What Is Osteitis Fibrosa?

Fibrotic osteitis is a hypertransportation bone disease caused by chronic renal failure secondary to hyperparathyroidism. The main clinical manifestations are advanced bone disease, skin itching, spontaneous tendon rupture, and soft tissue calcification.

Basic Information

English name: fibrosing osteitis
Visiting department: orthopedics

Common causes: Secondary hyperparathyroidism
Common symptoms: Itchy skin, spontaneous tendon rupture, soft tissue calcification, etc.

Causes of fibrous osteitis

The main cause is secondary hyperparathyroidism, which causes hyperparathyroidism and hyperfunction, leading to hypocalcemia and hyperphosphatemia in patients, especially lack of dihydroxycholesterol, advanced bone disease, skin itching, and spontaneous Sexual tendon rupture, soft tissue calcification, etc.

Clinical manifestations of fibrous osteitis

Itchy skin

Itchy skin is a common symptom of chronic renal failure, but its mechanism is unclear. In some patients, the amount of calcium in the skin is increased, and those whose blood calcium is> 2.4mmol / L are prone to pruritus, which is presumed to be related to the high amount of calcium in the skin. Plasma histamine levels in patients may also be one of the causes of itching.

2. Spontaneous tendon rupture

This phenomenon can be seen in chronic renal failure or secondary hyperparathyroidism caused by other reasons, so there may be a causal relationship between the two. Vitamin D deficiency can also cause degeneration of elastic tissue or chronic metabolic acidosis secondary to collagen synthesis disorders. Fractures of small tendon attachment points can also cause tendon rupture.

3. Growth is blocked

Children with advanced 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 blood growth hormone media.

4. Bone pain and fractures

People with fibrotic osteitis or osteomalacia can cause progressively worsening bone pain, which can be seen in the lower back, buttocks, lower legs, or knees. Rib pain may be the first symptom of a rib fracture. Lower back pain may be caused by compressive fractures of the vertebral body, osteopenia, and low conversion osteomalacia.

5. Bone deformation

Due to vitamin D deficiency, secondary epiphyseal dislocation caused by hyperparathyroidism causes long bones to bend, often spreading to the buttocks, and can also be found in the radius, ulna, lower end of humerus, lower end of femur, and lower end of tibia. Bone deformation is more common in adults with severe osteomalacia, which can cause scoliosis, humpback, and thoracic deformation.

6. Skin ulcers and tissue necrosis

Can be seen in a small number of patients with severe renal failure, renal transplantation and hemodialysis patients. Radiological examination can find subperiosteal bone resorption, normal or elevated blood calcium, severe pain and Raynaud's phenomenon before the onset. After the formation of ulcers, secondary infections can cause sepsis and death. The affected areas are fingers, toes, thighs, calves and ankles.

7. Soft tissue calcification

Soft tissue calcification (metastatic calcification) is mostly caused by persistent increased calcium and phosphorus deposition, which can be found in arteries, eyes, internal organs, joints and skin.

(1) Vascular calcification can be found in the back of the foot as early as it can invade any artery in the forearm, wrist, hand, eye, internal organs, joints and pelvis. More common in patients over 40 years of age. Generally speaking, the incidence often increases with the extension of dialysis time. In severe cases, the pulse cannot be touched and blood pressure cannot be measured.

(2) Eye calcification Eye calcification is the most common soft tissue calcification in patients with chronic renal failure treated with hemodialysis. Calcium deposition in the eye can cause inflammation and local irritation to form red eyes, which are often transient, but can occur repeatedly. The more common ones are asymptomatic white calcified spots on the conjunctiva, and the cornea can also be calcified to form "band keratopathy".

(3) Visceral calcification Visceral calcification can be seen in the lung, stomach, myocardium, skeletal muscle, and kidney and causes severe clinical symptoms. Calcium deposition in the myocardium or the cardiac conduction system can lead to heart failure, arrhythmias, and conduction blocks. Pulmonary calcification can cause pulmonary dysfunction, even pulmonary fibrosis, pulmonary hypertension, and right ventricular hypertrophy. Patients with uremia or dialysis, especially after taking a large amount of ascorbic acid, can increase oxalate and form calcium oxalate deposits in soft tissues. Deposits in myocardium or mitral and aortic valves can cause cardiomyopathy and congestive heart failure Or death.

(4) Peri-articular calcification Peri- articular calcification can be seen in patients with chronic renal failure dialysis, and its incidence increases with the duration of dialysis, and can be found in the shoulder, wrist, finger, toe and ankle joints. Occasionally large bumps around the joint can be seen, which can also be painless, but can limit joint movement. Eating phosphorus-rich foods such as milk can promote its development, and limiting phosphorus or subtotal thyroidectomy can alleviate the condition.

(5) Skin calcification Skin calcification is one of the causes of itching. Skin biopsy is helpful for diagnosis. Subtotal parathyroidectomy may reduce the calcium content in the skin.

8. Proximal muscle weakness

It is more prominent in renal osteopathy, which may be related to vitamin D deficiency, and may also be exacerbated by calcium interference with muscle metabolism.

Fibrous osteitis examination

1. There are often hypocalcemia and hyperphosphatemia, especially dihydroxycholesterol.

2. Radiological changes of secondary hyperparathyroidism include endosteal, cortical, and subperiosteal bone resorption, terminal finger and toe bone corrosion, cyst formation, and bone sclerosis, of which subperiosteal bone resorption is the most common Radiological changes are mainly found in the phalanx, but also in the pelvis, distal clavicle, and surface layers below the ribs, ulna, tibia, and mandible. The radiological changes of osteosclerosis, which is an increase in bone density, are commonly found in the vertebral body, pelvis, ribs, clavicle and metaphysis of various long bones, and the diagnosis of osteomalacia depends on bone biopsy. The only findings of radiology were the appearance of Loosers bands and pseudo fractures. Bone density often decreased, but not enough to diagnose osteomalacia. Osteopenia refers to a decrease in bone density found on radiological examinations. It is common in patients with long-term renal failure who are treated with hemodialysis. Osteomalacia, secondary hyperparathyroidism, and osteoporosis can be detected by radiological examination. It is difficult to determine the cause of bone loss based on radiological characteristics alone.

Diagnosis of fibrous osteitis

According to clinical manifestations, the characteristics of laboratory tests can be preliminary diagnosed.

Differential diagnosis of fibrous osteitis

This disease needs to be distinguished from uremic patients, aluminum-related bone disease and amyloidosis caused by 2-microglobulin deposition.

Fibrous osteitis treatment

Treatment includes control of phosphorus retention and hyperphosphatemia, correction of hypocalcemia, application of active vitamin D, control of dialysis calcium content, percutaneous injection of anhydrous alcohol or calcitriol ( Dihydroxycholesterol), subtotal parathyroidectomy, etc.

1. Controlling phosphorus retention and hyperphosphatemia

(1) Limit the intake of phosphorus in the diet The daily intake does not exceed 600-900mg, which is important for patients with GRF of 30-60ml / min. Care should be taken to avoid eating foods that contain more phosphorus, such as soybeans, laver, etc.

(2) Application of phosphorus binders When the phosphorus intake is unsatisfactory and blood phosphorus is increased, phosphorus binders should be used to convert the phosphorus in saliva, bile and intestinal fluid into non-absorbable ones, and eating too much phosphorus-containing food (> 2.0g / d) may reduce the effect of the phosphorus binder. Commonly used phosphorus binders are aluminum hydroxide, calcium preparations (calcium carbonate, calcium acetate) and magnesium preparations. Such as aluminum hydroxide, calcium acetate and calcium carbonate, lanthanum hydrochloride and so on.

2. Correct hypocalcemia

Hypocalcemia should be supplemented with calcium for a long time, which can increase blood calcium concentration and reduce serum alkaline phosphatase and parathyroid hormone.

If there is severe hyperphosphatemia, calcium supplementation will increase the calcium-phosphorus product and lead to calcification of soft tissues. Therefore, aluminum hydroxide should be used first, and the phosphorus binding agent should be used to reduce the blood phosphorus to <1.77mmol / L before calcium supplementation.

Supplementing a proper amount of calcium can correct hypocalcemia, and a large amount of calcium can cause hypercalcemia and cause ectopic soft tissue calcification, especially when combined with vitamin D preparations. Therefore, it is necessary to closely observe the blood calcium concentration when using calcium, especially for those receiving hemodialysis treatment.

3. Application of calcitriol

Dihydroxycholesterol deficiency is the most important cause of secondary parathyroidism. When GFR drops below 40ml / min, the level of dihydroxycholesterol begins to decrease, and it decreases significantly in end-stage renal failure. The reduction of functional kidney tissue and the inhibition of dihydroxycholesterol by early hyperphosphatemia are involved in the reduction of dihydroxycholesterol synthesis. At this time, it should be treated with calcitriol or other similar preparations, but in Before treatment, hyperphosphatemia must be basically controlled, or calcitriol can promote the absorption of phosphorus in the intestine and aggravate hyperphosphatemia.

4. Application of calcitriol in patients before dialysis

Whether patients with secondary hyperparathyroidism with renal failure before dialysis need to use calcitriol has not been determined. There have been concerns in the past that the application of calcitriol may accelerate the loss of renal function by causing hypercalcemia, hyperphosphatemia, and hyperuricemia. However, some reports indicate that as long as hypercalcemia is avoided, the use of calcitriol does not usually cause changes in renal function. Therefore, small doses of calcitriol appear to be safe and effective in reducing parathyroid hormone secretion.

5. Dihydroxycholesterol analogs

6. Calcium sensitive receptor synergist

Another way to reduce parathyroid hormone and reduce hypercalcemia is to use calcium mimics that activate calcium-sensitive receptors in the parathyroid glands.

7. Percutaneous injection of absolute alcohol or calcitriol

In summary, calcitriol and its analogs are a preferred method for the treatment of secondary hyperparathyroidism.

8. Calcium content of dialysate

Dialysis water must be purified and reverse osmosis water used. The calcium in the dialysate is ionic calcium, which can pass freely through the dialysis membrane, while only 60% of the ionic calcium in blood calcium. Blood calcium can be lost or increased during dialysis, depending on the concentration of calcium in the dialysate and blood, the amount of calcium in the dialysate, and the concentration of calcium that can diffuse in the blood. The use of low calcium dialysate also has the advantage of allowing patients to take larger doses of calcium orally in order to better combine with phosphorus and reduce blood phosphorus. However, if there is no oral calcium supplement, low calcium dialysate should not be used to avoid exacerbation of hypocalcemia and hyperparathyroidism.

9. Parathyroidectomy

Subtotal parathyroidectomy can be considered in the following cases: Plasma parathyroid hormone is significantly increased (often> 1000pg / ml); persistent hypercalcemia; severe skin pruritus is not effective after sufficient hemodialysis; Calcification of soft tissues; Fibrotic osteitis was ineffective with conservative treatment; Ischemic lesions of soft tissues, ulcers or necrosis occurred.