Hyperthyroid bone mineral disease

Introduction to hyperthyroidism bone mineral disease Hyperthyroidism (hyperthyroidism) is one of the more common endocrine system diseases, in addition to increased thyroid hormone secretion, hyperfunction, high metabolic syndrome, increased neurovascular excitability, but also thyroid enlargement, exophthalmos, nearly half Patients can develop osteoporosis and mineral metabolism disorders. basic knowledge The proportion of illness: 0.005% Susceptible people: no special people Mode of infection: non-infectious Complications: Osteoporosis Bone hyperplasia

Causes of hyperthyroidism bone mineral disease

(1) Causes of the disease

Hyperthyroidism and mineral metabolism disorders are caused not only by Graves' disease, but also by pituitary hyperthyroidism (increased TSH secretion from pituitary tumors), familial goiter with hyperthyroidism, neoplastic hyperthyroidism (early thyroid cancer), lithium hyperthyroidism, etc. The disease is caused by long-term treatment, the cause is multi-faceted, T3, T4, FT3 and FT4 increase in thyroid hormones, especially T3 and FT3, and more closely related to bone mineral metabolism.

(two) pathogenesis

Hyperthyroidism is increased during hyperthyroidism, causing abnormal bone and mineral metabolism. The severity of the disease is directly proportional to it. T3 is the main factor and the best indicator for the determination of hyperthyroidism. The bone turnover of hyperthyroidism patients is increased, which is characterized by elevated serum AKP and urine. Increased HOP excretion, increased bone turnover, often more bone resorption than bone formation, with a considerable degree of bone loss, bone histomorphometry studies indicate that when the hyperthyroidism, trabecular bone reduction, bone cortical pores increase, suggesting osteoclast activity and Osteoblast activity increased, serum BGP increased is a sensitive indicator of increased formation of patella, serum BGP returned to normal slower than T3, T4, indicating that after thyroid hormone returned to normal, bone turnover accelerated but not terminated, the role of thyroid hormone is promoted Bone resorption, which stimulates the bone remodeling cycle, increases osteoblast activity and increases bone formation. Hyperosmolarization is accelerated in patients with hyperthyroidism, bone resorption is more than bone formation, and bone calcium is increased. Some patients may have Hypercalcemia, which causes hypoparathyroidism to be suppressed and PTH to decrease, CT increases, due to high metabolic rate, phosphorus can be released from bone and soft tissue, blood phosphorus It can increase, the decrease of high blood phosphorus and PTH can inhibit the -hydroxylase activity of the kidney, and the secretion of 1,25-(OH)2D3 is reduced. The decrease of PTH and the increase of CT can inhibit the reabsorption of renal tubules. High urinary calcium occurs, because patients with hyperthyroidism often have diarrhea, consumption increases, 1,25-(OH)2D3 decreases, so intestinal calcium absorption decreases, often negative calcium balance and negative phosphorus balance, even negative magnesium balance, long course of disease Osteoporosis occurs due to bone mineral loss, bone calcium and magnesium are found in bone minerals, intracellular calcium and magnesium are accelerated, bone resorption is dominant, and osteoporosis occurs. Thyroid hormone in hyperthyroidism patients can directly mobilize bone. Calcium, not related to parathyroid glands, only a small number of patients with hyperparathyroidism, hyperthyroidism without hypophosphatemia, different from high blood calcium of parathyroidism, high blood calcium causes accelerated bone mineral turnover rate, slow Calcium renal clearance, AKP increased by about half in hyperthyroidism, urinary HOP, urinary cAMP, blood TrACP, BGP, etc. can be increased, when the thyroid function returns to normal after treatment, thyroid hormones return to normal levels, the condition can be restored to normal, indicating Thyroid function hyperactivity control After the bone transformation slows down, the osteoblast synthesis function predominates and lasts for a long time to repair the bone damage. The biochemical indicators of the patients with poor efficacy can not be reduced to normal, indicating that the bone is still destroying. Still need to improve the treatment.

In short, hyperthyroidism is common in hyperthyroidism, characterized by bone remodeling rate, blood calcium and urinary calcium can be increased, blood phosphorus is increased, urinary phosphorus can be more or less, blood magnesium is often reduced, urinary magnesium is often elevated, intestinal calcium Reduced absorption, thyroid hormone effect generally does not pass PTH on bone tissue, often negative calcium and negative magnesium balance, such as increased intake, can also be positive balance, hyperthyroidism, normal calcium level, indicating bone remodeling There is no parallel relationship between range and speed and serum. Under the great change of bone remodeling, blood calcium is kept constant, hyperthyroidism is remodeled at a high speed, intestinal absorption of calcium is reduced, and it can interfere with thyroid hormones 1,25-( OH) 2D3 catabolism or affecting 25-(OH)D3 is related to the reduction of 1-hydroxylation in the kidney, and can also affect the secretion and release of PTH and CT. The secretion of PTH is reduced during hyperthyroidism, and the blood phosphorus is high. Clearance reduction, or elevated blood calcium, inhibition of parathyroid gland, when PTH accelerates the rate of bone tissue renewal, must have a synergistic effect of thyroxine to complete.

Hyperthyroidism prevention of bone mineral disease

1. Hyperthyroidism and mineral metabolism disorders should mainly treat hyperthyroidism, and restore the normal levels and proportions of excessive secretion of thyroid hormones T3, T4, rT3, FT3 and FT4.

2. Hyperthyroidism should increase nutrition, especially in adolescence, increase calcium intake, increase bone peak in adulthood, slow down BMC loss, and moderate activity and outdoor exercise.

3. Calcium supplement 4 ~ 8g / d, it is best to supplement calcium calcium and other calcium containing calcium, daily vitamin D 5000 ~ 50000U, such as blood calcium is too low to increase the amount of vitamin D, If necessary, a vitamin D agent may be injected, and if appropriate, 1-(OH)D3 or 25-(OH)D3 or 1,25-(OH)2D3 may be added.

Hyperthyroidism bone mineral disease complications Complications Osteoporosis Bone hyperplasia

The most common form of osteosarcoma is osteoporosis, decreased bone density, osteoporosis and bone hyperplasia.

Symptoms of hyperthyroidism, bone mineral disease, common symptoms, calcification, weak cortical bone, thin body pain, osteoporosis, bone pain

1. Symptoms and signs

The most common form of osteosarcoma is osteoporosis, decreased bone density, osteoporosis and bone hyperplasia. All patients with bone changes have varying degrees of weakness, low back pain, generalized pain or headache. Symptoms, more common symptoms of hyperthyroidism, a small number of hyperthyroidism patients may have bone deformities or pathological fractures.

2. Bone X-ray performance and bone density performance

Patients with hyperthyroidism often have bone decalcification and varying degrees of osteoporosis, decreased bone density, or fibrous cystic osteitis, or acrure of the extremities. When the condition is severe, there are often bone pain, deformity, and even fractures. Rarely, mostly in patients with untreated hyperthyroidism, or poorly treated, often involving one, two, and five metacarpal bones, X-ray showed irregular lace-like or nearly needle-like periosteal new bone, and the middle part of the backbone became thicker. Shuttle shape.

Osteoporosis occurs mostly in weight-bearing parts. For example, lumbar vertebrae and pelvis often have decalcification of bone and thinning of cortex, bone density is consistently reduced, and trabecular bone is scarce. Bone histology shows that bone remodeling activity is enhanced and active. The bone resorption surface is enlarged, the osteolytic osteolytic absorption activity is enhanced, the number of osteoclasts is increased, the new bone formation surface is not enlarged, the osteoid surface is enlarged, the calcification front is normal, and the bone tissue changes are similar to the parathyroid function. Hyperthyroidism, both multinucleated osteoclasts with corresponding osteoblast activity, and epithelial mononuclear osteoclast activity, which can also occur in diabetes, acromegaly, hyperparathyroidism, etc. Therefore, it is still necessary to combine clinical features to diagnose hyperthyroidism.

A single photon bone densitometer was used to measure 58 cases of hyperthyroidism in Nanjing. The value was (0.59±0.10) g/cm2 (male), (0.54±0.08) g/cm2 (female), and the measurement site was humerus (left). /3, compared with the normal value (0.73 ± 0.13) g / cm2 (male), (0.69 ± 0.11) g / cm2 (female) significantly decreased, BMD after treatment was significantly increased (P <0.01).

Examination of hyperthyroidism bone mineral disease

1. Serum thyroid hormone (T4) and triiodothyronine (T3) are elevated.

2. Thyroid stimulating hormone releasing hormone stimulation test

After intravenous injection of 200 g, thyroid stimulating hormone did not increase or increase very little.

3. Lower serum cholesterol.

4. Blood sugar

Because thyroid hormone promotes gluconeogenesis, some patients with hyperthyroidism may have secondary diabetes or impaired glucose tolerance.

5. Serum Ca, P, AKP and osteocalcin were elevated, reflecting the increased activity of osteoclasts, increased bone turnover, and decreased blood parathyroid hormone and 1,25-(OH)2D3.

6. X-ray showed osteoporosis and reduced bone mass.

7. Bone density meter inspection

It can indicate a change in bone density.

Diagnosis and diagnosis of hyperthyroidism bone mineral disease

The diagnosis of abnormal mineral metabolism of the nail bone can be clearly diagnosed by combining clinical manifestations. The change of thyroid hormone level in hyperthyroidism can support the diagnosis of hyperthyroidism. There is a series of history of hyperthyroidism and hypermetabolic disease, and the enhancement of neurovascular excitability. Symptoms and signs associated with goiter or exophthalmos, laboratory biochemical abnormalities, decreased bone density and osteoporosis can diagnose the disease.

The diagnosis of hyperthyroidism mineral metabolism disorder should be associated with osteomalacia, renal osteodystrophy, hyperparathyroidism, senile osteoporosis, multiple myeloma, osteogenesis imperfecta, osteoarthritis, anti-vitamin D rickets, Low blood phosphorus (congenital) bone disease, metastatic cancer, and identification of diseases such as vitamin D poisoning and primary osteoporosis.

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