What Is the Treatment for Osteomalacia?

Osteomalacia

Osteomalacia (ricketsandosteomalacia) is a skeletal disease characterized by newly formed bone matrix mineralization disorders. As a result, non-mineralized bone-like tissue (osteoid) accumulates and the bone softens, resulting in a series of clinical symptoms and signs such as bone pain, bone deformity, and fracture. The epidemic characteristics of osteomalacia have important relations with living environment, nutritional level and living habits. In the past, this kind of disease mostly occurred in infants and young children with poor breastfeeding conditions, prolific women and long-term breastfeeding women, but now it is rare. The disease is more common among residents of industrial cities who have long lacked outdoor activities, lacked sunlight, and had severe environmental pollution. The prevalence of the disease is 36.2%, which is higher in women than in men. The high-incidence population is 30 to 39 years (55.85%).

Osteomalacia disease description

Vitamin D nutritional deficiency. Deficiency of metabolic activity of vitamin D. Deficiency of minerals in bone mineralization sites. Bone cells and bone matrix disorders.

Rickets occurs before puberty, that is, before the long bone growth plate is closed to the closed period. In adults, bone mineralization after the epiphyseal growth plate is closed is called osteomalacia. Osteomalacia begins in children. There is bone rebuilding in a person's life, that is, bone tissue is constantly undergoing renewal and replacement (bone conversion) of bone resorption and bone formation, and it affects all surfaces (or coatings) of bone Epiperiosteal surface, endoperiosteal surface, inner surface of cortex (inner surface of Haver's canal) and inner surface of trabecula. The pathological changes of osteomalacia are manifested in almost all bone surfaces due to mineralization disorders, and there is a large amount of osteoid accumulation, which makes the bone softer, the trabeculae thinner and reduced, the intracortical Haval system, It is irregular, and there are large pipelines. Osteoid hyperplasia is an important feature of rickets and osteomalacia, but it is not unique to them. It also occurs in diseases with a high rate of bone turnover, such as primary hyperthyroidism, Paget bone disease, hyperthyroidism and fluorosis, and after the administration of certain diphosphates.

Osteomalacia symptoms and signs

Osteomalacia Osteomalacia is because only 5% of adult epiphysis is newly added bone each year. It takes a considerable time to form new bone with insufficient mineralization, causing osteomalacia, so early symptoms are often not obvious. With the increase of osteomalacia, bone deformity caused by long-term weight-bearing or muscle stretching during activity, or the sensory nerve terminal that touches the periosteum causes obvious bone pain. Onset or intermittent, obvious in winter and spring, intensified in late pregnancy and lactation. After a few months or years, it becomes persistent, and develops into severe and severe generalized bone pain. He becomes more active during walking and walking, and may have lameness and duck gait. It is difficult to bend, comb, and turn over. In severe cases, the bone is further softened, and thoracic invagination and sternal protrusion can form chicken breasts, which affects heart and lung function. Long-term bed rest and sitting can shorten the cervical spine, lumbar lordosis, and thoracic kyphosis, leading to scoliosis, kyphosis, and shortened height. Bone becomes soft and bears weight for a long time, making the promontory sink and lordosis, the pubic protrusion protruding into a bird's beak shape, two acetabulums invading, the pubic bone arch forming an acute angle, the pelvis showing a chicken heart or trilobate deformity, which can cause dystocia. Muscle weakness is also prominent

Osteomalacia Symptoms, especially in patients with marked hypophosphatemia. Hands cannot hold heavy objects or lift up, cannot stand independently after squatting with both legs, often need to support or rely on others, can not turn over and sit up by themselves, or the above action requires a lot of effort to complete slowly, its The mechanism is related to phosphorus depletion in muscle cells. Loss of long-term activity can lead to atrophic muscle atrophy, more muscular weakness, and is easily confused with primary myopathy. In patients with this type of osteomalacia, minor trauma can lead to pathological fractures, especially fractures of the ribs, and the patient may not even know after the occurrence. Most osteomalacia are accompanied by increased levels of compensatory parathyroid function due to a decrease in blood calcium, and some even have obvious secondary hyperparathyroidism, which further aggravates bone disease and complicates the diagnosis. Although secondary hyperparathyroidism can increase blood calcium, but increase the hypophosphatemia, make muscle weakness and myopathy more obvious.

Causes of Osteomalacia

The disease is characterized by the inability of the newly formed bone matrix to mineralize in a normal manner. Bone mineralization is a complex process involving many factors such as calcium and phosphorus metabolism, osteoblast function, and the acid-base environment of the mineralized site. The causes of rickets and osteomalacia include the following:

1. Vitamin D deficiency Vitamin D plays an important role in the metabolism of calcium and phosphorus in the body, can promote the absorption of calcium and phosphorus in the small intestine, increase the reabsorption of calcium and phosphorus by the renal tubules; stimulate the resorption of bone calcium; Mobilize the dissolution of bone salts; maintain

Osteomalacia The normal concentration of calcium and phosphorus in the blood is conducive to the deposition of bone salts in bone and promotes the formation of new bone. Therefore, vitamin D deficiency and metabolic disorders are important causes of rickets and osteomalacia. There are many causes of vitamin D deficiency, including:

(1) Insufficient sunshine:

It is estimated that people exposed to sunlight can produce 6U vitamin D3 per square centimeter of skin per hour, and normal sunlight can produce vitamin D310 100g per day. If there is a sufficient calcium and phosphorus diet, it is enough to prevent rickets and osteomalacia. Occurs, but many factors can affect the amount of sunlight and UV absorption, such as season, temperature, air pollution, and so on. Season can significantly affect the amount of sunlight and the production of vitamin D. In winter and spring, due to the reduction of sunlight exposure, the relationship between 25- (OH) D3 level and ambient temperature is greater than the average daily sunlight exposure. With the development of industry, industrial smoke, Coal dust pollution further reduces useful UV light, and in fact rickets may be the first example of an air-polluting disease. In addition, skin pigmentation, traditional clothing habits, and reduced outdoor activities are also important reasons for reduced sunlight exposure. Deeper skin pigmentation can lead to a decrease in UV absorption. In cold regions or near the equator, babies are wrapped too tightly to avoid cold or hot sunlight. Asian girls and women are used to staying indoors, wearing traditional clothing and closing curtains in boudoirs. Can make mothers and children have insufficient sunlight. In recent years, cities have become increasingly crowded, with dense buildings, rapid rises in floors, gradual decrease in street sunlight, people's intense work, and reduced outdoor activities, especially the longevity of many elderly people and the decline of their internal metabolism. Causes nutritional vitamin D deficiency, osteomalacia or subclinical osteomalacia.

(2) Insufficient intake:

Rickets has been reported in some children in the United States as a vegetarian. There are also regions where flour contains higher amounts of phytate and lignin. Phytate can combine calcium and zinc to increase its excretion. Lignin can form a complex with bile acid and affect the absorption of vitamin D. Both Causes osteomalacia.

(3) Gastrointestinal lesions and postoperative malabsorption of vitamin D:

Biliary diseases such as biliary cirrhosis, biliary obstruction affect the absorption of fat, but also the absorption of fat-soluble vitamin D; poor pancreatic function can also cause decreased vitamin D absorption.

4) Malabsorption:

Many of the current causes of vitamin D deficiency are small bowel, hepatobiliary dysfunction, and pancreatic disorders with intestinal malabsorption. In the case of malabsorption syndrome, vitamin D loss includes not only vitamin D given orally, but also endogenous products. These disorders include: after gastrectomy, small bowel resection or bypass anastomosis, Crohn's disease, gluten refractory disease, regional enteritis, diverticulum multiple malnutrition, stagnation (blind) ring syndrome, scleroderma, exocrine pancreas Insufficiency, pancreatic duct obstruction, chronic fatty diarrhea, biliary obstruction, extrahepatic bile duct obstruction, congenital bile duct atresia, etc. A British report reported that 25% of patients with small bowel bypass surgery have histological evidence of osteomalacia and 25- (0H) D3 levels have been reduced, but X-ray findings of osteomalacia are less common. Osteomalacia is also one of the surgical complications of partial gastrectomy (usually Type II), but the reported incidence of bone disease varies widely. Edd compared the radiological examination of patients with gastrectomy and peptic ulcer without surgery, which showed that the anterior group had obvious lesions in the mineralization of the thorax and lumbar vertebra, and pathological fractures occurred in 5.8%. Most previous studies have suggested that an important common feature of vitamin D deficiency in gastrointestinal nutrition disorders and hepatobiliary disorders is to interfere with the enterohepatic circulation of 25- (0H) D3, but recent studies by Clement et al. Have shown that the intestines of 25- (OH) D3 Hepatic circulation is insignificant, so 25- (OH) D3's enterohepatic circulation is responsible for vitamin D deficiency, and there is no consensus. For the absorption of vitamin D, bile salts are necessary, and bile duct obstructions such as congenital atresia of the bile duct and extrahepatic duct bile duct obstruction all have reduced vitamin D levels. The incidence of osteomalacia with pancreatic disorders and malabsorption is not high, and 25- (OH) D3 levels are also different, but they may have significantly lower calcium and secondary parathyroidism. In short, rickets and osteomalacia caused by gastrointestinal and hepatobiliary disorders are often the result of multiple factors. In addition to vitamin D malabsorption disorders, calcium, phosphorus, and magnesium are often accompanied by malabsorption of calcium, phosphorus, and magnesium. Diarrhea causes systemic malnutrition, which can affect vitamin D levels and bone mineralization. There is also a drug cholestyramine that binds bile acid in the intestine, increasing the risk of osteomalacia, even exceeding the primary disease it treats.

(5) It is not uncommon for osteomalacia to occur in women who are relatively prone to early marriage and prolificacy due to increased vitamin D requirements, especially in Asia. This may be related to the tradition of having many children and blessings in the area, the custom of staying out of doors and closing doors and windows at the end of pregnancy and lactation. During pregnancy and lactation, the mother's calcium requirement is greatly increased. The bones of newborn babies contain about 23g of calcium and 14g of phosphorus. Most of these minerals are obtained from the mother at the end of pregnancy. Breastfeeding women pay 300-500mg of calcium every day. At this time, the mother does not have a large amount of vitamin D synthesis and a sufficient amount of calcium supplement, which can easily lead to osteomalacia. Babies, especially premature babies, are also at a period of increasing vitamin D requirements. In addition to artificially fed babies who are susceptible to rickets due to imbalanced intake of milk calcium and phosphorus, recent studies have shown that the content of vitamin D in breast milk is only 40-50 U / L. D sulfate activity is only 1% to 5%, which cannot prevent the occurrence of rickets. Furthermore, puberty (11-17 years) has strong bone development, blood 25- (0H) D3 level is low, and vitamin D supplement is often ignored during this period, which is an important cause of delayed osteomalacia.

Osteomalacia Pathology

Osteomalacia Vitamin D deficiency mainly causes osteomalacia, which is a metabolic skeletal disease caused by calcium D deficiency caused by vitamin D deficiency, which is characterized by poor calcification of bone-like tissue and bone growth disorders. In the absence of vitamin D, the absorption of calcium and phosphorus in the intestine decreases, which reduces blood calcium and blood phosphorus. The decrease in blood calcium promotes increased secretion of parathyroid glands, which promotes osteoclasts to dissolve bone salts, decalcifies old bones, and enters bone calcium. The blood maintains calcium near normal. However, parathyroid hormone can inhibit the reabsorption of renal tubular phosphorus, resulting in increased urine phosphorus, decreased blood phosphorus, and decreased calcium-phosphorus product in the blood (<40), hindering the calcification of bone formation in the body and compensating osteoblasts. Hyperplasia, causing the accumulation of osteoid tissue at the epiphyseal end and subperiosteal level, causing osteomalacia. If the parathyroid glands are unresponsive and bone calcium cannot be quickly released into the blood, the blood calcium decreases. If total blood calcium drops to 1.75 to 1.87 mmol / L (7 to 7.5 mg / dl), free blood calcium is less than 0.88 to 1.0 mol / L (3.5 to 4.0 mg / dl), and hypocalcemic convulsions occur.

Osteomalacia epidemiology

diagnosis

The epidemic characteristics of osteomalacia have important relations with living environment, nutritional level and living habits. In the past, this kind of disease mostly occurred in infants and young children with poor breastfeeding conditions, prolific women and long-term breastfeeding women, but now it is rare. The disease is more common among residents of industrial cities who have long lacked outdoor activities, lacked sunlight, and had severe environmental pollution. In terms of geographical distribution, the incidence of rickets and osteomalacia in southern China is much lower than in the north, where winter is long and the sun is short. As the rate of rickets and osteomalacia related to environmental and nutritional disorders declines, due to the patient's own abnormal vitamin D and phosphorus metabolism, family inheritance or drugs, and rickets associated with tumors or other diseases (osteomalacia The proportion of patients is increasing. With the improvement of people's quality of life, the incidence of traditional osteomalacia has decreased significantly in some developed regions, while the incidence of osteomalacia caused by environmental factors and lifestyle changes is rising. Many cases of low-conversion uremic bone disease caused by aluminum poisoning and severe bone diseases including osteomalacia caused by living habits in rural Guiding County, Guizhou, have been reported in China. Guo Kaijin and others carried out an epidemiological survey of osteomalacia in 2743 ordinary people and found that the prevalence of the disease is 36.2%, and women are higher than men. The high-incidence population is 30 to 39 years (55.85%), and the disease The rate was normal distribution with age, and the military population was higher (47.5%). Piedre and Oliveri reported osteomalacia caused by dieting in Spain (41 cases) and Argentina (1 case), respectively. Patients with severe anorexia can develop osteoporosis or osteomalacia, with spine or rib fractures.

Osteomalacia diagnosis test

Diagnosis: should be based on medical history, clinical manifestations, blood biochemical examination and X-ray bone examination. The latter two tests are more diagnostic for atypical cases and staging of rickets.

(1) Developmental delay and height below normal range.

(2) The child's expression is indifferent and irritable, or he is very quiet, he is not willing to move, prefer to sit, not stand and walk.

(3) In the sitting position, the abdomen is swollen (his diseased abdomen).

(4) Skulls of young children become soft, square skull and forehead protrusions and dentin defects.

diagnosis

(5) The junction of rib cartilage on the chest wall is beaded. The lower ribs are uneven and become Harrison sulcus. The posterior process of the thoracic vertebrae but rare scoliosis are rare.

(6) The wrist, ankle, knee, and elbow joints are significantly enlarged, and arch deformities of the lower limbs. Sometimes accompanied by fractures, a few may have femoral skull condyle slippage.

X-rays of rickets show the following characteristics: The length and length of the growth plate are increased, the calcification is poor, and the arrangement is disordered. The edge of the ossification center of the epiphyseal plate is uncertain. Bone softening, bending deformity, etc.

2. Osteomalacia has relatively fewer positive signs. Patients often complain of fatigue, fever and bone pain. Bone pain is diffuse, difficult to locate, and may be accompanied by extensive tenderness of the bone. The latest findings of osteoporosis caused by osteoporosis in older people may be the latest findings.

3. X-ray film is also non-specific for the difficulty of diagnosis of osteomalacia due to bone loss. Many changes include malformations of long bones, pelvis and spine, and skull that are the same as rickets. The total number of trabeculae decreases and the remaining trabeculae appear marked and rough. There are hyaline areas in the cortical bone area. Pseudo fractures can occur, similar to stress fractures, but the difference is that the pseudo fracture can occur in non-weight-bearing bones and can exist symmetrically.

4 Blood biochemical examination Osteomalacia can be normal or low in the active phase, [normal 2.2 2.7mmol / L (9 11mg / dl)]; blood phosphorus decreased [0.9 1.3mmol / L (2.8 4mg) normal for adults / dl)], [children's normal 1.3 to 1.9 mmol / L (4 to 6 mg / dl)], calcium-phosphorus product <30 (normal 40). Increased serum alkaline phosphatase (normally 15-30 Gin units). This method is a commonly used indicator for the diagnosis of rickets, but it lacks specificity and is greatly affected by liver disease. In recent years, the measurement of bone alkaline phosphatase has been promoted, and the normal reference value is 200 g / L. Bone alkaline phosphatase is the main alkaline phosphatase in serum and is secreted by osteoblasts. When vitamin D deficiency, the cell is active. Serum bone alkaline phosphatase is elevated, and the degree of elevation is closely related to the severity of osteomalacia, and it is highly sensitive to the early diagnosis of rickets. Serum 25- (OH) D3 [normal 12 200nmol / L (5 80ng / ml)]; serum 1,25- (0H) 2D3 [normal 40 160pmol / L (16 65pg / ml)] in the early stage of activity It has been reduced and is more sensitive to early diagnosis (but the values measured by different laboratories vary widely). Blood biochemical examination during the recovery period returned to normal.

5. X-ray skeletal features Early stage of rickets only showed a temporary thinning of the temporary calcification band on the metaphysis of the long bone, and the angle of wear on both sides disappeared. The typical change of the active period was the disappearance of the temporary calcification band. The shape changes, the distance between the epiphysis and the metaphysis is increased, the long bones are decalcified, the bones are thinned, the bones are significantly sparse, the density is reduced, the trabecular bones are thickened and the arrangement is disordered. There may be a bent or fractured backbone. During the recovery period, the temporary calcification zone reappeared, gradually tidy, dense, and bone density increased.

Early X-rays of osteomalacia may have no special changes. Most patients have varying degrees of osteoporosis, decreased bone density, thin long cortex, and some with pathological fractures. In severe cases, the X-ray showed anteroposterior and lateral curvature of the spine, severe decalcification and atrophy of the vertebrae, and a double concave deformity.

Osteomalacia Shape, pelvic stenosis, pseudo fracture (also known as Looser band); the characteristics of X-ray changes in adult osteomalacia can be considered to be band-shaped decalcification, and the length on the X-ray film ranges from a few millimeters to a few centimeters. The light-transmitting belt is generally perpendicular to the bone surface. These light-transmitting bands are often bilateral and symmetrical, especially the pubic bone, ischium, femoral neck, ribs, and axillary margin of the scapula. Bone mineral content has become an important indicator for studying bone mineralization abnormalities caused by various pathological factors of bone metabolic diseases. At present, the single photon absorption method is more commonly used in China. This method was used to determine the bone mineral content of rickets in different stages, and it was found that the bone mineral content of rickets was reduced in the early and acute stages, which has great significance for the diagnosis of rickets and osteomalacia.

Osteomalacia laboratory test

Biochemical change

(1) Blood calcium and phosphorus: due to different causes and degrees of rickets and osteomalacia and secondary hyperparathyroidism, the blood calcium and phosphorus can have the following six changes:

blood calcium is reduced, blood phosphorus is normal or low, such as mild nutritional vitamin D deficiency rickets.

Blood calcium is normal or low, and blood phosphorus is significantly reduced, such as X-linked hypophosphatemia, renal tubules, and tumorous osteomalacia.

Calcium and phosphorus were significantly reduced, such as vitamin D-dependent rickets type and severe vitamin D deficiency rickets with secondary hyperparathyroidism.

Hypocalcemia and normal blood phosphorus, such as idiopathic hypoparathyroidism and renal bone disease (uremic bone disease).

Normal or elevated blood calcium and normal blood phosphorus, such as familial hypoalkaline phosphatase.

Blood calcium and phosphorus are normal, such as axial osteomalacia and bone fibrosis.

(2) urinary calcium and phosphorus: urinary calcium of osteomalacia caused by various reasons is different, but most of the rickets and osteomalacia have a prominent feature, that is, the 24h urine calcium is significantly reduced, generally at 50mg Left and right, some can't even be measured. A small number of osteomalacia and osteomalacia, urinary calcium can be normal or increased. There are many inconsistencies in urine phosphorus, which are related to phosphorus intake and the presence or absence of secondary parathyroidism.

(3) Blood alkaline phosphatase (AKP) and urinary hydroxyproline (HOP): most rickets and osteomalacia, blood AKP and 24h urine HOP are mild and moderately elevated, and often associated with bone lesions The severity is related. However, familial hypophosphataemia is reduced, dysplasia at the metaphysis, and axial osteomalacia are normal.

Differential diagnosis of osteomalacia

Osteomalacia First, it should be distinguished from rickets caused by other causes. For the clinical diagnosis of vitamin D deficiency rickets, the effect is not good after treatment with a sufficient amount of vitamin D 30,000 g (1.2 million U), anti-vitamin D rickets should be considered, often related to kidney disease. Such diseases include:

1. Vitamin D-dependent rickets have a family history. Type occurs in infants less than 1 year old, with short stature and incomplete enamel growth. Rickety skeletal deformity. Blood biochemical features include hypocalcemia, hypophosphatemia, markedly increased alkaline phosphatase activity, and amino aciduria. The onset of type is early, and it is characterized by hair loss in the first few months after birth. Skin damage also has type clinical characteristics.

2. Hypophosphatemic anti-D rickets are sex-linked inheritance, and can also be autosomal dominant or recessive, so they often have family history. It is more common after 1 year old, and active rickets still appear after 2 to 3 years old, often with severe bone deformity. Blood biochemical characteristics are extremely low blood phosphorus and increased urine phosphorus. These patients need to be replenished with phosphorus for life.

3. Distal renal tubular acidosis is congenital deficiency of distally curved renal tubules, which causes insufficient loss of hydrogen ions, causing sodium, potassium, and calcium cations to be lost from the urine, alkaline urine excretion, blood biochemical changes, and low blood calcium, phosphorus, and potassium High blood chlorine, often with metabolic acidosis. These patients have severe skeletal deformities, decalcified bones, and children with short stature.

4. Renal rickets can cause renal dysfunction due to congenital or acquired causes, leading to low blood calcium and high blood phosphorus, 1,25- (0H) 2D3 production decline and secondary hyperparathyroidism, and bone decalcification generally , More common in late childhood, there are symptoms of primary disease and changes in urine and renal function. The skeletal system changes of rickets, such as large head, large front palate, slow closing, and slow growth and development should be distinguished from petty disease and cartilage malnutrition. The sickness has a special face, the lower part is extremely short, with low intelligence, normal blood calcium and phosphorus, X-ray examination of the ossification center appears delayed, but the calcification is normal. Cartilage is malnourished, limbs are short, blood calcium and phosphorus are normal, X-rays show that long bones are short and thick, and the metaphysis is broadened to a trumpet shape, but the outline is smooth.

Osteomalacia treatment options

medical treatement:

Find the cause, and treat the cause, such as vitamin D and derivatives, calcitonin, phosphate and so on. There are no effective treatments for rickets and osteomalacia caused by genetic factors in some patients. For nutritional vitamin D deficiency rickets and osteomalacia, usually small to moderate doses of vitamin D treatment can cure it. In addition to etiological treatment, vitamins and calcium supplements are mainly used.

1. Vitamin D The currently commonly used vitamin D preparations are cod liver oil, concentrated cod liver oil, vitamin D2 and D3, and some vitamin D active metabolites and vitamin D derivatives, such as 25- (OH) D3, 1- (OH) D3, 1, 25- (0H) 2D3, DHT. Generally use the parent vitamin D preparation, that is, vitamin D2 or D3 is sufficient to be effective, both have the same effect. Colic liver oil or concentrated cod liver in mild cases

medical treatement Oil, heavier patients need direct intramuscular injection of vitamin D2 or D3. Unless the patient has severe rickets and osteomalacia or is accompanied by severe hypocalcemia, the use of active vitamin D may be effective about one month earlier than the mother's vitamin D. However, dihydrotachysterol is not effective in treating this disease, and the drug has similar PTH. Effect, better treatment of hypoparathyroidism.

(1) Vitamin D metabolism deficiency liver 25- (OH) D3 production is reduced: this kind of rickets and osteomalacia should actively treat the primary disease, and in addition, daily doses of vitamin D or 25- (OH) D3 can be taken orally cure. However, in patients with primary biliary cirrhosis, chronic vitamin D depletion is shown, short-term vitamin D is ineffective, and longer-term vitamin D treatment is required. Patients with liver disease are better treated with 25- (OH) D3, because it does not need to be hydroxylated in the liver, is easily soluble in water and can be better absorbed, and less dependent on bile salts than vitamin D2 or D3 absorption. Dosage: mild patients can start from 50g / d, severe patients can take 1130 200g / d orally, and the maximum can be 300g / d. Prevent oral 20g daily. The vitamin D requirement of premature infants is 3 to 6 times higher than that of full-term infants, so the vitamin D dose for treatment is larger than the recommended dose for normal children, 4000U per day.

(2) Hereditary vitamin D-dependent rickets: Treatment with general doses of vitamin D and 25- (0H) D3 is ineffective, and symptoms can be alleviated only by giving large doses of vitamin D (that is, several times to tens of times the general treatment amount). A physiological dose of alfacalcidol is 100 times less effective than the parent's vitamin D dose. However, life-long medication is needed. Once the medication is interrupted, the performance can reappear, so it is called vitamin D-dependent rickets. During the disease active period, the mother's vitamin D is required to be 40,000 to 80,000 U / d or 25- (0H) D375 to 150 g / d, and the maintenance amount of vitamin D is 200,000 U / week or 25- (OH) D350 to 70 g / d. For example, 1,25- (0H) 2D3 can give 1.5 2.5g / d, the maintenance amount is 0.75 1g / d, and l- (OH) D32 4g / d can also be used.

(3) Rickets and osteomalacia (nephrotic bone disease) caused by chronic kidney disease: First of all, actively treat the primary disease and correct metabolic acidosis. Patients with renal insufficiency should be given phosphate binder aluminum hydroxide gel early to inhibit hyperphosphatemia, which can prevent and delay the occurrence of renal bone disease, and can also reduce soft tissue calcification. It is not effective to give ordinary vitamin D preparations. Alfacalciferol should preferably be 0.25 to 2 g / d, and 1- (OH) D31 to 3 g / d can also be used. When ordinary vitamin D is given unconditionally, large doses should be used.

(4) Hypoparathyroidism and pseudohypoparathyroidism: If the mother's vitamin D is used, a large dose is required, ranging from 10,000 to 400,000 U / d, and blood and urine calcium should be regularly reviewed. Note that often high blood calcium can occur before the blood calcium completely reaches normal. In this case, reduce the amount of urine in time to prevent excessive urine calcium from causing urinary stones and kidney calcification. Thiazine derivatives can reduce urine Calcium is lost. Dihydrotachysterol (DHT) has a similar effect to PTH, and has obvious efficacy in the treatment of this disease. Its oil (also known as AT10) is 1 to 3 ml per day, and it is changed to 0.5 to 1 ml / d after improvement. It can also use 1- (0H) D32 4g / d, or 1,25- (OH) 2D30.5 2.5g / d. When taking the above vitamin D preparation, you need to add calcium and pay attention to reduce blood phosphorus. Aluminum hydroxide gel.

Osteomalacia complications

1. Most osteomalacia are accompanied by increased levels of compensatory parathyroid function due to a decrease in blood calcium, and some even have obvious secondary hyperparathyroidism.

2. Rickets long bones and bones are deficient in calcium and softened due to stress, and "O" -shaped legs (knee varus), "X" -shaped legs (knee valgus), and lower tibia are tilted forward, forming saber deformities. Patients with severe rickets and infants with rickets can develop hand-foot convulsions due to severe hypocalcemia, and can even cause systemic convulsions, laryngeal spasms, suffocation and death.

3. Osteomalacia can cause the pelvis to become smaller. Due to the softening of the pelvic bone, it cannot effectively support the spine, causing the pelvic organs to move down and causing pelvic stenosis.

Prevention of osteomalacia

As calcium and vitamin D fortified foods have not been widely used in China, the dietary calcium and vitamin D content is generally low. In addition, the northern region of China has longer winters and shorter sunshine hours. The incidence of rickets in children under 3 years of age is higher, and Subclinical vitamin D deficiency in older children and osteomalacia in pregnancy and lactation often occur, so it is very important for the prevention of rickets and osteomalacia

prevent disease Necessary and permanent. According to the survey of calcium intake in the Chinese population, the vast majority of people are below 80% of the nutritional standard, and some children are only 20% to 50%. Therefore, the appropriate amount of calcium supplementation for infants and young children and late pregnancy, lactation, postmenopause Women and older people with malabsorption are also necessary. Calcium supplementation for children should be 20-30mg / (kg? D), 500mg / d for postmenopausal women and the elderly, and 500-1000mg / d for pregnant and lactating women. If you take calcium for a long time, it is more reasonable to take it intermittently, because it has been proven that high calcium can increase the net absorption rate of aluminum, which is especially bad for the elderly. It can promote the occurrence of brain softening and osteoporosis. There will be a decrease in the net absorption rate of compensatory intestinal calcium. Therefore, taking calcium for 2 months can be interrupted for 1 month. Each fixed amount of calcium supplement should be divided into 550mg doses or smaller, so that the net absorption rate of calcium will be higher. When long-term application of calcium to a few children, there will be loss of appetite, constipation, and even anemia. At this time, it is not necessary to emphasize the supply of conventional calcium, and a high-calcium diet should be given. ^[1]