Osteitis fibrosus

Introduction to fibrous osteitis Fibrous osteitis is a highly transportable bone disease caused by hyperparathyroidism secondary to chronic renal failure. The main cause is secondary hyperparathyroidism, hyperparathyroidism, hyperfunction, leading to hypocalcemia, hyperphosphatemia, especially the lack of dihydroxycholecalciferol, advanced skeletal lesions, itchy skin, spontaneous Muscle tendon rupture, soft tissue calcification, etc. Clinically, it mainly manifests as pathological changes of fibrotic osteitis. basic knowledge The proportion of illness: 0.03% Susceptible people: no specific population Mode of infection: non-infectious Complications: fractures

Cause of fibrotic osteitis

(1) Causes of the disease

Chronic renal failure is the main cause of fibrotic osteitis.

(two) pathogenesis

In renal failure, due to the destruction of renal tissue, urinary phosphorus is reduced, blood phosphorus is increased, and the synthesis of 1,25-(OH)2D3 is reduced, which reduces the ability of the intestinal tract to absorb calcium and produces hypocalcemia. Among them, the synthesis of 1,25-(OH)2D3 is reduced, causing parathyroid hyperplasia and hyperfunction, leading to pathological changes mainly manifested in fibrotic osteitis, in addition to osteoporosis, osteosclerosis or osteomalacia. .

In the early stage of renal failure, secondary hyperparathyroidism may occur. When the glomerular filtration rate (GFR) is reduced to 50-60 ml/min, the whole plasma parathyroid hormone (iPTH) tends to increase. This is mainly due to the disorder of the parathyroid hormone-VD axis, that is, the synthesis of dihydroxycholecalciferol [1,25-(OH)2D3] is disturbed, and the early stage of renal failure, serum 1,25-(OH)2D3 The level is often at or below normal, and its low level can lead to excessive secretion of the parathyroid glands and reduce intestinal absorption of calcium.

The synthesis of dihydroxycholecalciferol is reduced in the early stage of renal failure, unlike the result of small kidney volume, because the early kidney volume does not become small, probably due to functional damage of the kidney biosynthesis of dihydroxycholecalciferol Because the restriction of phosphorus intake in this patient can increase the level of dihydroxycholecalciferol, and the accumulation of phosphorus in the renal tubular cells in the early stage of renal failure can lead to a decrease in the biosynthesis of dihydroxycholecalciferol. And raise the level of parathyroid hormone.

Other additional factors may also be involved in the occurrence of secondary hyperparathyroidism. The theory of "correction of imbalance" proposed by Bricker et al. suggests that blood phosphorus increases in the early stage of renal failure and directly reduces the amount of ionized calcium in the blood. Liach and Massry found that In the early stage of renal failure, plasma ionized calcium levels decrease, and then the release of parathyroid hormone may be promoted by the release of pre-formed parathyroid hormone and the synthesis of mRNA of proparathyroid hormone. However, other scholars believe that Hypocalcemia is not a necessary factor for secondary hyperparathyroidism. In summary, the biosynthesis disorder of dihydroxycholecalciferol in early renal failure is an important factor in promoting secondary hyperparathyroidism.

In the late stage of renal failure, the production of secondary hyperparathyroidism is often associated with hypocalcemia, hyperphosphatemia, and especially the lack of dihydroxycholecalciferol.

1. Hypocalcemia leads to at least three factors, namely, phosphorus retention, bone resistance to hypercalcemia of parathyroid hormone (PTH) and vitamin D metabolism disorder.

Acute intake of large amounts of inorganic phosphorus in normal people can cause a transient increase in blood phosphorus, and can also reduce blood calcium and a significant increase in parathyroid hormone. Hyperphosphatemia does not necessarily directly cause hypocalcemia, chronic kidney. Phosphorus retention can cause hypocalcemia by other pathways, so phosphorus retention is one of the causes of hypocalcemia.

Increased blood parathyroid hormone levels can mobilize bone calcium into the blood, which should increase blood calcium, but in renal failure, although the level of blood parathyroid hormone is elevated, often hypocalcemia occurs, suggesting chronic renal function. In the event of depletion, the bones have a resistance to the mobilization of bone-calcium in parathyroid hormone. Animal experiments have shown that this bone is responsive to parathyroid hormone mobilization of bone calcium, which is partly due to insufficient 1,25-(OH)2D3. Correcting this phenomenon relies on providing sufficient amounts of 1,25-(OH)2D3 and 24,25-(OH)2D3, and other studies have shown that this resistance is partly due to downregulation of the parathyroid hormone receptor.

The lack of vitamin D has a major impact on the production of hypocalcemia. Vitamin D in the body comes from the diet, and more importantly, it is formed in the skin. The vitamin D3 present in the skin is irradiated with sunlight (especially ultraviolet rays). , converted to pre-vitamin D3, the former vitamin D3 is further converted into vitamin D3 after the skin's heat, and the vitamin D3 in the skin combines with the vitamin D-binding protein (DBP) in the blood to enter the blood in the form of DBP-D3. The 25-hydroxylase in the liver hydroxylates vitamin D3 on the 25th carbon chain to form 25-(OH)2D3, which is then formed by the 25-(OH)D3-1 hydroxylase produced by the kidney. The powerful 1,25-(OH)2D3,1,25-(OH)2D3 promotes the absorption of calcium in the intestine.

In the late stage of renal failure, due to dietary restrictions, calcium intake is often reduced, and calcium absorption in the intestine is also reduced, which is one of the causes of hypocalcemia.

Clinically, the level of blood calcium in the late stage of renal failure can be low, normal or even increased, the latter often due to severe hyperparathyroidism, aluminum poisoning or excessive vitamin D.

2. Phosphorus in plasma of hyperphosphatemia, only 12% to 15% bind to protein. Therefore, the concentration of phosphorus in the glomerular filtrate is about 90% of the plasma phosphorus concentration, and most of the filtered phosphorus is in the renal tubule. (mainly in the proximal tubules) is reabsorbed, only 15% to 20% of filtered phosphorus is excreted. Under normal conditions, parathyroid hormone can reduce the reabsorption of phosphorus by the renal tubules and increase the excretion of urinary phosphorus. Reduce blood phosphorus levels and keep them in the normal range. Even in the early renal failure, even if the glomerular filtration rate decreases, the increase in plasma parathyroid hormone causes the renal tubular to reduce the reabsorption of phosphorus. Blood phosphorus, still maintained in the normal range, when the glomerular filtration rate drops to about 20ml / min, because the amount of filtered phosphorus is greatly reduced, even if the plasma parathyroid hormone concentration is high, it can not stop the rise of blood phosphorus High, when the glomerular filtration rate drops below 10ml/min, blood phosphorus will increase significantly, leading to hyperphosphatemia, increased parathyroid hormone also promotes bone resorption, and calcium and phosphorus released from bones enters. Extracellular fluid, phosphorus can not be excreted from the urine, so the blood phosphorus level High, leading to hyperphosphataemia, excessive dietary intake of phosphorus-containing foods, beyond the discharge capacity of the kidneys, is also a factor.

In chronic renal failure, phosphorus retention can participate in the development of secondary hyperparathyroidism in three ways:

(1) The synthesis of 1,25-(OH)2D3 can be reduced in the early stage.

(2) Late stage can directly stimulate the secretion of parathyroid hormone and the growth of parathyroid glands.

(3) Promote the gene expression of parathyroid hormone: It has been reported that the experimental end-stage renal disease limits the intake of phosphorus in the diet of the animal, so that the blood phosphorus reaches a normal level, and the plasma parathyroid hormone level can be lowered from 130 pg/ml. By 35pg/ml without affecting blood calcium and dihydroxycholecalciferol levels, the volume of parathyroid glands is also reduced, suggesting that hyperphosphatemia can stimulate the growth of parathyroid glands during renal failure.

In an in vitro experiment, hyperplasia of parathyroid tissue in patients with renal failure was exposed to high concentrations of phosphorus, resulting in an increase in prepro-PTH mRNA (preproPTH mRNA), which promoted the secretion of parathyroid hormone from this parathyroid tissue. .

3. Dihydroxycholecalciferol synthesis reduces 1-hydroxylase when the renal parenchyma undergoes progressive destruction, resulting in inhibition of the biosynthesis of dihydroxycholecalciferol in the kidney, making the dihydroxycholecalciferol thyroid The negative feedback signal of parathyroid hormone weakens and increases the synthesis and release of parathyroid hormone. In addition, the retention of phosphorus (or the increase of the level of phosphorus in the proximal renal tubule) can directly inhibit the kidney to dihydroxycholecalciferol. The synthesis, which reduces the absorption of calcium in the intestines, lowers the level of blood calcium and increases the secretion of parathyroid hormone. It may be more important to reduce the inhibition of the parathyroid hormone by dihydroxycholecalciferol and cause it to proliferate. Increase the secretion of parathyroid hormone, it is also believed that the deficiency of dihydroxycholecalciferol can change the set point between the parathyroid hormone and the serum calcium ion concentration, so that the normal level of calcium ions is also insufficient. To inhibit the secretion of parathyroid hormone, however, other studies have failed to confirm this.

When the glomerular filtration rate (GFR) drops below 30 ml/min, the level of dihydroxycholecalciferol may fall below the normal level due to the retention of phosphorus and the decrease of functional kidney tissue. In patients with renal failure (GFR 40-80 ml/min), dihydroxycholecalciferol levels are reduced, and treatment with dihydroxycholecalcitol can reverse hyperparathyroidism in early and late renal failure.

In addition to the retention of phosphorus, experimental studies suggest that retention of some substances, including uremic toxins and uric acid, in renal failure can reduce the conversion of 25-hydroxycholecalciferol to dihydroxycholecalciferol. The phenomenon has also been confirmed in patients. It has been reported that 9 patients with chronic renal failure (mean serum creatinine concentration of 3.6 mg / dl or 316 mol / L) reduced serum uric acid from 7.3 mg / dl to 4.0 mg / dl (434 238 mol/L) resulted in an increase in dihydroxycholecalciferol levels from 31 pg/ml to 38 pg/ml, while plasma calcium, phosphorus and parathyroid hormone levels did not change.

There are also indications that the hypoparathyroidism is low in response to dihydroxycholecalciferol and is also involved in the progression of hyperparathyroidism. The physiological concentration of dihydroxycholecalciferol does not inhibit the secretion of parathyroid hormone, which may be Due to a decrease in the number of dihydroxycholecalciferol receptors in the parathyroid glands, low dihydroxycholecalciferol levels may play an important role in reducing their receptors because a therapeutic dose of dihydroxycholecalciferol can be administered. To correct this phenomenon, in the late stage of the disease, the retained uremic toxins play a role by reducing receptor synthesis and reducing the binding of the active hormone-receptor complex to the vitamin D response component in the nucleus.

Observations in maintenance hemodialysis patients have shown that the reduction in receptor density in nodular parathyroid glands is more pronounced than in diffuse proliferative parathyroid glands, so the reduction in the number of dihydroxycholecalciferol receptors may be in thyroid Progression of parathyroidism and proliferation of parathyroid cells are involved in the formation of nodules, which may also explain the super-physiological level of dihydroxycholecalciferol (administered intravenously or intraperitoneally) to significantly inhibit maintenance blood. The release of parathyroid hormone in patients is relatively common, while conventional oral doses are relatively less effective.

4. Calcium-sensitive receptors may be accompanied by a decrease in calcium-sensitive receptor mRNA and protein in the nodule-forming region. This change may cause the secretion of parathyroid hormone, which is inhibited by calcium, and the reaction is less intense, and calcium is sensitive. Receptor regulation of parathyroid function may have therapeutic implications, and administration of a calcium-sensitive receptor potentiator in experimental or human chronic renal failure can reduce plasma parathyroid hormone by more than 50% and inhibit the parathyroid of experimental animals. Glandular cell hyperplasia.

5. Skeletal resistance to parathyroid hormones The resistance of bones to parathyroid hormone mobilization of bone calcium may be involved in the pathogenesis of secondary hyperparathyroidism. This resistance to parathyroid hormone is mainly due to high circulation. Parathyroid hormone receptor downregulation caused by parathyroid hormone levels, in addition to the deficiency of dihydroxycholecalciferol and hyperphosphatemia also play a role.

Metabolic acidosis can damage bone function in advanced renal failure. Some excess hydrogen ions can cause calcium release through the buffering action of bone carbonate, which reduces the storage of bone calcium and provides maintenance hemodialysis patients. Alkaline drugs to maintain normal plasma bicarbonate concentrations can slow the progression of uremic bone disease. In addition, animal experiments have shown that correcting acidosis can reduce muscle consumption and delay the development of kidney disease.

6. Skeletal lesions In renal failure, the two most common bone lesions are bone resorption and bone mineralization defects, osteosclerosis may also occur, and osteoporosis is uncommon.

(1) Parathyroidism-induced bone disease (high-transportation bone disease): Increased blood parathyroid hormone can lead to increased osteoclast activity and enhanced bone resorption. When these processes become more and more serious, bones show obvious fibers. It constitutes a histological lesion of fibrotic osteitis. This osteoclast bone resorption is found in the subperiosteal, subendocardial, cortical bone and the trabecular bone surface. These changes are more common in cortical bone and are rare in small Beam bone, parathyroid hormone can also stimulate bone cell osteolysis, leading to the absorption of cortical bone, hyperparathyroidism can also cause the appearance of braided bone and braided bone.

(2) Incomplete mineralization of bone lesions: Incomplete bone mineralization causes rickets in children, and rickets in adults occur due to delayed bone mineralization, leading to excessive unmineralized bone.

The mechanism of osteoid mineralization is mainly due to the relative or absolute deficiency of vitamin D or its active products and/or the resistance of bone to vitamin D. Vitamin D can affect bone mineralization through several ways: it can affect collagen Synthetic and mature, directly stimulate bone mineralization, or increase the level of calcium and phosphorus in the extracellular fluid around the bone by promoting the absorption of calcium and phosphorus in the intestine. Vitamin D deficiency can cause abnormal metabolism of collagen, and can also make amorphous calcium and The process of converting phosphorus into crystal form is inhibited. In addition to vitamin D deficiency, aluminum poisoning may also be the cause of some mineralization deficiency, and it is resistant to vitamin D treatment, so-called low-transport osteomalacia.

(3) Osteospermia: Osteosclerosis is a unique manifestation of renal osteodystrophy. Radiological examination shows an increase in bone density. Histological examination shows an increase in unmineralized trabecular bone and an increase in total bone volume in the spine and pelvis. The ribs and the long bones of the long bones are most prominent in the trabecular bone.

There is no correlation between bone lesions in patients with osteopetrosis and various biochemical indicators such as calcium, phosphorus and alkaline phosphatase. Some experimental and clinical observations suggest that osteosclerosis may be caused by excessive secretion of parathyroid hormone, parathyroid function. Patients with hyperthyroidism may have radiological changes in osteosclerosis.

(4) Osteoporosis: Osteoporosis refers to the reduction of the volume of normal mineralized bone. Osteoarthritis, calcium deficiency and chronic protein intake may be the cause of osteoporosis. Patients over 50 years old with uremia, menopause After the period, factors such as idiopathic or senile osteoporosis may also be involved in the occurrence of this bone disease.

Fibrous osteitis prevention

1. Population prevention With the prolongation of life expectancy and the improvement of detection methods for patients with chronic renal failure, the detection rate of this disease has an increasing trend. The bone biopsy and radionuclide scanning can be used to diagnose the disease early.

Population control measures include controlling high blood phosphorus, correcting hypocalcemia, supplementing vitamin D, preventing hyperthyroidism, hemodialysis or kidney transplantation, but the key is to control hyperphosphatemia early.

2. Personal prevention

(1) Primary prevention:

1 control of high blood phosphorus: first should control the intake of phosphate in the diet, phosphate is mainly from protein in food, patients with advanced renal failure such as daily phosphorus intake >1.2g, and not taking phosphorus binder, then Hyperphosphatemia can occur, followed by the use of phosphorus binders as appropriate, and the use of small doses of calcium carbonate or calcium lactate under strict monitoring of blood calcium is currently the first recommended method.

2) Correcting hypocalcemia: Maintaining normal calcium balance is beneficial to bone mineralization and inhibiting hyperparathyroidism. Calcium absorption is reduced in patients with advanced renal failure, while calcium intake in diet is only 400-700 mg per day. It should be supplemented with 1~2g of elemental calcium per day to supplement calcium acetate and calcium gluconate.

3 application of active vitamin D: kidney produces l,25-dihydroxyvitamin D3 failure, plays an important role in the occurrence and development of renal osteopathy, 1,25-dihydroxyvitamin D3 can make blood calcium in uremic patients The level of blood is significantly increased, and the level of blood parathyroid hormone is significantly decreased. Currently, vitamin D preparations commonly used include vitamin D2, alfacalcidol and calcitriol (Rosin Calcium).

4 Dialysis and kidney transplantation: Dialysis can partially replace renal function, while kidney transplantation can completely replace renal function, thereby treating renal bone disease.

(2) secondary prevention: the incidence of renal osteopathy is concealed, often without self-conscious symptoms, blood calcium is reduced, elevated blood phosphorus and alkaline phosphatase can be used as the basis for early diagnosis, tibia biopsy, photon absorption bone density determination and 99Tc ECT scan can improve the early diagnosis rate. Diagnostic points: 1 diagnosis basis of renal failure, 2 children with rickets, adults with bone pain, lower limbs with weight-bearing bones, 3X line examination showing specific bone disease performance .

Once renal osteopathy is discovered, the above preventive measures should be implemented immediately. Subtotal thyroidectomy should be performed for patients with obvious secondary hyperparathyroidism, persistent hypercalcemia, metastatic calcification and severe itchy skin. .

(3) Tertiary prevention: When fractures and significant skeletal deformities occur, surgery can be considered to correct them, but preoperative preparation should be sufficient, such as correcting the patient's anemia, nutritional status, etc., and doing intraoperative monitoring.

Complications of fibrotic osteitis Complications

Can be complicated by bone pain and fractures, skin ulcers and tissue necrosis, arterial calcium deposition and tissue ischemia and necrosis, children's growth is blocked, resulting in rickets.

Fibrous osteoinflammation symptoms Common symptoms Skin itching Skin Calcified tendon fracture Calcium deposit Hypercalcemia Humpback severe pain Bone pain Parathyroid function Hyperactive red eye

1. Itchy skin Itching is a common symptom of chronic renal failure, but its mechanism is unclear. Some patients have increased calcium in the skin. Blood calcium >2.4mmol/L is prone to itching. It is speculated that it contains calcium in the skin. The amount is related, but the itching may be improved within a few days after parathyroidectomy, and the reduction of calcium in the skin takes a long time. It seems that it is not good to explain the itching, parathyroid gland with more calcium in the skin. After resection, although itching is relieved, if hypercalcemia is caused by treatment with active vitamin D, itching may recur, and it is not easy to explain the increase in plasma parathyroid hormone alone. The plasma histamine level may also be caused by the patient. One of the causes of itching, treatment with recombinant erythropoietin improves anemia, reduces plasma histamine levels, and reduces itching. Full hemodialysis can improve or eliminate itching. Some patients are effective with lidocaine or ultraviolet radiation. Parathyroidectomy should be performed in patients with adequate hemodialysis and no improvement in skin itching and a significant increase in plasma parathyroid hormone levels.

2. Spontaneous tendon rupture can be seen in chronic renal failure or other secondary hyperparathyroidism caused by other causes, so there may be a causal relationship between the two, vitamin D deficiency causes elastic tissue degeneration or chronic metabolism Acidosis is also a possible cause of collagen synthesis disorders. Fractures with small tendon attachment points can also cause tendon rupture.

3. Growth retarded children with chronic renal failure are often shorter than normal children, due to malnutrition, vitamin D deficiency, chronic metabolic acidosis, intestinal absorption of calcium, bone disease and low levels of growth hormone media in the blood. Etc., the treatment of recombinant auxin in prepubertal children can promote its growth rate.

4. Bone pain and fractures with fibrous osteitis or osteomalacia can lead to progressively exacerbated bone pain, visible in the lower back, buttocks, calves or knees. Rib pain may be the first symptom of rib fracture, lower back pain May be due to compression fractures of the vertebral body, bone loss and low conversion type softening.

5. Bone deformation due to vitamin D deficiency, secondary hyperparathyroidism caused by osteophyte dislocation, long bones, often wave and hip, can also be seen in the humerus, ulna, lower end of the tibia, lower femur and lower end of the tibia.

Bone deformation is more common in adults with severe osteomalacia, which can cause scoliosis, kyphosis and thoracic deformation. Several vertebral compression fractures can make people shorter, and children are prone to rickets.

6. Skin ulcers and tissue necrosis can be seen in a small number of patients with severe renal failure. After renal transplantation and hemodialysis, radioactive examination can find subperiosteal bone resorption, normal or elevated blood calcium, and severe pain before the onset. Raynaud's phenomenon, after ulcer formation, secondary infection can cause sepsis and death, the pathogenesis is unclear, and the ulcers heal after subtotal resection of the parathyroid glands. It is speculated that secondary hyperparathyroidism may be the cause. These symptoms are not common. The site of the disease is the fingers, toes, thighs, calves and ankles.

7. Soft tissue calcification Soft tissue calcification (metastatic calcification) is mostly caused by persistent calcium and phosphorus deposition, which can be seen in arteries, eyes, viscera, joints and skin. The continuous increase of parathyroid hormone levels in addition to causing bone disease, It can lead to the deposition of calcium phosphate in small arteries, joints, soft tissues and viscera. It is most likely to occur when the calcium-phosphorus product exceeds 70. A more severe metastatic calcification called calciphylaxis is often accompanied by significant arteries. Calcium deposition and tissue ischemia and necrosis.

Because parathyroid hormone inhibits the reabsorption of phosphorus in the proximal tubules, only 15% of the filtered phosphorus is reabsorbed in severe renal failure, but the glomerular filtration rate is significantly reduced due to glomerular filtration rate. Significantly reduced, at this time parathyroid hormone is no longer possible to increase the excretion of phosphorus, but can continue to cause the release of calcium phosphate, the result is that parathyroid hormone aggravates hyperphosphatemia, in this case, oral phosphorus binder For example, calcium carbonate has little effect on lowering blood phosphorus, and parathyroidectomy and forearm transplantation of part of the parathyroid gland can achieve the purpose of reducing blood phosphorus. This surgery through the reduction of bone resorption and calcium phosphate deposition in the previous due to the parathyroid Glandular function, which in turn loses mineral bone, reduces blood calcium and blood phosphorus.

(1) vascular calcification: the earliest visible in the back of the foot, can also invade any artery in the forearm, wrist, hand, eye, internal organs, joints and pelvis, etc., more common in patients over 40 years old, generally speaking, the incidence often followed by dialysis The time is prolonged and increased. In severe cases, the pulse cannot be touched, blood pressure is not detected, and radiological examination shows that the blood vessel wall has fine granular compacts, which is the result of deposition of calcium on the inner elastic membrane of the middle layer of the artery. Membrane can also form atheromatous plaques, which can be eliminated in some patients after a kidney transplant or subtotal parathyroidectomy for several months or years.

(2) ocular calcification: ocular calcification is the most common soft tissue calcification in patients with chronic renal failure for hemodialysis. Calcium deposition in the eye can cause inflammation and local irritation to form red eyes, often transient, but can appear repeatedly, more Commonly known as the asymptomatic white calcification spots of the conjunctiva, the cornea can also be calcified to form a "band keratopathy", the mechanism of eye calcification may be that CO2 can not be discharged into the air through the surface of the conjunctiva, causing the pH in the eye tissue to increase, resulting in Calcium deposition.

(3) visceral calcification: visceral calcification can be seen in the lungs, stomach, heart muscle, skeletal muscles and kidneys and produce severe clinical symptoms. Calcium deposition in the myocardium or cardiac conduction system can lead to heart failure, arrhythmia and conduction block, pulmonary calcification Can cause pulmonary dysfunction, even pulmonary fibrosis, pulmonary hypertension and right ventricular hypertrophy, uremia or dialysis patients, especially after taking large amounts of ascorbic acid, can increase oxalate, form calcium oxalate deposition in soft tissue, or in the myocardium The mitral valve, deposited in the aortic valve, can cause cardiomyopathy, congestive heart failure, or death.

(4) Periarticular calcification: Periarticular calcification can be seen in dialysis patients with chronic renal failure, and its incidence increases with the duration of dialysis, which can be seen in the shoulders, wrists, fingers, toe joints and ankle joints. Patients often suffer from pain. Radioactive examination, visible scattered radioactive dense, occasionally visible large mass around the joint, can also be painless, but can limit joint activity, eating more phosphorus-containing foods such as milk can promote its development, limit phosphorus or thyroid Subtotal resection can ease the condition.

(5) Skin calcification: Skin calcification is one of the causes of itching. Skin biopsy is helpful for diagnosis. Subtotal removal of parathyroid gland may reduce the amount of calcium in the skin.

8. Proximal myasthenia proximal muscle weakness is more prominent in renal osteodystrophy, may be related to vitamin D deficiency, but also may be aggravated by calcium interference with muscle metabolism.

Examination of fibrous osteitis

Laboratory tests often have hypocalcemia, hyperphosphatemia, especially dihydroxycholecalciferol.

Radiological examination: Radiological changes in secondary hyperparathyroidism include bone endothelium, bone resorption in the cortex and subperiosteum, terminal fingering, erosion of the phalanx, cyst formation, neostosis of the periosteum and osteosclerosis, in which subperiosteal Bone resorption is the most common radiological change, mainly found in the phalanx, but also in the pelvic bone, the distal clavicle and the surface of the ribs, ulna, humerus and mandible. The radiological changes of the bone sclerosis increase the density of the bone. In the vertebral body, pelvis, ribs, clavicle and various metaphyseal trunks, the diagnosis of osteomalacia depends on bone biopsy. The only findings of radiology are the appearance of Loosers and pseudo-fractures. Bone mineral density is often reduced, but not enough. Diagnosis of osteomalacia, osteopenia refers to the reduction of bone density found in radiological examination, common in long-term renal failure for hemodialysis treatment, osteomalacia, secondary hyperparathyroidism and osteoporosis by radiology It can be found that the bone density is reduced, and it is difficult to judge the cause of bone loss by radioactivity alone.

Diagnosis and diagnosis of fibrotic osteitis

According to the clinical manifestations, the characteristics of laboratory examination can be initially diagnosed. The 2-microglobulin amyloidosis has no special changes in various examination indexes. The contents of Table 1 are for reference. The examination of blood calcium and phosphorus is for identification. Secondary hyperparathyroidism and aluminum-associated bone disease do not help much, severe hyperparathyroidism and aluminum-associated bone disease, both may have hypercalcemia, while phosphorus levels It depends on factors such as phosphorus intake, decomposition rate, residual renal function, and dialysis effect.

Alkaline phosphatase activity is often an index of osteoblast function, which is significantly increased in advanced fibrotic osteitis, while aluminum-related bone disease is often normal or low, and 1,25-(OH)2D3 levels are detected. Certainly, low levels suggest vitamin D deficiency. Blood parathyroid hormone is often significantly elevated in hyperparathyroidism, and is often lower than secondary hyperparathyroidism or normal in aluminum-related bone disease. It may be due to the inhibition of the secretion of parathyroid hormone by aluminum. When the serum aluminum is lower than 60g/L, the possibility of aluminum poisoning is small, and the positive deferoxamine (DFO) test is helpful for the diagnosis of aluminum-related bone disease.

The disease needs to be differentiated from uremia patients, possible aluminum-associated bone diseases and amyloidosis caused by 2-microglobulin deposition.

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