| disease | Vitamin D Deficiency Rickets |
| alias | Rickets |
Vitamin D deficiency rickets is a common childhood disease, accounting for over 95% of all rickets cases. This condition arises from insufficient vitamin D in the body, leading to systemic calcium and phosphorus metabolism disorders that prevent calcium salts from properly depositing in the growing parts of bones, ultimately resulting in skeletal deformities. Although rickets rarely directly threatens life, its slow onset makes it easy to overlook. Once obvious symptoms appear, the body's resistance weakens, increasing susceptibility to complications such as pneumonia, diarrhea, anemia, and other diseases.
bubble_chart Epidemiology
Between 1977 and 1983, a survey was conducted in 26 provinces, municipalities, and autonomous regions across China, examining 84,901 children under the age of 3. Among them, 75,259 were found to have rickets, resulting in a national average prevalence rate of 40.70%. The average prevalence rates were 49.39% in the northern region, 33.11% in the central region, and 24.64% in the southern region. Compared to the local incidence rate of 79.60% reported in 1957, this represented an almost 50% reduction, with a significant decline in severe cases of rickets. In a 1987 survey across nine provinces and autonomous regions, the average prevalence rate of rickets among children under 3 years old dropped further to 27.2%, showing another notable decrease. In Harbin, Heilongjiang Province, the northernmost part of China, the incidence rate of rickets among children under 3 fell gradually from 60.84% in 1977 to 11.0% in 1991. These findings demonstrate the effectiveness of China's efforts in the prevention and treatment of rickets.
bubble_chart Etiology1. Vitamin D Deficiency Vitamin D deficiency is the primary cause of this disease. There are two sources of Vitamin D: one is endogenous, where ultraviolet light with a wavelength of 296–310 μm from sunlight converts 7-dehydrocholesterol stored in the basal layer of the skin into cholecalciferol, also known as Vitamin D3 (VitD3). The other source is exogenous, obtained through dietary intake of foods containing Vitamin D, such as liver (15–50 IU/kg①), milk (3–40 IU/L), and egg yolks (25 IU each). However, the Vitamin D content in these foods is minimal and insufficient for the body's needs. Ergosterol can be converted into Vitamin D2 (calciferol) upon exposure to ultraviolet light. Both VD2 and VD3 can be synthesized artificially and have the same effects on humans.
2. Insufficient Ultraviolet Exposure Another major cause of Vitamin D deficiency, especially in northern regions. Exposure of the skin to ultraviolet light can provide adequate Vitamin D3. China has a vast territory with varying natural conditions between the north and south, particularly in terms of sunlight duration. Southern regions have longer sunlight exposure and lower rickets incidence, while northern regions have shorter sunlight exposure and higher incidence. However, ultraviolet light in sunlight is easily blocked or absorbed by dust, smoke, clothing, and ordinary glass. Rapid industrial development, urban construction, air pollution in some areas, skyscrapers blocking light, and indoor lifestyles all reduce exposure to ultraviolet light.
3. Other Factors
⑴ Rapid Growth: Faster growth increases the demand for Vitamin D. Thus, rapidly growing children are more prone to rickets. Premature infants have insufficient calcium and phosphorus reserves and grow quickly after birth; if Vitamin D is lacking, rickets is highly likely.
⑶ Excessive Cereal Consumption: Cereals contain high levels of phytic acid, which binds with calcium and phosphorus in the small intestine to form insoluble calcium phytate, hindering absorption.
⑷ Chronic Respiratory Infections, Gastrointestinal Disorders, and Liver, Pancreas, or Kidney Diseases: These can impair Vitamin D, calcium, and phosphorus metabolism.
⑸ Improper Acidity or Alkalinity: This affects intestinal absorption of calcium and phosphorus. Generally, lower intestinal pH enhances calcium and phosphorus absorption.
Calcium and Phosphorus Metabolism and Bone Development
Vitamin D deficiency affects the absorption of calcium and phosphorus, leading to metabolic disorders of calcium and phosphorus. Apart from vitamin D, other factors in the body are involved in calcium and phosphorus metabolism, interacting and interrelating to exert positive and negative feedback effects, thereby maintaining normal calcium and phosphorus metabolism and bone development. These factors include parathyroid hormone, calcitonin, chondrocytes, osteoblasts, and matrix vesicles. Additionally, growth hormone, androgens, estrogens, thyroid hormone, and glucocorticoids also influence calcium and phosphorus metabolism. A brief overview of these factors is provided below.
Vitamin D, whether absorbed through the skin or the digestive tract, is stored in the plasma, liver, fat, and muscles. Absorbed vitamin D is inactive and requiresNeijingtwo hydroxylation steps to exert its hormone-like biological effects.
First, vitamin D is transported to the liver, where it is converted by the 25-hydroxylase system in the endoplasmic reticulum and microsomes of hepatocytes, transforming vitamin D3 into 25-hydroxycholecalciferol (25-(OH)D3). The latter exerts a negative feedback inhibition on the activity of 25-hydroxylase, regulating the concentration of 25-(OH)D3 in the blood. 25-(OH)D3 is then transported to the kidneys, where it undergoes further hydroxylation by the mitochondrial 25-(OH)D3-1-hydroxylase system (1-hydroxylase) in the proximal tubule epithelial cells, producing 1,25-dihydroxycholecalciferol (1,25-(OH)D3). The latter inhibits the activity of 1-hydroxylase via negative feedback. 1,25-(OH)D3 is highly active, with effects on calcium and phosphorus metabolism 200 times stronger than 25-(OH)D3 and 100 times more potent in promoting bone salt formation.
Active vitamin D is influenced by blood calcium and phosphorus levels. Low calcium and phosphorus stimulate 1-hydroxylase activity, accelerating the formation of 1,25-(OH)D3; conversely, high blood calcium and phosphorus inhibit 1-hydroxylase activity. High blood calcium and phosphorus also promote the conversion of 25-(OH)D3 into 24,25-(OH)D3, which loses vitamin D activity or has minimal effects.
The functions of 1,25-(OH)D3 include: ① Promoting calcium and phosphorus absorption in the small intestine mucosa. 1,25-(OH)D3 binds to specific receptors in target cells of the small intestine mucosa, forming a vitamin D-binding protein-calcium complex, which is transported from the mucosal side to the serosal side and absorbed into the blood via capillaries. ② 1,25-(OH)D3 enhances the reabsorption of calcium and phosphorus in the renal proximal tubules, increasing blood calcium and phosphorus levels. ③ 1,25-(OH)D3 promotes the differentiation of undifferentiated mesenchymal cells into osteoclasts, stimulating bone resorption and dissolving bone salts from old bone tissue, thereby elevating blood calcium and phosphorus levels. ④ 1,25-(OH)D3 directly stimulates osteoblasts, promoting calcium salt deposition.
From this, it is evident that liver or kidney dysfunction can impair the hydroxylation process of vitamin D, which is also the pathogenic cause of hepatic and renal rickets.
2. The role of parathyroid hormone (PTH) ① The secretion of PTH depends on blood calcium concentration. When blood calcium is below normal, PTH increases, whereas high blood calcium suppresses PTH secretion. High blood calcium inhibits the adenylate cyclase in target organs, reducing the formation of cyclic adenosine monophosphate (c-AMP). Conversely, low blood calcium has the opposite effect, increasing c-AMP. PTH acts on the adenylate cyclase system of target cells, elevating intracellular c-AMP, which promotes the transfer of calcium ions from mitochondria to the cytoplasm. The increased cytoplasmic calcium concentration activates the calcium pump on the cell membrane, facilitating the outward transfer of calcium ions and raising blood calcium levels. ② The effect of PTH on bone: When PTH increases, it enhances the ability of undifferentiated mesenchymal cells to differentiate into osteoclasts, thereby increasing bone resorption and elevating blood calcium and phosphorus levels. PTH inhibits bone formation, antagonizing the action of 1,25-(OH)D3. ③ The effect of PTH on the kidneys: PTH acts on renal tubules, promoting calcium reabsorption and facilitating calcium ion entry into the blood via the calcium pump on the plasma membrane. PTH inhibits renal tubular reabsorption of phosphorus, increasing urinary phosphorus excretion, and antagonizes the action of 1,25-(OH)D3. Another role of PTH is to accelerate the conversion of 25-(OH)D3 into 1,25-(OH)D3. ④ PTH promotes intestinal calcium absorption, primarily due to increased 1,25-(OH)D3 levels, though some suggest PTH may also have a direct effect on intestinal calcium absorption.
3. Calcitonin (CT) is derived from the parathyroid glands and the parafollicular cells ("C" cells) of the thyroid gland. Calcitonin is influenced by blood calcium levels; the normal value of CT in the blood is below 72±7 ng/L. An increase in blood calcium promotes a rise in CT, while a decrease has the opposite effect. ① The effect of CT on bones: It inhibits the formation of osteoclasts, suppresses bone resorption, and prevents the dissolution of bone salts and the breakdown of bone matrix. CT promotes the transformation of osteoclasts into osteoblasts, enhancing calcium deposition. The biological effects of calcitonin are more active in young animals. ② The effect of CT on the kidneys: It inhibits the reabsorption of calcium and phosphorus by the renal proximal tubules, increasing the excretion of calcium and phosphorus in the urine. ③ The effect of CT on the intestines: It inhibits the absorption of calcium in the digestive tract. CT also suppresses the absorption of sodium, potassium, and phosphorus in the intestines.
Vitamin D, PTH, and CT have synergistic and antagonistic effects on calcium and phosphorus metabolism in the intestines, bones, and kidneys. There is a clear mutual feedback mechanism among them, maintaining normal calcium and phosphorus metabolism in the body and the proper development of bones.
4. Normal Bone Development Normal bone development occurs in two forms: endochondral ossification and intramembranous ossification. The former primarily takes place at the ends of long bones, causing bones to lengthen, while the latter occurs in the bone cortex and flat bones, making bones thicker or wider.
During developmental ages, the epiphyseal cartilage proliferates and differentiates chondrocytes from the ossification center toward the bone shaft. The differentiation of chondrocytes from the ossification center to the metaphyseal epiphyseal cartilage can be divided into: ① The germinal cell layer, consisting of small, undifferentiated, flattened cells. ② The proliferative chondrocyte layer, formed by the division of germinal cells, with flattened cells tightly arranged in columns and increased cartilage matrix between the columns. ③ The osteogenic chondrocyte layer, where the cells gradually enlarge and arrange in a square pattern. ④ The hypertrophic chondrocyte layer, where the cells become larger, mature, and align neatly in columns. Calcium and phosphorus transported by metaphyseal blood vessels begin to deposit in the matrix of hypertrophic chondrocytes in layers ③ and ④, leading to chondrocyte degeneration. ⑤ The degenerative layer represents the final stage of cell degeneration, where cells undergo necrosis and dissolution. This is also the temporary calcification zone visible on X-ray films. Calcified tubes contain capillary-like structures, with osteogenic cells arranged orderly around the blood vessels. ⑥ The osteogenic zone, or the newly formed spongy bone region. Osteoblasts adhere closely to the calcified tube walls, secrete bone matrix, and subsequently deposit calcium, becoming embedded themselves to form initial-stage [first-stage] trabeculae, which are later remodeled into mature trabeculae and longitudinally arranged spongy bone in the metaphysis.
Some researchers suggest the presence of matrix vesicles in bone tissue, which originate from chondrocytes and osteoblasts. These vesicles are named matrix vesicles due to their location in the matrix. Matrix vesicles have a membrane and a diameter of about 30–300 nm, containing abundant alkaline phosphatase, ATPase, and pyrophosphatase (some believe these enzymes are the same entity). In the hypertrophic chondrocyte layer, under the action of phosphatase on the biological membrane of matrix vesicles, pyrophosphate salts and bone salt crystals interact within the vesicles. Pyrophosphatase breaks down pyrophosphate, and alkaline phosphatase further decomposes other phosphates into inorganic phosphorus. This locally increases calcium and phosphorus concentrations, leading to the formation of bone salt crystals within the matrix vesicles. These crystals protrude from the vesicle membrane, extend outward, and deposit bone salts, eventually forming apatite. This constitutes the calcified portion of the bone matrix synthesized by hypertrophic chondrocytes and osteoblasts in the metaphysis—the temporary calcification zone.
During childhood bone growth, chondrocytes continuously proliferate, the temporary calcification zone advances, and spongy bone undergoes constant remodeling, allowing long bones to lengthen.
bubble_chart Pathological Changes
The main pathological change is osteomalacia (normally, two-thirds of a child's bone consists of inorganic matter and one-third organic matter, whereas in rickets, these proportions are reversed), where incompletely calcified osteoid tissue proliferates, replacing the normal provisional calcification line. This severely impairs longitudinal bone growth, leading to a dwarfism-like condition.
bubble_chart Clinical Manifestations
1. General Symptoms When VitD deficiency reaches a certain degree, a series of neuropsychiatric symptoms may appear clinically, such as profuse sweating, especially during feeding and crying, with an abnormal odor to the sweat; irritability, night terrors, and night crying. These are not specific symptoms of rickets, but in high-prevalence areas, they can serve as reference points for early clinical diagnosis when considered alongside other relevant conditions.
2. Skeletal Lesions
(1) Head: In the early stages, an enlarged fontanelle or delayed closure may be observed, along with delayed tooth eruption. The sutures may widen, with softened edges, and in severe cases, a "ping-pong ball" craniotabes may appear. By 7–8 months, frontal and parietal bossing may develop, forming a square-shaped skull. If the bossing worsens, saddle-shaped, buttock-shaped, or cross-shaped skull deformities may occur.
(2) Chest: During infancy, swelling of the costal cartilage regions may appear, primarily at the 5th–8th ribs, forming round, bulbous enlargements known as "rachitic rosary." If the rosary expands inward, it may compress the lungs. Due to prolonged traction from the diaphragm attachment, the softened ribs may exhibit inward invasion at the upper rib margins, leading to flaring of the lower ribs and the formation of a groove-like deformity called Harrison's groove. When inward invasion occurs at the junction of the 6th–8th ribs and the sternum, it may cause protrusion of the sternum, known as pigeon breast. When these signs coexist and worsen, thoracic deformities may develop, compounded by abdominal muscle laxity and protrusion, resulting in a violin-shaped thoracoabdominal appearance. Such deformities can impair cardiopulmonary function. Some children with rickets may exhibit increased curvature of the clavicles and shortened length, causing the shoulders to hunch forward and restricting chest expansion. Funnel chest, characterized by inward invasion centered at the xiphoid process, may also occur and should be distinguished from familial funnel chest. In some older children, the sternal manubrium may appear shallowly grooved, which is one of the sequelae of rickets.
(3) Spine: In active rickets, prolonged sitting may lead to kyphosis, and occasionally scoliosis.
(4) Pelvis: In severe cases, pelvic deformation may occur, often with a shortened anteroposterior diameter, which may contribute to difficult delivery in females later in life.
(5) Limbs: In children with rickets aged 7–8 months or older, the epiphyseal regions of the limbs may appear enlarged, particularly at the distal ends of the ulna and radius, forming round, blunt, and thickened bulbous structures known as "rachitic bracelets." Before and during the early walking stage, due to bone softening and the effects of gravity and tension, "O"-shaped legs may develop. The bending of "O"-shaped legs may occur at the lower third of the calf, mid-calf, knee joint, femur, or even the femoral neck, with the latter being more difficult to correct. "O"-shaped legs appearing before walking should be distinguished from physiological bowing. After walking begins, the lower limbs may develop an "X"-shaped configuration. Severe lower limb deformities may lead to an unsteady gait, as the wide stance prevents adduction, causing a waddling "duck-like" gait to maintain balance. Deformities affecting the femoral neck angle or causing valgus primarily at the knee joint are less likely to resolve naturally.
Severe cases of rickets may result in pathological fractures from minor trauma, often going unnoticed.
(6) Others: Severe rickets may be accompanied by hepatosplenomegaly, anemia, and Jaksch's syndrome. Some children may experience delayed intellectual development. Certain newborns may develop laryngeal stridor within the first 1–2 weeks of life, with inspiratory dyspnea, inspiratory retractions, and a three-sign depression, worsening during feeding and crying. This condition is related to congenital dysplasia and may gradually resolve with vitamin D supplementation as the child grows. Severe rickets may delay the development of motor skills, such as sitting, standing, and walking. Even established motor skills may regress due to active rickets.
3. Blood generation and transformation findings: In the VD deficiency stage of rickets, the blood level of 25-OHD3 decreases, while 1,25-(OH)2D3 decreases or remains normal. Subsequently, blood calcium, phosphorus, and alkaline phosphatase levels also change. In the initial stage [first stage], blood phosphorus decreases, followed by a drop in blood calcium, an increase in alkaline phosphatase, and a rise in PTH. During the active stage, both blood calcium and phosphorus decrease, while alkaline phosphatase rises significantly. In the stage of convalescence, serum 25-OHD3 and 1,25-(OH)2D3 levels increase, calcium and phosphorus begin to rise, alkaline phosphatase decreases accordingly, PTH also declines, and eventually returns to normal levels.
4. X-ray findings X-rays cannot reflect the early stage of rickets, but the signs of rickets shown on X-rays reflect the corresponding histopathological changes in bone tissue, providing strong objectivity for the diagnosis of rickets. The X-ray signs of rickets at various stages are closely related to serum calcium, phosphorus, and alkaline phosphatase levels. X-rays also demonstrate corresponding changes in the occurrence, progression, and outcome of clinical rickets.
In the early stage of rickets, X-ray findings appear normal. During the initial stage (first stage), the provisional calcification zone may be normal, blurred, or absent. In the early active stage, flattening or depression of the metaphysis at the wrist joint can be observed, along with thinning of the cortex and widening of the nuclear distance (the distance between the epiphyseal nucleus and the metaphysis, normally 2mm, less than 3mm) to more than 3mm. The peak active stage represents the height of rickets activity, with X-rays showing widened metaphysis, cup-shaped deformities, deepening of the cup, a woolly appearance at the base of the cup, porous or lamellar changes in the bone cortex, sparse or reticular trabeculae, further widening of the nuclear distance (up to 8mm at its maximum), disappearance of the epiphyseal nucleus (making nuclear distance unmeasurable), and delayed bone age. In the early recovery stage, the provisional calcification zone may reappear as dotted or linear, the epiphyseal nucleus reappears, and further changes include a linear or double-layered provisional calcification zone, increased density of the metaphysis, denser and more numerous trabeculae, increased cortical density of the bone shaft, and possible periosteal reaction, with shortening of the nuclear distance. In some cases transitioning from the active stage to the late recovery stage, the metaphysis may show a uniform "candle wax dripping" appearance. In the cured stage, the provisional calcification zone may become denser and thicker or remodel to normal.
Dynamic X-ray observations show that in active rickets, the ulna is affected first, followed by the radius. During the stage of convalescence, the radius recovers before the ulna. The metaphysis widens first and then narrows. In children under 6 months of age, cup-shaped deformities of the metaphysis are rare in rickets, with fan-shaped expansion and a woolly appearance at the end being more common. After 8 months, cup-shaped deformities in the active stage become more frequent. If the nuclear distance is too wide, the cup-shaped deformity may not be visible, indicating not only hyperplasia of chondrocytes and their matrix but also severe decalcification.
The diagnosis of rickets is primarily based on a history of vitamin D deficiency and clinical symptoms and signs, with the option to measure generation and transformation and take X-rays when conditions permit.
A history of vitamin D deficiency refers to: ① During pregnancy or the advanced stage of pregnancy, the mother consumed little or no vitamin D-rich foods, had limited sun exposure, and exhibited symptoms of calcium deficiency. ② Infants born in winter or spring, artificially fed during infancy, not supplemented with vitamin C preparations, lacking or having inadequate complementary foods, or having insufficient sun exposure (i.e., limited outdoor activity). For infants, rickets may be linked to breastfeeding history, while for children aged 2–3 years, it is unrelated to maternal pregnancy history.
The diagnostic criteria for rickets are as follows.
1. Disease stages
⑴ Vitamin D deficiency stage or initial stage of vitamin D deficiency: This stage occurs before clinical symptoms of rickets appear. There may be a history of vitamin D deficiency, and generation and transformation may show 25-(OH)D3 levels below 25 nmol/L, or 1,25-(OH)2D3 below the lower limit. (Normal serum levels of 25-(OH)D3 are 27.5–170 nmol/L (11–68 ng/ml); 1,25-(OH)2D3 are 75–150 pmol/L (30–60 pg/ml)).
⑵ Initial stage [first stage]: Clinical manifestations include neuropsychiatric symptoms or grade I cranial softening and grade I rachitic rosary or "bracelets," with grade I decreases in blood calcium and phosphorus and grade I increases in alkaline phosphatase. X-rays may appear normal or show initial stage changes. This stage typically occurs at 3–4 months of age, often in winter.
⑶ Active stage: Neuropsychiatric symptoms, cranial softening, and prominent rachitic rosary or "bracelets" are present. Blood calcium and phosphorus levels drop significantly, and alkaline phosphatase rises markedly. X-rays show various active-stage changes. The peak age for this stage is 7–8 months to around 2 years, commonly in winter and spring.
⑷ Stage of convalescence: The aforementioned neuropsychiatric symptoms and signs improve significantly after treatment and sun exposure. Blood calcium and phosphorus levels rebound, and alkaline phosphatase decreases. X-rays display various convalescent-stage changes. The age range is similar to the active stage, and the season is typically late spring, summer, or early autumn.
⑸ Sequela stage: No active skeletal changes or the above symptoms are present, only varying degrees of skeletal deformities. Generation and transformation return to normal, and X-rays show recovery. This stage occurs after approximately 3 years of age.
2. Severity grading: Skeletal deformities are classified as:
⑴ Grade I: Square skull, grade I rachitic rosary and Harrison's groove, grade I "O" legs (standing with feet together, knee joint distance below 3 cm).
⑵ Grade II: Cranial softening, prominent rachitic rosary and "bracelets," and Harrison's groove; grade II "O" legs (knee joint distance 3–6 cm), or grade II or higher "X" legs (standing with knees together, ankle distance exceeding 3 cm).
⑶ Grade III: Impairs physiological and motor functions, such as rounded rachitic rosary and bracelets, prominent Harrison's groove and pigeon breast, or "O" or "X" legs affecting gait, possibly accompanied by pathological fractures.
bubble_chart Treatment Measures
1. Vitamin D Treatment
⑴ Grade I (initial stage [first stage]): Oral administration of vitamin D preparations at 1000–2000 IU daily or a single oral dose of 100,000–200,000 IU of VitD.
⑵ Grade II (pre-active stage): Oral administration of 2000–5000 IU of VitD daily or a single oral dose of 200,000–300,000 IU.
⑶ Grade III (active stage): Oral administration of 5000–5000 IU of VitD daily or a single oral dose of 300,000–400,000 IU.
The above daily oral doses should be continued for 1 month, along with 200 mg/day of elemental calcium. If clinical and biochemical tests do not show preventive efficacy, the medication duration may be appropriately extended before switching to a preventive dose.
2. Intensive Therapy For severe active-stage cases or children with other conditions such as chronic diarrhea, jaundice, acute infectious diseases, prolonged illnesses, or congenital rickets, intensive VitD therapy may be administered. However, this should always be under medical supervision and not abused.
⑴ Oral method: High-concentration VitD (50,000 IU per pill) is taken daily for 1 week, followed by a preventive dose. Long-term or excessive use must be avoided, especially for those with sequelae, as cases of toxicity have been reported with daily doses of 20,000–40,000 IU for 4 weeks.
⑵ Injection method: A single intramuscular injection of 150,000–200,000 IU of VitD2 or VitD3 is administered, followed by a preventive dose. Repeated injections should be avoided to prevent toxicity.
Before intensive therapy, oral administration of 10% calcium chloride for 3 days is generally recommended to prevent hypocalcemic spasms. Some argue that intensive therapy rapidly increases serum calcium levels, making prior calcium administration unnecessary. However, clinical cases of convulsions after high-dose VitD injections have been observed, warranting further study. Additionally, intensive therapy should be used cautiously in frail children or those with a predisposition to spasms.
3. Artificial Ultraviolet Radiation Therapy.
4. Orthopedic Therapy For bone deformities due to rickets in children over 3 years old, which are mostly sequelae, VitD preparations are not suitable. Orthopedic therapy should be considered. For pigeon chest, prone positioning, push-ups, or pull-ups can help expand the chest. For Grade I "O" or "X" leg deformities, massage of the corresponding muscle groups (e.g., lateral muscles for "O" legs, medial muscles for "X" legs) can improve muscle tone. Swimming is the best orthopedic method. For Grade III sequelae or cases affecting physiology and physique, surgical correction may be considered in adolescence.
Children with active rickets should limit sitting, standing, and walking during treatment to avoid worsening spinal curvature or "O"/"X" leg deformities.
1. Popularization of Preventive Measures
(1) Strengthen publicity efforts, including rational knowledge on preventing rickets among pregnant women, the perinatal period, and the infant stage, specifically implemented within the maternal and child health management system.
(2) Promote legally mandated vitamin D-fortified foods. In recent years, the Nutrition Research Laboratory of the Beijing Pediatric Research Institute developed vitamin AD-fortified milk (AD milk), containing 2000 IU/L of vitamin A and 600 IU/L of vitamin D. Trials have proven that this fortified milk eliminates the need for additional vitamin D supplements, making it the safest, most effective, convenient, and economical method to address vitamin A and D deficiencies in milk-fed infants while preventing overdosing. It has already been promoted in Beijing and is worth introducing for application in other regions.
(3) Enhance the proper management and feeding of infants and young children, advocating breastfeeding for up to 8 months and timely introduction of complementary foods.
(4) Increase outdoor activities for children, with group-based children participating in the "three baths" exercise (air baths, sunlight baths, and water baths).
(5) Prevent and treat common illnesses in infants and young children at an early stage.
(6) Urban planning departments should consider sunlight exposure angles in residential designs. Child (and elderly) green activity zones should be incorporated within building complexes, or rooftop activity areas for children should be established, especially in northern regions where this is urgently needed.
(7) Artificial ultraviolet light devices should be introduced into qualified childcare institutions.
2. Pharmacological Prevention Methods
(1) During pregnancy, emphasize outdoor activities not only for the preventive effects of sunlight and ultraviolet rays against rickets but also for broader health benefits. Especially in the last three months of pregnancy, supplement with 400 IU of vitamin D daily in addition to sunlight exposure.
(2) From 1–2 weeks after birth, administer 400 IU of vitamin D orally per day, or a single dose of 30,000–50,000 IU of vitamin D daily, or 100,000–150,000 IU of vitamin D quarterly. Infants fed breast milk or cow’s milk consuming 400–500 ml daily do not require calcium supplementation, as calcium from general calcium supplements is less easily absorbed and utilized compared to that in milk. Sunlight exposure can be fully utilized in summer and autumn. Starting each winter, administer 100,000–150,000 IU of vitamin D orally, repeating every 2–3 months (i.e., by the end of the following winter) for three consecutive years—this method is particularly suitable for rural areas.
(3) For premature infants, twins, and children with gastrointestinal diseases, the preventive dose of vitamin D may be slightly increased as appropriate, but overdosing must be avoided to prevent toxicity.
Given China’s vast territory, varying conditions between northern and southern regions, urban and rural areas, differences between scattered and grouped childcare settings, and varying levels of crowding in high-rise buildings versus single-story homes, preventive measures should be implemented in accordance with local conditions.
1. Renal osteodystrophy, also known as renal rickets. The disease is caused by chronic renal dysfunction resulting from congenital renal hypoplasia, polycystic kidney, hydronephrosis due to urinary tract obstruction, chronic nephritis, or pyelonephritis, all of which can lead to reduced production of 1,25-(OH)2D3, resulting in rickets and bone deformities. Serum calcium is often decreased, while serum phosphorus is significantly elevated. This condition affects normal body development and easily leads to a state of dwarfism. Although blood calcium is compensated, convulsions of the hands and feet rarely occur, which is due to metabolic acidosis and hypoproteinemia, causing a relative increase in free calcium in the blood. X-rays often show generalized osteoporosis and decalcification, with rickets-like changes at the ends of long bones. Fibrocystic changes may appear in the bone shafts and pelvis. Treatment with conventional doses of VD is ineffective, but administration of 1,25(OH)2D3 at 0.04μg/kg/d can yield significant therapeutic effects.
2. Renal tubular acidosis
3. Hypophosphatemic vitamin D-resistant rickets
4. Fanconi syndrome
5. Rickets induced by antiepileptic drugs Long-term oral administration of antiepileptic drugs such as phenobarbital sodium and phenytoin sodium can cause hypocalcemia. The mechanism is believed to be that these drugs activate the hepatic microsomal oxidase system, leading to increased catabolism of various steroid hormones, forming inactive metabolites excreted in bile or urine. The breakdown of 25-(OH)D3 in the liver is also increased, thereby reducing the production of 1,25-(OH)2D3, resulting in hypocalcemia and the development of rickets. When antiepileptic drugs are used long-term, weekly administration of VD 6000–10000 IU can prevent this condition.
