Risk Factors and genetics
An elevated risk of developing tertiary hyperparathyroidism exists when late stage kidney disease is not corrected timely. This is due to a hyperphosphatemia acting directly on the parathyroid glands. Genetically, those who have an X-linked dominant disorder that disrupts phosphate transport at the renal tubules (X-Linked hypophosphatemic rickets) and are receiving oral phosphate treatment have shown to be at high risk of developing tertiary hyperparathyroidism in the absence of secondary hyperparathyroidism. Recurring tertiary hyperparathyroidism is generally seen to be caused by incomplete parathyroidectomy without renal transplant and the risk is increased when the parathyroid tissue left after surgery is that of a nodular type.Other risk factors of tertiary hyperparathyroidism include an elevated risk of developing acute pancreatitis, mainly due to the hypercalcemia associated with the hyperparathyroidism. Other studies have shown a significant increase in the risk of developing malignancies of the urinary tract and renal system with women being more at risk. Though there is some conjecture as to the correlation between hyperparathyroidism and thyroid carcinoma development, there is however a correlation between the two, which is thought to be due to prolonged irradiation of the neck and head for parathyroid adenomas and increased parathyroid hormone.Other studies have found some correlation in the development of renal disease following parathyroidectomy. However, the mechanism for this effect remains unknown. Pathophysiology
Tertiary Hyperparathyroidism is almost always related to end stage kidney disease and a secondary hyperparathyroidism. Physiological changes due to the kidney damage adversely affect feedback loops that control secretion of parathyroid hormone.
Surgical options for tertiary hyperparathyroidism include subtotal parathyroidectomy (three and one half of total tissue) and total parathyroidectomy with autotransplatation of resected tissue. Outcomes from surgery are generally favourable and a return to normalised blood calcium levels and parathyroid function is seen. History
In 1962, Dr C.E Dent reported that autonomous hyperparathyroidism may result from malabsorption syndromes and chronic kidney disease. The term tertiary hyperparathyroidism was first used in 1963 by Dr Walter St. Gaur to describe a case reported on at Massachusetts General hospital. This case involved a patient who had presented with autonomous parathyroid adenoma causing hypercalcemia with a background of parathyroid hyperplasia. Further reports were recorded in 1964, 65 and 67 of suspected tertiary hyperparathyroidism.In 1968 Davies, Dent and Watson produced a historic case study where they reviewed 200 cases of previously diagnosed primary hyperparathyroidism and found the majority of these cases should be reclassified as tertiary. These were important findings as it allowed an understanding into distinguishing features of primary, secondary and tertiary hyperparathyroidism which then allows appropriate medical treatment.It is now understood that tertiary hyperparathyroidism is defined as the presence of hypercalcemia, hyperphosphatemia and parathyroid hormone due to terminally biased parathyroid-bone-kidney feedback loop. Although there is still conjecture as to whether tertiary hyperparathyroidism is also due to adenomatous growth or hyperplasia it is clear that tertiary hyperparathyroidism presents with some form of tissue enlargement in all four parathyroid glands. See also
Hyperparathyroidism
Primary hyperparathyroidism
Secondary hyperparathyroidism

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