Etiology
As follows from the classification, the main causes of secondary hyperparathyroidism are renal failure and diseases of the digestive system. In accordance with this, renal and intestinal secondary hyperparathyroidism is distinguished.
Due to the widespread use of hemodialysis and an increase in the life expectancy of patients with chronic renal failure (CRF), secondary hyperparathyroidism became more common.
Pathogenesis
By the time of transfer of patients to hemodialysis, histological changes of varying degrees in bone tissue are present in 90% of patients. The development of secondary hyperparathyroidism in chronic renal failure is primarily associated with impaired formation of active vitamin D3 in the kidneys. A progressive increase in the plasma level of inorganic phosphorus begins as soon as the glomerular filtration rate decreases to 60 ml / min or less. Hypocalcemia stimulates parathyroid hormone secretion by the parathyroid glands. Renal osteopathy is a combination of osteomalacia and increased bone resorption resulting from parathyroid hormone hyperproduction.
The basis of the pathogenesis of the intestinal form of VHP lies in the small absorption of calcium and vitamin D, which leads to over stimulation of the parathyroid glands. In patients after gastrectomy, osteopathy occurs in approximately 30% of cases. Patients after the Billroth II operation and the total gastrectomy have a greater risk of osteomalacia than after the Billroth I operation.
In liver diseases, the development of secondary hyperparathyroidism is associated with impaired cholecalciferol conversion. Most often occurs in primary biliary cirrhosis. The pathogenesis of tertiary hyperparathyroidism may be associated with the gradual formation of autonomy of hyperfunctioning parathyroid glands with a disturbance of the feedback mechanism between calcium levels and excessive production of parathyroid hormone.
Clinic
The clinical picture of secondary and tertiary hyperparathyroidism is usually dominated by symptoms of the underlying disease, most often CRF. The specific symptoms are pain in the bones, weakness in the proximal muscles, arthralgia. Spontaneous fractures and skeletal deformity may occur. Formation of extra bone bones calcinations has various clinical manifestations. Calcification of the arteries may develop ischemic changes. Periarticular calcinates can be detected on the arms and legs. Calcification of the conjunctiva and cornea in combination with recurrent conjunctivitis is referred to as red eye syndrome.
Diagnostics
Laboratory tests reveal hyperphosphatemia, normal or slightly reduced calcium levels.
in blood plasma, high levels of alkaline phosphatase. The most sensitive marker of secondary hyperparathyroidism, in particular, incipient renal osteopathy, is an increase in the level of intact parathyroid hormone in the blood plasma.
Typical radiological signs of secondary hyperparathyroidism are subperiosteal and subchondral resorption of the bones of the hand (acroosteolysis), as well as the elbow and hip joints.
Treatment and Prevention
In chronic renal failure, prophylaxis of osteopathy is indicated with an increase in the level of inorganic phosphorus in the plasma of more than 1.5 mmol / l. Calcium-containing preparations that bind phosphates (calcium gluconate, lactate, citrate), and also phosphate-binding preparations of aluminum are prescribed. In addition, prescribed drugs (rocaltrol) under the control of excretion of calcium in the urine, which should not exceed 300 mg per day. In case of tertiary hyperparathyroidism, when autonomic adenoma is formed, in some cases surgical treatment is indicated.