beaded, the middle part of the sternum protrudes like a "chicken chest", or it sinks into a "funnel chest", and the lower edge of the thorax is turned outwards to "the rib valgus"; the spine is protruding and the side is protruding; the standing, walking children Because the weight is pressed against the unstable long bones of the lower limbs, the legs will form an inward or outward bending deformity, that is, an "O" or "X" leg.
The muscle ligament of the child is slack and weak. Because the abdominal muscles are weak, the abdomen is swollen. When lying down, it is a "frog-shaped abdomen". Because of the muscle weakness of the limbs, learning to sit, standing, and walking are later, because the legs are weak and easy to fall. The teeth are delayed, the teeth are not neat, and caries are prone to occur.
Abnormal cerebral cortex, conditioned reflex formation, children with apathy, language development retardation, low immunity, easy to concurrent infection, anemia.
3. Recovery period: After a certain treatment, various clinical manifestations disappeared, muscle tension recovered, blood biochemical changes and X-ray performance also returned to normal.
4. sequelae: more common in children after 3 years of age, after treatment or natural recovery, clinical symptoms disappeared, only severe rickets left different parts, varying degrees of skeletal deformities.
Examine
Examination of vitamin D deficiency rickets in children
1. Blood biochemical examination: determination of blood calcium, phosphorus, alkaline phosphatase, serum 25-(OH)D3 (normal 10 ~ 80g / L) and 1,25- (OH) 2D3 (normal 0.03 ~ 0.06g / L) It is significantly reduced in the early stage of rickets, and it is a reliable early diagnosis index, and alkaline phosphatase is elevated in plasma.
2. Determination of urinary calcium: The determination of urinary calcium also contributes to the diagnosis of rickets, and the excretion of alkaline phosphatase in the urine is increased.
3. X-ray of the long bones of the epiphysis: The specific X-ray findings of the long bone humerus were found. The calcification reserve line of the early X-ray long bone was blurred; the polar calcification reserve disappeared, the end of the humerus was widened, and the sacral end was cupped or The brush is changed, the bone is sparse, and the backbone is bent or deformed.
4. X-ray bone age film: found bone age behind.
Diagnosis
Diagnosis and identification of vitamin D deficiency rickets in children
diagnosis
Diagnosis can be made based on medical history, symptoms, signs, and changes in blood biochemical examinations and bone X-ray examinations.
Differential diagnosis
Identification with children with hypothyroidism, cartilage dystrophy, hydrocephalus and anti-vitamin D rickets.
Cartilage dystrophy is a type of disease that affects the conversion of cartilage into bone. Of course, achondroplasia is the easiest to understand, and they are all characterized by gnome signs (usually with a normal height of the trunk but short limbs) and often accompanied by other malformations.
Hypothyroidism is a syndrome in which thyroxine secretion is insufficient or insufficient.
