Tertiary parathyroid

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Tertiary hyperparathyroidism (HPT III) occurs when an excess of parathyroid hormone (PTH) is secreted by parathyroid glands, usually after longstanding secondary hyperparathyroidism. Some authorities reserve the term for secondary hyperparathyroidism that persists after successful renal transplantation. Long-standing chronic kidney disease (CKD) is associated with several metabolic disturbances that lead to increased secretion of PTH, including hyperphosphatemia, calcit-riol deficiency, and hypocalcaemia. Hyperphosphatemia has a direct stimulatory effect on the parathyroid gland cell resulting in nodular hyperplasia and increased PTH secretion. Prolonged hypocalcaemia also causes parathyroid chief cell hyperplasia and excess PTH. Af-ter correction of the primary disorder CKD by renal transplant, the hypertrophied parathyroid tissue fails to resolute, enlarge over and continues to oversecrete PTH, despite serum calcium levels that are within the reference range or even elevated. They also may become resistant to calcimimetic treatment. The main indication for treatment is persistent hypercalcemia and/or an increased PTH, and the primary treatment is surgery. Three procedures are commonly performed: total parathyroidectomy with or without autotransplantation, subtotal parathyroidectomy, and limited parathyroidectomy. It is important to remove superior parts of thymus as well. The most appropriate surgical procedure, whether it be total, subtotal, or anything less than subtotal including "limited" or "focused" parathyroidectomies, continues to be unclear and controversial. Surgical complications are rare, and para-thyroidectomy appears to be a safe and feasible treatment option for HPT III.


What are the signs and symptoms of tertiary hyperparathyroidism? The signs and symptoms are usually similar to primary hyperparathyroidism with a risk of reduced bone density (osteoporosis), muscle weakness, bone pain, constipation, abdominal pain, poor concentration or confusion.


Tertiary disease is characterized by the development of autonomous hypersecretion of parathyroid hormone causing hypercalcemia. The etiology is unknown but may be due to monoclonal expansion of parathyroid cells (nodule formation within hyperplastic glands).

Risk factors

Tertiary hyperparathyroidism can follow any secondary hyperparathyroidism, but is usually due to chronic kidney disease. A history of external neck irradiation is also a risk factor. Polymorphisms in the VDR gene (encoding the vitamin D receptor) may also be risk factors.

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If you and your health care provider have chosen to monitor, rather than treat, your primary hyperparathyroidism, the following suggestions can help prevent complications:

Monitor how much calcium and vitamin D you get in your diet. ...

Drink plenty of fluids. ...

Exercise regularly. ...

Don't smoke.