Rickets is a metabolic bone disease in which the newly formed bone matrix is not properly mineralized. I. Etiology The etiology is divided into the following categories, which can be one or several combined: 1. Insufficient intake of vitamin D in the diet or Et photo deficiency. 2, increased vitamin D requirements without timely supplementation (e.g., pregnancy, lactation). 3, vitamin D absorption and metabolism disorders 4, hereditary, acquired or tumor hypophosphatemia. 5, nephrotic syndrome, chronic renal failure and renal tubular acidosis. 6. Others: calcium deficiency, bone matrix production disorder …… II. Clinical manifestations Depending on the etiology, the clinical manifestations and severity of children with rickets may vary. The main manifestations are skeletal pain, deformity, fracture, epiphysis enlargement and slow growth. Early manifestations of rickets include emotional abnormalities and developmental delays, secondary short stature and deformities with excessive sweating, abdominal distention and constipation, and in severe cases, inability to stand and walk. Hypophosphatemic rickets often shows symptoms such as muscle weakness and hypotonia; hypocalcemia often has hand and foot twitching; vitamin D-dependent rickets type II often has baldness. The typical signs of children are square skull, occipital baldness, chicken chest, beaded ribs, Henry’s groove, wrist enlargement in the form of bracelet, “0” or “x” shaped legs. It may be associated with anemia and hepatomegaly. The main manifestations are generalized osteoporosis of the diaphysis and epiphysis, thinning of the cortex, pathological fractures, small epiphyseal ossification centers with blurred margins, thickening of the epiphyseal growth plate, blurred brush-like epiphyseal margins, and cup-like depressions. The long bones are bent and deformed, often with inversion or valgus of the knee. Bone densitometry reveals a generalized decrease in bone density, which is more obvious in cortical bone. Serum alkaline phosphatase level is significantly increased in almost all patients with rickets. Prevention and treatment 1. Vitamin D intake of vitamin D-rich food, increased sunlight, supplementation of appropriate amount of vitamin D preparations, etc. The preventive dose of vitamin D deficiency depends on the age, generally 400-800 U/d. It can be increased during pregnancy and lactation as appropriate, and the general preventive treatment time is 3-6 months. Treatment of rickets: 2,000-4,000 U of oral vitamin D daily, which can be reduced to a preventive dose when the condition improves significantly. Those who cannot take it orally or severe patients can be injected intramuscularly 200,000-300,000 U once, and change to preventive amount after 3 months. Attention must be paid to calcium supplementation 800-1,000 megd before and during oral or intramuscular injection of high-dose vitamin D. Blood calcium, phosphorus and alkaline phosphatase levels should be monitored regularly, and attention should be paid to adjusting calcium and vitamin D dosage at any time. If the disease does not recover, it should be differentiated from anti-vitamin D rickets. The selected preparations can be vitamin D: pills, vitamin D: tablets, vitamin AD pills, vitamin AD drops, vitamin D: colloidal calcium injection, osteopontin, alfa osteopontin, etc. 2, calcium infants 0-1 years old, breastfeeding can intake 225 mg / d calcium, the appropriate intake (AI) is 400 mg / d, artificial feeding is often lower calcium content of food, calcium should be supplemented so that AI up to 400 mg / d. Children 1 to 3 years old, 4-6 years old, ≥ 7 years old A1 are 600 mg / d, 800 If you can drink 250 ml of milk in the morning and 250 ml in the evening (containing 300 mg of calcium x 2), plus other food containing calcium, the AI can be reached. 3, other nutrients Osteomalacia (or rickets) patients are often accompanied by malnutrition and various vitamin deficiencies, depending on the need If necessary, supplement with adequate protein and multivitamins, etc. 4.Other treatment Actively treat the original disease. In case of tumor, remove the tumor as soon as possible; in case of high fluorine intake, isolate the fluorine source and treat with fluoride removal; in case of drug-induced disease, discontinue the corresponding drugs; in case of low phosphorus anti-vitamin D chondroplasia or rickets, in addition to active vitamin D and calcium supplements, oral neutral phosphate preparations should be taken. In renal tubular acidosis, the body needs to be provided with sufficient HCO3 to counteract the excess H+ and correct the acidosis. NaHCO3, or Shohl’s combination, can be given, and orthopedic surgery can be considered for those with severe skeletal deformities, provided that the condition is controlled.