Aluminum bone disease

Introduction to aluminum bone disease Chronic renal failure can cause renal osteodystrophy, a type that is caused by secondary hyperparathyroidism (SHPT). This is a high-transfer-overbonedisease, and the other is lowturn-overbonedisease, which is characterized by osteomalacia, mostly due to the deposition of aluminum in the bone. Aluminum-relatedbonedisease. There is also a bone disease that has both of these changes, called mixed osteodystrophy (troped dystrophy). basic knowledge The proportion of illness: 0.0035% Susceptible people: no special people Mode of infection: non-infectious Complications: dementia, epilepsy, fracture

Cause of aluminum bone disease

Excessive aluminum content in the dialysate (25%):

When the aluminum content in the dialysate is close to 50g/L, the incidence of aluminum-associated bone disease is very high. Therefore, some authors suggest that the aluminum content in the dialysate should be at least 10g/L, preferably less than 5g/L. This source of aluminum poisoning has been greatly reduced after seepage as a dialysate.

Oral aluminum-containing preparations (20%):

For example, aluminum hydroxide, only a small amount of aluminum is absorbed after oral administration of aluminum hydroxide, but the kidney is the only way to excrete aluminum. Aluminum absorbed during chronic renal failure accumulates in the body and causes aluminum poisoning. The disease drug sucralfate is also one of the reasons. Orange juice and sodium citrate can also promote the absorption of aluminum. Calcium citrate can also promote the absorption of aluminum. The pH value in gastric juice can increase the solubility of aluminum. It suggests that the pH value of gastric juice can change the absorption of aluminum. Therefore, it is believed that the H2 receptor inhibitor ranitidine can reduce aluminum poisoning in patients with chronic renal failure. In China, some people are used to making aluminum products (rice pot, kettle, wok). Cooking rice with water and eating foods containing aluminum condiments (such as oil cakes, fritters, etc.) may also be the cause of excessive intake of aluminum.

Excessive amount of aluminum in the fluid of the parenteral rehydration (15%):

Such as albumin.

Iron deficiency (10%):

Since aluminum and iron have common pathways in the intestinal absorption, serum transport and cellular uptake, iron storage can affect the kinetics of aluminum, so iron deficiency may increase the risk of aluminum poisoning, and sufficient iron storage seems to be able to poison aluminum. It has a protective effect.

Individual factor (5%):

Some people have low bone remodeling and/or hypoparathyroidism, including patients with parathyroidectomy, renal transplant rejection with corticosteroids, diabetes, and excessive parathyroid hormone after treatment with dihydroxycholediol Decreased and bilateral nephrectomy are sensitive to the toxic effects of aluminum.

In patients with end-stage renal disease, the excretion of aluminum is blocked, and the accumulation of aluminum in the body makes the body's aluminum content 20 times higher than normal. The organs with the most aluminum accumulation are bone, liver and spleen, and the content of aluminum in the bone increases with aluminum. Related to poisoning, it can lead to aluminum-related bone disease. Although the aluminum content in the liver and spleen is high, it does not cause poisoning.

Pathogenesis

Bone softening is characterized by low bone turnover, bone formation, decreased bone resorption cells, and increased unmineralized bone volume. Vitamin D deficiency has been considered an important factor in the past, but most modern reports are attributed to aluminum poisoning, and aluminum is mainly deposited. Bone calcification of the bone edge, ie mineralized bone, unmineralized bone interface causes bone softening, the severity of histological changes of osteomalacia is related to the degree of deposition of aluminum on the edge of calcified bone, while aplastic bone disease may be aluminum. A prelude to osteomalacia, a renal bone dystrophy first reported in 1982, is now considered to be a major bone lesion in patients with chronic renal failure undergoing peritoneal dialysis, in some cases by aluminum Excessive accumulation, but excessive inhibition of parathyroid hormone may be a more important cause. Parathyroid hormone plays an important role in maintaining normal bone metabolism. Parathyroid hormone may prevent aluminum by increasing bone transport. Deposition of the mineralization front, and parathyroidectomy is a risk factor for the occurrence of aluminum-related bone disease, which can reduce the rate of bone formation and renewal rate, so that aluminum Accumulate on the edge of calcified bone, thereby interfering with the mineralization process of bone. Clinically, in patients with secondary hyperparathyroidism, aluminum-related bone disease should be excluded before considering parathyroidectomy because lowering parathyroid hormone levels It accelerates the deposition of aluminum in the bone in patients with bone softening and accelerates the occurrence of aluminum-related bone disease.

Aluminum bone disease prevention

Prevention of aluminum-related diseases is not easy, and the following measures can be considered.

1. Avoid using aluminum-containing phosphorus binders instead of calcium carbonate or calcium acetate.

2. Use a reverse osmosis device to make dialysate.

3. Avoid using aluminum products to boil water for cooking, and avoid eating too much aluminum-containing foods such as oil cakes and fritters.

Aluminum bone disease complications Complications, dementia, epilepsy fracture

Can cause aluminum-related encephalopathy, or dialysis dementia, advanced language disorders, flapping tremor, myoclonus, seizures, personality changes, thinking disorder, disorientation, progressive dementia and aphasia, recurrent Fracture, bone deformation, etc.

Symptoms of aluminum bone disease Common symptoms Joint pain Dementia Progressive dementia Myoclonus weakness Self-directed disorder Stuttering thinking disorder Quiver

The clinical manifestations of aluminum-associated bone disease are extensive bone and joint pain, which can be located on the back, buttocks and ribs, proximal muscle weakness, recurrent fractures commonly found in ribs, femoral neck, spine and femoral shaft, and can also be expressed as bone Deformation, these symptoms reflect the content of aluminum in the synovial cavity, and the dose of patients taking aluminum-containing phosphorus binder is 2 to 10 times higher than that of those who do not contain aluminum.

Increased aluminum content in the bone can also affect the formation of red blood cells. The clinical manifestations are reversible small cell hypoechoic anemia, and iron supplementation cannot be improved. One of the reasons is that too much aluminum can interfere with iron absorption and is treated with erythropoietin. The response was also poor. Deferoxamine was used to correct the effect of erythropoietin on anemia after aluminum poisoning.

Although aluminum-associated bone disease can be seen in patients with chronic renal failure who take aluminum-containing preparations, the risk of developing diabetes is greater, which may be related to the lower than normal bone formation rate. Type 1 diabetes forms bone formation before clinical diabetic nephropathy. The rate is down, the cause is unclear, but the plasma parathyroid hormone levels in these patients tend to be low.

The content of aluminum in brain tissue is relatively low, but it can cause aluminum-related encephalopathy. It was called dialysis encephalopathy or dialysis dementia in the early stage. It has been recognized that aluminum is a pathogenic factor of neurotoxin, and it is a kind of nervous system synthesis for long-term dialysis patients. Signs, early manifestations of intermittent language disorders (stutter), the use of obstacles, late manifested as persistent language disorders, flapping tremor, myoclonus, seizures, personality changes, thinking disorders, disorientation, progressive dementia and Aphasia, EEG changes to a mild rhythm of dominant rhythm.

Aluminum bone disease examination

Bone biopsy is a gold indicator for the diagnosis of aluminum poisoning, but the procedure is complicated and difficult for patients to accept, so it can not be used as a routine means of diagnosis. Atomic absorption spectroscopy can accurately measure plasma aluminum content, but plasma aluminum content can only reflect the recent aluminum load. It does not reflect the presence of aluminum poisoning because plasma aluminum concentrations are not closely related to the storage of aluminum in tissues, but plasma aluminum levels are significantly elevated in most patients with aluminum-associated bone disease (ie, >75-100 g/L, Normal value <10g/L) If the patient is exposed to aluminum for a long time and the plasma aluminum level is significantly increased (for example, more than 150-200g/L), aluminum-related bone disease or encephalopathy is likely to occur.

It has been recognized that the deferoxamine (DFO) test is a reliable indicator for the diagnosis of aluminum poisoning-related diseases. Deferoxamine is a chelating agent that combines with trivalent ions such as Fe3 and Al3 to form a complex for patients. After a certain dose of deferoxamine, it combines with the excess aluminum in the tissue to enter the blood circulation. The increase of serum aluminum can be used as an indicator of the overall aluminum load. The commonly used method is to use deferoxamine 40mg/kg body weight after dialysis. The patient was given an intravenous infusion within 30 minutes to determine the serum aluminum content before the dialysis (before deferoxamine) and before the next dialysis (after 44 hours of administration), the difference between the two was over 150 g/L (recommended >200 g) /L) is positive, Yacoob et al. consider that although the test is carried out with a larger dose of deferoxamine (40 mg/kg), its sensitivity and specificity are still limited, and larger doses of deferoxamine may also cause Visual side effects and hemodynamic side effects, so they recommend a small dose of deferoxamine test method, regardless of the patient's weight, given a dose of deferoxamine (500mg diluted in 100ml of normal saline), in dialysis Intravenous infusion within 2 hours after the start Before intravenous infusion of deferoxamine and after 48 h, each blood was taken to measure serum aluminum content, if the second blood aluminum concentration was >150 g / L, or 3 times the first blood aluminum concentration was considered positive, and bone biopsy Results Control, the false positive rate was 11%.

1. Radiological changes

The only radiological feature of adult osteomalacia is the looser zone or pseudofractures, which are linear loose ray transmissive bands adjacent to the cortical bone, often perpendicular to the long axis of the bone, which can be bilateral and Symmetrical, with or without a stenotic hardened area or a small, incompletely metabolized epiphysis, this loose band is not common in aluminum-associated bone disease, true fractures of the ribs and hips, and compression fractures of the vertebral body Common in dialysis patients with osteomalacia and less common in fibrous osteitis, bone mineral loss can be seen in bone softening, but no specificity, adult osteophytes have been closed, like the widening and opening of bone growth discs, typical radiation of rickets Learning changes do not occur, and changes in slow bone softening with osteomalacia are mainly under the microscope, so its diagnosis can only be established by histological examination of the bone.

2. Changes in bone histology

The histological changes of bone softening are characterized by excessive unmineralized bone, which is caused by bone mineralization of the bone matrix. The main change is the expansion of unmineralized bone, fiber. This type of change can also occur to some extent in osteoarthritis due to delayed bone mineralization. Therefore, tetracycline labeling is needed to identify damaged mineralization rates. Markers for identifying bone softening include:

(1) Measurement of the width of the bone-like suture.

(2) Determination of the number of bone-like bone plates in the suture.

(3) The extent of coverage of the bone surface covered by the osteoid.

(4) The volume of osteoid in the total bone surface.

(5) The mineralization retardation indicated by the tetracycline labeling. The detection of aluminum by Maloney staining can be found that most bone-softening dialysis patients have a large amount of aluminum deposition in the bone, typically in the interface between trabecular bone and osteoid. There is a line of aluminum deposited.

Most of the aplastic (or motility-deficient) bone diseases are caused by aluminum poisoning, which is similar to bone softening. The main difference is that it has no large osteoids.

Diagnosis and diagnosis of aluminum bone disease

diagnosis

According to clinical manifestations, deferoxamine test, bone biopsy features can be diagnosed, bone biopsy is a gold indicator for the diagnosis of aluminum poisoning, but the procedures are more complicated and not easy for patients to accept, so can not be used as a routine means of diagnosis, atomic absorption spectroscopy can be accurate Plasma aluminum content is measured, but plasma aluminum content can only reflect the recent aluminum load, can not reflect whether there is aluminum poisoning, the plasma aluminum level of most patients with aluminum-related bone disease is significantly increased (ie >75 ~ 100g / L, normal Value <10g / L), if the patient is exposed to aluminum for a long time, and the plasma aluminum level is significantly increased (for example, more than 150 ~ 200g / L or more), it is likely to occur aluminum-related bone disease or encephalopathy, can also be initially diagnosed.

Differential diagnosis

Attention to the identification of other related bone diseases, this disease has chronic renal failure can cause renal osteodystrophy, low turn-over bone disease (low turn-over bone disease), manifested as osteomalacia (osteomalacia), onset and chronic kidney Functional failure is associated with dialysis treatment.

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