Overview of hyperthyroidism
Hyperthyroidism (hyperthyroidism) is one of the more common endocrine system diseases, in addition to increased secretion of thyroid hormones, hypermetabolic syndrome, neurovascular excitability, but also goiter, proptosis, nearly half of the patients may occur osteoporosis and mineral metabolism disorders.
A variety of endocrine hormones and biologically active substances and mineral metabolism are closely related, thyroid hormone, parathyroid hormone, calcitonin, growth hormone, adrenocorticotropic hormone, sex hormones, insulin, vitamin D and its active metabolite, osteocalcin, alkaline phosphatase and other metabolites and enzymes can affect the mineral metabolism of the bone; conversely, calcium, phosphorus, magnesium and other disorders of mineral metabolism, but also directly or indirectly, make various kinds of hormone relationship changes. Conversely, disorders of mineral metabolism, such as calcium, phosphorus and magnesium, can also directly or indirectly cause changes in the relationship between various hormones, resulting in bone mineral and salt metabolism. Both hyperthyroidism and hypothyroidism can cause metabolic bone disease due to excess or deficiency of thyroid hormones. The interstitial C cells of the thyroid, also known as parafollicular cells, also secrete calcitonin (cT), which plays an important role in the regulation of calcium and phosphorus metabolism.
Etiology
Hyperthyroidism osteoporosis and mineral metabolism disorders are not only caused by Graves’ disease, but also due to pituitary hyperthyroidism (pituitary TSH tumor secretion of TSH increased), familial goiter with hyperthyroidism, thyroid tumors with hyperthyroidism (early stage thyroid carcinoma), lithium hyperthyroidism and other diseases that have not been treated for a long time. Excessive thyroid hormone stimulates osteoclasts in the bones, promotes bone resorption, increased release of bone mineral salts into the blood, so that urinary calcium and phosphorus rise, blood calcium and phosphorus remain normal, the body is in a negative balance of calcium and phosphorus. At the same time, the decomposition of bone matrix is also exuberant, so that the urinary hydroxyproline discharge increased significantly. While bone resorption increases, compensatory bone formation also increases. Most alkaline phosphatase is normal, and a few patients have elevated alkaline phosphatase. In addition, excess thyroid hormone contributes to insufficient protein matrix in the bones and massive calcium loss.
Symptoms.
Hyperthyroidism patients who have bone changes have different degrees of weakness, back and leg pain, generalized pain or headache, etc., which are more obvious than the general symptoms of hyperthyroidism, and a small number of hyperthyroidism patients may have bone deformity or pathological fracture. Although osteoporosis is more common in patients with hyperthyroidism, fractures are rare.
Hyperthyroid patients often have bone decalcification and varying degrees of osteoporosis, low bone density, or fibrocystic osteitis, or thickening of the limbs (acropathy), most patients with hyperthyroidism do not have low bone density on X-ray, and a few patients with severe disease, low body weight, or postmenopausal women, may show osteoporosis. When the disease is more serious, there is often bone pain, deformity, or even fracture, mainly involving the spine and pelvis, followed by the skull, long bones and hand bones. It mostly occurs in untreated patients with advanced hyperthyroidism or poorly treated patients, often involving the first, second and fifth metacarpal bones.
Osteoporosis mostly occurs in weight-bearing areas, such as the lumbar spine and pelvis often have bone decalcification, these manifestations in diabetes mellitus, acromegaly, hyperparathyroidism and so on can also appear, therefore, still need to combine with clinical features to diagnose hyperthyroidism bone lesions.
Examination
1. Serum thyroid hormone (T4) and triiodothyronine (T3) are elevated, and TSH is decreased.
2. thyrotropin-releasing hormone excitability test with no or little increase in thyrotropin after intravenous injection of 200 µg.
3. Serum cholesterol decreased.
4. Blood glucose: Because thyroid hormone promotes glycogen isomerization, some patients with hyperthyroidism may develop secondary diabetes mellitus or hypoglycemic tolerance.
5. Serum Ca, P, AKP and osteocalcin are elevated, reflecting increased osteoclast activity and faster bone turnover. Blood parathyroid hormone and 1,25-(OH)2D3 are decreased.
6. X-rays show osteoporosis and decreased bone mass.
7. Bone densitometry may indicate decreased bone density.
Diagnosis
The diagnosis of abnormal bone mineral salt metabolism in hyperthyroidism can be made clearly by combining it with clinical manifestations. Changes in thyroid hormone levels in hyperthyroidism can support the diagnosis of hyperthyroidism. Clinical history of hyperthyroidism, hypermetabolic syndrome, increased neurovascular excitability, accompanied by symptoms and signs such as goiter or proptosis, abnormal laboratory biochemical tests, decreased bone density and osteoporosis, except for other causes of osteoporosis, can be used to diagnose this disease.
Differential diagnosis
The diagnosis of hyperthyroidism bone mineral salt metabolism disorder should be differentiated from osteochondrosis, renal osteodystrophy, hyperparathyroidism, senile osteoporosis, multiple myeloma, osteogenesis imperfecta, osteitis deformans, anti-vitamin D rickets, hypophosphatemic (congenital) osteopathy, metastatic carcinoma, as well as vitamin D intoxication and primary osteomalacia.
Treatment
1.Drugs
Methimazole (Tabazole), 3 times/d or propylthiouracil, 3 times/d. The dosage should be gradually reduced after symptom control. When applying these drugs, attention should be paid to the bone marrow, hepatotoxicity and allergic reactions to these drugs, and blood and liver function should be monitored regularly. The course of drug treatment is generally longer, often takes 1 to 2 years, and the recurrence rate is high.
2. Surgery
Subtotal thyroidectomy can be performed after controlling hyperthyroidism with drugs, and the cure rate reaches 90%.
3.131I therapy
It is suitable for those who are allergic to oral medication; or those who have recurrence after long-term medication; or those who have recurrence after surgery; or those whose hyperthyroidism is combined with severe cardiac, hepatic and renal function damage, granulocytopenia and bleeding.
4. Other treatments
Those with hypokalemia should have potassium supplementation in time.
Prognosis
Hyperthyroidism is easy to relapse, and the resistance of the more serious patients is lowered and easy to relapse. Treatment should be adhered to and medication should be prolonged to prevent relapse and complications from reoccurring and aggravating.