Vitamin D deficiency

Introduction

Introduction to vitamin D deficiency

Vitamin D deficiency (vitaminDdeficiency) is due to less sun exposure (the skin can be converted into effective vitamin D after UV irradiation), insufficient intake (milk, eggs, liver, fish and other foods), malabsorption (small bowel disease) and increased demand (children, pregnant women, lactating mothers) and other factors, resulting in systemic calcium, phosphorus metabolism disorders and bone changes caused by insufficient vitamin D in the body. Its outstanding performance is rickets in children and osteomalacia in adults and osteoporosis (osteoporosis), affecting the functions of nerves, muscles, hematopoiesis, immunity and other organs and organs, seriously affecting children. Growth and development.

basic knowledge

Sickness ratio: 0.05%

Susceptible people: children

Mode of infection: non-infectious

Complications: anemia, chicken breast, funnel chest

Pathogen

Vitamin D deficiency

(1) Causes of the disease

1. Insufficient sunlight. If there is sufficient ultraviolet radiation, human skin can produce enough vitamin D. The amount of vitamin D produced is proportional to the intensity of ultraviolet light. The exposure time is proportional to the exposed area of the skin. In the winter and spring, it lacks outdoor due to cold. Activities or in foggy areas, industrial cities have serious air pollution, and high-rise buildings can make ultraviolet radiation insufficient.

2. Insufficient intake of vitamin D is more common in infants who have not eaten vitamin D fortified dairy products before the age of 2 and children who have not been supplemented with cod liver oil in the long-term breastfeeding. Children are relatively short of growth due to rapid growth, especially in premature infants. The twins and low birth weight infants have less vitamin D, calcium and phosphorus storage at birth, and are prone to rickets after birth. The mothers who have multiple pregnancies and long-term breastfeeding consume a large amount of calcium, if vitamin D intake is insufficient. There is a bone softening disease.

3. Vitamin D malabsorption and activation disorders Chronic celiac disease, liver, gallbladder, pancreatic diseases affect the absorption and utilization of vitamin D, in the elderly due to the reduction of the efficiency of skin vitamin D synthesis and intestinal vitamin D absorption rate of osteoporosis The disease is aggravated, and severe liver and kidney diseases affect the hydroxylation of vitamin D to active 25-(0H)D and 1,25-(OH)2D.

Vitamin D-dependent rickets are autosomal recessive syndromes, type I is impaired in the function of 25-(OH)D 1 hydroxylase, and type II gene mutations cause damage to 1,25-(OH)2D receptors.

Phenobarbital drugs can induce changes in liver microsomal enzymes, reduce the activity of vitamin D 25-hydroxylase, and promote bile secretion, which accelerates the degradation of vitamin D, thereby reducing serum vitamin D and 25-(OH)D. concentration.

(two) pathogenesis

When vitamin D is deficient, the absorption of calcium and phosphorus in the intestine is reduced, causing blood calcium and blood phosphorus to decrease. The decrease of blood calcium promotes the secretion of parathyroid glands. The latter promotes the dissolution of bone salts by osteoclasts, decalcifying old bones and entering bone calcium. Blood maintains blood calcium close to normal, but parathyroid hormone can inhibit renal tubular phosphorus reabsorption, resulting in increased urinary phosphorus, decreased blood phosphorus, and reduced calcium and phosphorus in the blood (<40), which hinders calcification of bone formation in the body. Osteoclast compensatory hyperplasia, resulting in accumulation of osteophytes and subperiosteal bone-like tissue, causing rickets and osteomalacia.

If the parathyroid gland is unresponsive and bone calcium cannot be quickly released into the blood, the blood calcium will decrease. For example, the total calcium in the blood drops to 1.75 to 1.87 mmol/L (7 to 7.5 mg/dl), and the blood free calcium is lower than 0.88. Below 1.0 mmol/L (3.5 to 4.0 mg/dl), there is a low calcium convulsion in the hand, foot and ankle.

Prevention

Vitamin D deficiency prevention

The prevention of vitamin D deficiency should start from the perinatal period. Pregnant women should have outdoor activities, and they should be exposed to the sun. They should be rich in vitamin D, calcium, phosphorus and protein. In the late 7 to 9 months of pregnancy, they can take vitamin D 25g per day. (1000U) or vitamin D2 2500 ~ 5000g (100,000 ~ 200,000 U) once orally, every day should be supplemented with 1000mg elemental calcium in the diet, insufficient calcium supplementation, breastfeeding should be initiated in the neonatal period to start outdoor activities as soon as possible , contact with sunlight.

Because ultraviolet light can not penetrate the glass, it should be opened to the sun. It is considered that the newborn has the risk of vitamin D deficiency or subclinical vitamin D deficiency. The recommended amount of vitamin D in China is 10g/d (400U/d). Young children need to take comprehensive preventive measures, such as promoting breastfeeding, adding complementary foods in a timely manner, 1~2h daily activities, supplementing vitamin D, increasing vitamin D to strengthen the intake of dairy products, etc. For premature infants, twins, and weak children, Children with particularly rapid growth and development can use intramuscular injection of vitamin D3 7500g (300,000 U), or oral administration of bividin emulsion (commercial name Yingkang) 15mg / support, containing vitamin D3 300,000 U, adolescents, adults Older people and menopausal women should also take vitamin D and calcium to prevent osteomalacia and osteoporosis.

Complication

Vitamin D deficiency complications Complications Anemia chicken chest funnel chest

Complications are more common in children, mainly causing the baby to look up, sit, stand, and walk later. The joints are loose and overextended, and the cerebral cortex is abnormally characterized by slow conditioned reflexes, backward language development, and anemia. In some of the more severe cases of vitamin D deficiency, other bone deformations such as chicken breasts, funnel chests, X-legs, O-legs, ribbed beads, bracelets and anklets can be found.

Symptom

Vitamin D deficiency symptoms common symptoms night irritability irritability irritability diarrhea vitamin D poisoning convulsions pale pale hyperhidrosis liver splenomegaly

Rickets and osteomalacia are clinically unique manifestations of vitamin D deficiency. Rickets occur in infants and children during growth and development. Osteomalacia occurs in adults and clinical manifestations vary significantly.

Rickets

(1) Symptoms: mainly for mental and neurological symptoms found in the initial and extreme stages of rickets, irritability, irritability, restlessness, night terrors, night crying, sweating, sweating, often shaking your head while sleeping, so that Post-occipital alopecia (occipital baldness), as the disease progresses, the muscle tension is low, the joint ligament is slack, the abdomen is swollen like a frog belly, the child's movement is slow, independent walking is late, severe rickets are often accompanied by anemia, hepatosplenomegaly, Malnutrition, weakened systemic immunity, prone to diarrhea, pneumonia, and prone to prolonged, low calcium in children, low calcium convulsions (hand and foot snoring), increased neuromuscular excitability, facial and hand muscles Convulsions or generalized seizures, the episodes are stopped in a few minutes, but intermittent episodes can occur. Severe convulsions can cause suffocation due to the throat.

(2) Bone changes: As the disease progresses, bone changes occur, which are more common in the extreme period of rickets. The changes in bones are related to age, growth rate and vitamin D deficiency.

1 The softening of the skull in the head is more common in infants from 3 to 6 months. The occipital or parietal bone is obvious. When the finger is pressed, the skull is sunken. When the pressure is removed, the original state (such as table tennis feeling) is removed. After 6 months, the growth rate of the skull is slowed down. For the subperiosteal bone-like tissue hyperplasia, the frontal bone, the parietal bone bulge into a square skull, serious fashion can be a cross skull, saddle-shaped cranium, in addition to the anterior palpebral late closure, teeth out of the teeth, the teeth are not strong, the arrangement is not neat.

2 The ribs on both sides of the chest and the costal cartilage are blunt-rounded and called "ribbed beads", which are marked by the 7th to 10th ribs; the ribs are softened and pulled by the diaphragm, and the ribs in the attachment are formed into lateral grooves. For Hee's ditch); severe rickets anterior sternal formation of chicken breast; sternal xiphoid invagination to form a funnel chest, due to chest deformity affecting lung expansion and pulmonary circulation, easy to be combined with severe pneumonia or atelectasis, the above deformity is more common in 6 months ~ 1 Older baby.

3 The spine and limbs can be bent forward or backward, the long bones of the extremities are hypertrophied, and the wrists and ankles are swollen like "bangles" and "ankles", which are common in 7-8 months. After 1 year old, children begin to walk, long bones of lower limbs. Because the weight is bent, it is an "O" shape or an "X" shape leg. When the two feet are close together, the distance between the knee joints is 3cm or less, and the weight is more than 3cm. When the "X" shape legs are close together, The distance between the two ankle joints and the light and heavy criteria are the same as the "O" shaped legs.

Early light rickets can be completely restored if they can be treated in time, leaving no skeletal deformities, and skeletal deformities can be left in the recovery period, such as square skull, chicken breast, "O" or "X" shaped legs, mostly found in After 3 years old.

2. Common symptoms of osteomalacia are bone pain, muscle weakness, tendon and bone tenderness. Early symptoms may not be obvious. Common back and waist and leg pains are aggravated. When exercise is aggravated, muscle weakness is an important manifestation of vitamin D deficiency. It is very difficult to get up the stairs or stand up from the seat. The bone pain and muscle weakness are both present. The patient's gait is special. It is called duck step. Finally, it is difficult to walk, forcing the patient to be bedridden. The patient's sternum, ribs and pelvis during physical examination. At the large joints, there is often obvious tenderness. The skeletal deformities have shortened neck, head sinking, and posterior scoliosis. Chicken breast and pelvic stenosis cause difficulty in childbirth. Many patients have pathological fractures.

3. Other clinical types

(1) Congenital rickets: more common in cold regions of the north, the incidence rate is 16.4%, the disease is more common in premature babies, multiple births, low birth weight infants, babies born in winter and spring, have a history of vitamin D deficiency during pregnancy, lack of animal food, Rare sun; or pregnant women are sick and sick, suffering from liver and kidney or other endocrine diseases, pregnant women often have hand and foot spasm, gastrocnemius tendon, bone pain, low back pain and other symptoms, severe cases may have osteomalacia, neonatal clinical symptoms may not be obvious, some have Easy to be shocked, sleepless at night, crying, physical signs with softening of the skull, anterior iliac crest, straight sputum, cranial suture width, edge softening, chest bone changes such as rib soft groove, funnel chest is rare, X-ray examination of the wrist The Orthotopic Tablet is the main basis for the diagnosis of this disease. Congenital rickets show typical rickets changes, and blood biochemical changes can only be used for diagnostic reference.

(2) Late-type rickets: more common in the northern temperate zone, occurs in the late winter and early spring season, children aged 5 to 15 years old, lack of sun exposure, insufficient intake of vitamin D, and the growth rate or the height increase Clinical manifestations of poor walking, lower limb pain, especially knee, ankle or heel pain, often complained of gastrocnemius tendon, in addition, there are symptoms such as excessive sweating, restlessness, and long-term deformity ("O" shape or "X" shaped legs), a few visible rib valgus or thoracic deformities such as chicken breasts, laboratory tests showed a decrease in 25-(OH)D (<24-96 nmol/L) and an increase in alkaline phosphatase (>30 gram units) Blood calcium, blood phosphorus decreased, X-ray wrist film can show the change of vitamin D deficiency rickets of light and heavy, according to laboratory and X-ray examination can exclude growth pain, rheumatism, rheumatoid disease.

Examine

Vitamin D deficiency check

Blood biochemical examination: rickets, osteomalacia active blood calcium can be normal or low [normal 2.2 ~ 2.7mmol / L (9 ~ 11mg / dl)]; blood phosphorus decreased [adult normal 0.9 ~ 1.3mmol / L (2.8 ~ 4mg / dl), children normal 1.3 ~ 1.9mmol / L (4 ~ 6mg / dl)], calcium and phosphorus product <30 (normal 40).

Increased blood alkaline phosphatase (normal 15 ~ 30 gold units), this method is a commonly used indicator for the diagnosis of rickets, but lacks specificity, and is greatly affected by liver disease, in recent years advocated bone alkaline phosphatase determination, normal reference The value is 200g/L. The alkaline phosphatase in serum is mainly composed of bone alkaline phosphatase, which is secreted by osteoblasts. When vitamin D is deficient, the cells are active and the serum alkaline phosphatase is elevated. The degree is closely related to the severity of rickets, and the sensitivity to early diagnosis of rickets is high. Serum 25-(OH)D is normal 12-200 nmol/L (5-80 ng/ml); serum 1,25-(0H)2D is normal 40-160 pmol. /L (16 ~ 65pg / ml), because the concentration of 25-(OH)D is three levels higher than 1,25-(OH)2D, even if the 25-(OH)D is at a low level, patients with vitamin D deficiency have enough The matrix of 25(OH)D-1 hydroxylase, therefore the serum 1,25-(OH)2D concentration has little value in evaluating vitamin D deficiency, and the blood biochemical tests in the recovery period return to normal.

1. X-ray examination of the early stage of rickets only shows that the temporary calcification of the long bones is blurred and thinned, and the grinding angle disappears on both sides. The typical change is that the temporary calcification band disappears. The cartilage of the osteophytes is brush-like, the cup is changed, and the epiphysis is The distance between the metaphysis is increased, the bone of the long bone is decalcified, the bone is thinned, the bone is obviously sparse, the density is reduced, the trabecular bone is thickened, the arrangement is disordered, and the backbone can be bent or fractured. The temporary calcification zone is restored during the recovery period. It is neat, dense, and has an increased bone density.

There is no special change in the early X-ray of osteomalacia. Most patients have different degrees of osteoporosis, bone density decreases, the long cortical bone becomes thinner, some have pathological fractures, and severe X-ray shows anterior and posterior curvature of the spine and vertebral body. Severe decalcification and atrophy, biconcave deformity, pelvic stenosis, pseudo-fracture (also known as Looser belt); can be considered as a feature of X-ray changes in adult osteomalacia, decalcification of banded bone, length on X-ray films Light-transmissive tapes ranging from a few millimeters to a few centimeters are generally perpendicular to the bone surface. These light-transmissive bands are often bilateral and symmetrical, especially at the pubic, ischial, femoral neck, rib and shoulder rim. As typical.

2. Bone mineral content has become an important indicator of bone mineralization abnormalities caused by various pathological factors of bone metabolic diseases. At present, single photon absorption method is widely used in China, and this method is used to measure sputum bone minerals in different stages. The content of the skeletal and bone softening disease was found to be significant in the initial stage of rickets and in the final stage.

Diagnosis

Diagnosis and identification of vitamin D deficiency

Diagnostic criteria

1 medical history

(1) Mother's eating habits, whether vitamin D and calcium are added during pregnancy.

(2) Whether the child is a premature or immature child, birth season, feeding history and supplementary food addition, living conditions, sunshine, vitamin D and calcium addition.

2. Symptoms early due to low blood calcium visible sweating, especially in the head sweating, regardless of room temperature and season, sleep convulsions, easy to cry, irritability, hand and foot sputum (blood calcium decreased to 1.996mmol / L, that is, 80mg / L), anemia, repeated respiratory infections, the above symptoms are more common in infants within 6 months, adult osteomalacia, more common in women, may have limbs sore, especially at night, mostly in the lower back along the spinal nerves.

3. Signs pale, muscle relaxation, occipital alopecia, deciduous teeth late, late closure of the cardia, delayed development, "ping-pong head" caused by softening of the skull, chest examination; ribs at the junction of ribs and costal cartilage Beaded, ribbed eversion, ribbed soft groove (Harrison ditch) and "chicken chest", the wrist of the limbs has a blunt rounded "bangle", "ankle bracelet", the two legs are close together and the two knees are separated It is an "O" shaped leg; otherwise, the knee joint is close and the ankle joint is an "X" shaped leg, leaving 3 cm as mild, 3 to 6 cm as moderate, and >6 cm as severe.

Differential diagnosis

1. Renal rickets (renal rickets) caused by congenital renal hypoplasia, chronic nephritis and other renal dysfunction, causing skeletal deformities, although low blood calcium, but rarely cause hand and foot spasm.

2. The clinical manifestations of renal tubular acidosis are mainly hypokalemia and rickets, and renal calcification or kidney stones may occur.

3. Fanconi syndrome is characterized by amino aciduria, renal glucosuria, increased urinary phosphorus, hypophosphatemia, developmental delay and severe rickets. 4. Others should be weakened with sweat and mild hydrocephalus. , intelligent low caused by various reasons, slow development of motion, cretinism (back bone age) and cartilage malnutrition (hereditary diseases) and other diseases.

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