Introduction: This is a systemic, chronic nutritional disease characterized by bone diseases caused by the lack of vitamin D in infants, children and adolescents, resulting in calcium and phosphorus metabolism disorders. Osteochondrosis is manifested by poor growth of cartilage plates at the epiphyseal end of the long stem, incomplete calcification of bone tissue, incomplete calcification of mature bone, and vitamin D deficiency. The high-risk group for the disease is in infants under 2 years of age (especially 3 to 18 months), and taking enough vitamin D can prevent the disease.
First, vitamin D deficiency rickets, the cause of insufficient sunshine, and fast growth rate
1, insufficient sunshine
Due to the high-rise buildings in urban life blocking the sun; air pollution; short sunshine in cold winter; weak ultraviolet rays; insufficient outdoor activity time; or less skin contact during outdoor activities; regardless of climate, season, cloud cover, latitude, skin color, skin exposure, it will affect endogenous vitamin D production.
2, the growth rate is too fast
For example, factors such as low weight, premature birth, twins, disease, etc., can cause babies to recover, grow and develop faster, and need more vitamin D, but the body's vitamin D reserves are insufficient and prone to rickets.
3. Insufficient vitamin D supplementation in food
The increased risk of vitamin D deficiency is due to low vitamin D content in natural foods, exclusive breastfeeding and lack of vitamin D supplementation, such as outdoor activities such as vitamin D supplementation.
4. Disease and drug effects
Gastrointestinal or hepatobiliary diseases will affect the absorption of vitamin D, such as infantile hepatitis syndrome, chronic diarrhea, etc., severe liver and kidney damage can lead to poor vitamin D hydroxylation, and rickets can lead to the formation of 125-oh4-d3 deficiency. Prolonged use of anticonvulsant drugs can lead to a deficiency of vitamin D.
Second, suffering from vitamin D deficiency rickets, the main clinical manifestations of patients are osteoporosis
1. The incidence is more common in children
Found in infants, especially in infants aged 3-18 months. Osteoporosis is characterized by bone changes in rapidly growing sites that can affect muscle development and nerve excitement. Clinical manifestations vary with age.
2. Hyperhidrosis occurs in the early stage
Half a year, especially three months. Most patients experience increased nervous excitability, such as irritability, annoyance, sweating, baldness, etc. In this case, there is no bone injury, the bone x-ray may be normal, or the calcification area may be slightly blurred, the serum level of 25-oh-d3 is decreased, and parathyroid hormone, blood calcium, phosphorus, and alkaline phosphatase are normal or slightly elevated.
3. The patient's head circumference will increase
When symptoms persist, typical hyperthyroid hormone and calcium and phosphorus metabolism disorders may occur. Within half a year, rickets mainly occur in the skull, the soft front edge of the skull, the head is thin, and the light press has a "ping-pong" feeling. After half a year, a ping-pong ball-like sensation may appear around the bone slit, but the middle of the frontal bone and parietal bone often gradually thickens. In seven to eight months, the head becomes a "square skull" and the head circumference increases normally.
In addition to hypocalcemia, changes in other indicators at this stage are more pronounced. X-rays show vanished calcification areas, brush-shaped epiphysis, cup-shaped, osteoporosis, thinning of the cortex, axial bending deformity or branch fractures, and the clinical symptoms of fractures are not obvious.
4. After treatment, the patient's symptoms will gradually disappear
Clinical signs and symptoms gradually resolve or disappear after treatment or sun exposure. Blood calcium and phosphorus gradually return to normal, while alkaline phosphatase needs to return to normal within one to two months. After 2-3 weeks of treatment, the bone x-ray was significantly improved, the calcified line was irregular, the calcified area was dense and thickened, and gradually returned to normal.
Third, vitamin D deficiency rickets, the main examination methods are X-ray examination, as well as biochemical examination
1. Diagnostic methods
Diagnosis is made according to clinical presentation, blood biochemical indicators and bone x-ray examination.
2. Differential diagnosis
Early symptoms of the excitatory phase are nonspecific and need to be differentiated from the following disorders.
(1) Cartilage malnutrition
The disease is hereditary cartilage development disorder, congenital short limbs, large head, protruding forehead, protruding waist, and kyphosis of the buttocks. Diagnosis is based on specific position (short-sided dwarf) and bone x-rays.
(2) Distal renal tubular acidosis
Due to insufficient hydrogen secretion in the distal canal, a large amount of sodium, potassium and calcium loss in the urine, secondary hyperparathyroidism, bone decalcification, rickets. Children with obvious bone malformations, short stature, metabolic acidosis, polyuria, alkaline urine, in addition to low blood calcium and blood phosphorus, blood potassium is also low, blood ammonia is increased, and often has symptoms of decreased blood potassium.
Due to congenital or acquired reasons, chronic renal insufficiency causes calcium and phosphorus metabolism disorders, low blood calcium and blood phosphorus, secondary hyperparathyroidism, systemic bone decalcification, osteoseopathy, etc. Children gradually become more pronounced after multiple symptoms, forming a short state.
3. Treatment methods
Control active period and prevent skeletal deformities. Calcium and vitamin D supplementation is required at doses of 2000 iu to 4000 iu or 1,25-oh 2-d30.5 μ g to 2.0 μ g or 400 iu/day after 1 month of prophylaxis. There should be strict indications for large doses. If there are complications or severe rickets that cannot be taken orally, a larger dose of vitamin D can be injected intramuscularly and then changed after 3 months. Review after one month of treatment. If there are no signs of recovery in clinical manifestations, blood biochemistry, and bone x-ray changes, they should be differentiated from anti-vitamin rickets.
4. It is necessary to pay attention to supplementing nutrition
In addition to the treatment of vitamin D, we must also pay attention to strengthening nutrition, ensuring that milk is sufficient, adding milk transport food in time, and insisting on going out every day. The sequelae of bone deformities in children should be strengthened and corrected by active exercise and passive exercise. Early weight-bearing exercise should be avoided when there are risk factors for vitamin D deficiency during the growth phase. Surgical correction may be considered for skeletal deformities.
5. Prevention methods
Vitamin D deficiency rickets is a preventable disease that can be prevented if infants and children have enough time to spend outdoors. So ensuring that children take vitamin d400iu every day is the key to prevention and treatment. For infants who are exclusively or partially breastfed, vitamin D400iu/day should be supplemented within 2 weeks of birth, and in preterm, low birth weight and twins within 1 week of life. Both make up to 2 years old. Even in the summer, when the sun is shining, vitamin D should not be reduced or stopped if it grows rapidly. Generally speaking, calcium cannot be added, but milk and malnutrition can be appropriately supplemented with micronutrients and calcium.
Conclusion: Most patients are children, because rickets develop in infancy and childhood, resulting in different degrees of distortion. For example, there are loop legs, dwarfism, etc. The patient's biochemical examination is generally normal. X-rays show significant lesions.