This is a prevention and control recommendation issued by the Pediatric Branch of the Chinese Medical Association.
Pregnant women should take regular outdoor activities and eat foods rich in calcium and phosphorus. Women in late pregnancy in autumn and winter should add VitD400-1000U / d (10-25μg / d) appropriately. If there are conditions, pregnant women should monitor the concentration of 25- (OH) D 3 months after pregnancy, there is obvious VitD deficiency, VitD should be supplemented to maintain 25- (OH) D levels within the normal range.
Clinical manifestations The clinical manifestations of rickets include non-specific symptoms, changes in skeletal characteristics and other systemic changes.
The active period of rickets is divided into early stage, acute stage, recovery period and sequelae period.
Early stage: More common in infants within 6 months (especially within 3 months). There may be non-specific neuropsychiatric symptoms such as hyperhidrosis, occipital alopecia, irritability, and night terrors. There is no bone disease at this stage. Blood calcium and blood phosphorus are normal or slightly lower, alkaline phosphatase (AKP) is normal or slightly higher, and blood 25- (OH) D is reduced. There was no abnormality in the long metaphysis of the bone X-ray film or the temporary calcification zone was blurred and thinned, and the metaphysis was slightly wider.
Stress period: Skeletal signs: <6 months infant, visible signs of skull softening (table tennis);> 6 months infant, visible square skull, hand (foot) bracelet, rib bead, rib cartilage groove, chicken breast, O-shaped leg, X-shaped legs and other signs. Blood calcium is normally low or reduced, blood phosphorus is significantly reduced, and AKP is increased. Blood 25- (OH) D and 1,25 (OH) 2D were significantly reduced. Bone X-ray film widened the epiphysis of the long bone, the temporary calcification zone disappeared, and appeared as a brush or cup-shaped, and the epiphyseal cartilage disc was widened> 2mm .
Recovery period: The symptoms of the children in the early or active period disappear after sun exposure or treatment, and the signs gradually reduce or disappear. Blood calcium, blood phosphorus, AKP, 25- (OH) D, 1,25- (OH) 2D gradually returned to normal. Temporary calcification zone of the long metaphysis of the bone X-ray film reproduced, widened, and increased in density, and the epiphyseal cartilage disc was <2mm.
Sequelae: more common in children after the age of 3, due to severe rickets in infants and young children, different degrees of bone deformation can be left behind. Generally no clinical symptoms, blood biochemical examination is normal.
The lack of VitD, in addition to changes in skeletal disease, can also affect other tissues and organs, delaying motor development, such as muscle relaxation, decreased muscle strength (muscle tone); decreased immune function and repeated infections. VitD deficiency in children may be related to certain chronic diseases in adulthood, such as diabetes, asthma, and multiple sclerosis.
VitD's lack of high-risk factors, clinical symptoms and signs are helpful for diagnosis, and blood biochemistry and bone X-ray radiography are needed to confirm the diagnosis. Serum 25- (OH) D is the best indicator of VitD nutritional status and should be carried out gradually.
Differential diagnosis
VitD-deficiency rickets need to be combined with other non-VitD-deficiency rickets (such as renal osteodystrophy, renal tubular acidosis, hypophosphatemia-resistant VitD rickets, Fanconi syndrome), endocrine, bone metabolic diseases (such as thyroid Identification of reduced function, achondroplasia, mucopolysaccharidosis).
Children suffering from chronic diarrhea or hepatobiliary, pancreatic diseases or taking antiepileptic drugs can affect VitD absorption, metabolism, and hydroxylation in the body, leading to secondary VitD deficiency, which also needs to be identified.
The therapeutic effect of children with rickets is monitored to control the condition and prevent bone deformity. The principle of treatment is mainly oral. The choice of VitD preparation, dose size, length of treatment, single or multiple times, the route (oral or intramuscular injection) should be determined according to the specific circumstances of the child, emphasizing individualized administration.
When the dose is 2000-4000U / d (50-100μg / d), it will be changed to 400U / d (10μg / d) after 1 month.
When oral intake is difficult or diarrhea affects absorption, high-dose assault therapy can be used, VitD150-300,000 U (3.75-7.5mg) / time, intramuscular injection, VitD at 400U / d (10μg / d) 1-3 months maintain. Follow up after 1 month of medication. If symptoms, signs, and laboratory tests are not improved, other diseases should be considered, and differential diagnosis should be considered. At the same time, hypercalcemia, hypercalciuria, and VitD overdose should be avoided.
Excerpt from "Vitamin D Deficiency Rickets Prevention Recommendations", "Chinese Journal of Pediatrics" editorial committee, Chinese Medical Association Pediatric Branch Child Health Science Group National Rickets Prevention Scientific Research Collaboration Group, "Chinese Pediatrics" March 2008 Vol. 46 No. 3 .
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