Rickets, or vitamin D deficiency rickets, is a systemic, chronic, nutritional disease characterized by skeletal lesions due to disorders of calcium and phosphorus metabolism caused by vitamin D deficiency in infants, children, and adolescents. The main feature is incomplete calcification of the cartilage plate and bone tissue of the growing long bone epiphysis, and incomplete calcification of mature bone due to vitamin D deficiency. The high risk group for this disease is infants and children under 2 years of age (especially 3 to 18 months), which can be prevented by adequate intake of vitamin D.
I. Etiology.
1. Perinatal vitamin D insufficiency.
Studies have pointed out that although the mother’s daily supplementation of 400 IU of vitamin D in the second trimester has little effect on the 25-OH-D3 in the blood circulation of full-term infants, the vitamin D of newborns quickly drops to deficient levels when compared to mothers who supplement regularly during pregnancy, and therefore preterm births and twin births are more likely to be under-stored.
2. Insufficient sunlight.
Due to tall buildings blocking sunlight in urban life; atmospheric pollution; short sunlight and weak ultraviolet light in cold winter; not enough time for outdoor activities; or little skin exposure during outdoor activities; regardless of climate, season, atmospheric cloudiness, latitude, skin color, and skin exposure can affect the production of endogenous vitamin D.
3. Fast growth rate.
Such as low weight, premature birth, twin births, disease and other factors, after the infant recovers, growth is relatively faster and requires more vitamin D. However, the body does not have enough stored vitamin D and is prone to rickets.
4. Inadequate vitamin D supplementation in food.
Because natural food contains little vitamin D, exclusive breastfeeding, there is no adequate outdoor activities, such as not supplementing vitamin D, vitamin D deficiency rickets increased risk of developing rickets.
5, disease and drug effects.
Gastrointestinal or hepatobiliary diseases affect vitamin D absorption, such as infantile hepatitis syndrome, chronic diarrhea, etc. Serious damage to the liver and kidneys can lead to vitamin D hydroxylation disorders, 1,25-OH2-D3 generation deficiency and cause rickets. Long-term use of anticonvulsant drugs can cause vitamin D deficiency in the body, such as sodium phenytoin and phenobarbital, which can stimulate the increased activity of the oxidase system of hepatocyte microsomes and accelerate the decomposition of vitamin D and 25-OH-D3 into inactive metabolites. Glucocorticoids have an antagonistic effect on the transport of calcium by vitamin D.
II. Treatment.
1. The aim is to control the active phase and prevent skeletal deformities. The principle of treatment should be based on oral vitamin D. The general dose is 2,000 IU to 4,000 IU per day, or 1,25-OH2-D30.5 μg to 2.0 μg, with a change to a preventive dose of 400 IU/day after one month. High-dose treatment should have strict indications. When severe rickets has complications or cannot be given orally, vitamin D can be injected intramuscularly in high doses, and the preventive amount should be changed after 3 months. After 1 month of treatment, it should be reviewed, and if there is no sign of recovery in clinical manifestations, blood biochemistry and bone X-ray changes, it should be differentiated from anti-vitamin D rickets.
2. The Chinese Nutrition Society recommends a daily dietary calcium supply of 300mg for 0-6 months, 400mg for 7-12 months, and 600mg for l-3 years. as long as breast milk is sufficient or enough formula is consumed, calcium nutrition for infants and young children can be met. The treatment of rickets generally does not require calcium supplementation, unless it is complicated by low calcium manifestations such as hand-foot twitching.
3. In addition to vitamin D treatment, attention should be paid to strengthening nutrition, ensuring adequate milk intake, timely addition of foods for lactation transfer, and insisting on daily outdoor activities.
4. For children with skeletal deformities in the posterior period, physical exercise should be strengthened, and active or passive exercise can be used to correct them. For children with high risk factors for vitamin D deficiency rickets, premature force-bearing exercises should be avoided during growth and development (e.g., avoiding premature practice of sitting, standing, bouncing under the support tuck, etc.). If lower limb deformity has already appeared, muscle massage (O-shaped leg massage lateral muscle, X-shaped leg massage medial muscle) can be done to increase muscle tone to correct the deformity. Severe skeletal deformity can be considered surgical orthopedic treatment.
III. Prevention.
Vitamin D deficiency rickets is a preventable disease, the onset of which can be prevented if infants and children spend enough time outdoors. Therefore, it is now considered that ensuring that children receive 400 IU of vitamin D daily is the key to prevention and treatment.
1. Breastfed or partially breastfed full-term infants should be supplemented with 400 IU/day of vitamin D starting 2 weeks after birth, and 800 IU/day of vitamin D starting 1 week after birth for preterm, low birth weight, and twin-born infants; all until 2 years of age. If the growth rate is fast, it is not advisable to reduce or stop the use of vitamin D. Generally, calcium supplements may not be added, but micronutrients and calcium supplements may be appropriate when milk intake is insufficient and nutrition is poor.
2, non-breast-fed infants, children whose daily milk intake is less than 1000ml, should supplement with vitamin D 400IU/day.
3, adolescents whose intake does not reach 400 IU/day of vitamin D, such as insufficient intake of dairy products, eggs or fortified vitamin D food, should be supplemented with 400 IU/day of vitamin D.