TERTIARY HYPERPARATHYROIDISM

TERTIARY HYPERPARATHYROIDISM

• Tertiary hyperparathyroidism is a persistent autonomous hypercalcaemic hyperparathyroidism occurring after kidney transplantation. A number of proposed factors may prevent involution of the hyperplastic parathyroid glands following resolution of the underlying renal impairment. These include impaired graft function, non-suppressible PTH secretion, slow involution of enlarged glands or insu ffi cient calcitriol conver - sion by the transplanted kidney . The biochemical diagnosis is confirmed by an elevated - total or ionised calcium, with an associated elevated or unsup - pressed PTH and a reduced phosphate occurring at least 1 year post renal transplantation. Di ff erentiation from PHPT can be di ffi cult. Few er than 1% of patients with tertiary hyperpara - thyroidism will require sur gical intervention ( Table 56.5 ). The only new evidence for intervention is the presence of nodular hyperplasia of the glands themselv es. Traditionally , localisa - tion studies or imaging of the neck was not indicated in tertiary hyperparathyroidism. However, increasing knowledge of the clonal nature of gland h yperplasia suggests that where there is a nodule within the parathyroid with a volume of tissue greater 3 than 500 /uni00A0 mm , then resolution of electrolyte abnormalities is unlikely . /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF The use of calcimimetics in tertiary hyperparathyroidism remains controversial and has not been approved for this indication. However, isolated reports have documented control of hypercalcaemia with minimal side e ff ects in individual patients. Surgical intervention remains the definitive management strategy . Subtotal parathyroidectomy or total

TABLE 56.5 Indications for surgical intervention in tertiary hyperparathyroidism. Subacute severe hypercalcaemia (>3 /uni00A0 mmol/L) Impaired graft function Nodular hyperplasia of the parathyroid gland(s) Progressive symptoms (>2 years following transplantation) Worsening bone disease (pain, fracture, bone loss) Renal stones/nephrocalcinosis Soft-tissue or vascular calci /f_i cations

surgical options. The majority of endocrine surgeons will opt for a subtotal parathyroidectomy in this setting, leaving a gland approximately four times normal in volume to minimise postoperative complications. Total parathyroidectomy without an autograft is not a treatment option because of the postoperative and persistent di ffi culties in managing the associated hypocalcaemia. Summary box 56.3 Tertiary hyperparathyroidism /uni25CF /uni25CF /uni25CF /uni25CF

Persistent autonomous hypercalcaemic hyperparathyroidism occurring after kidney transplantation Diagnosis is made by demonstrating an elevated total or ionised calcium with an associated elevated or unsuppressed PTH and a reduced phosphate occurring at least 1 year post renal transplantation Localisation studies are not required but a focused neck ultrasonography may con /f_i rm the presence of nodular enlargement Surgical intervention remains the mainstay of treatment and involves a subtotal parathyroidectomy

TERTIARY HYPERPARATHYROIDISM

• Tertiary hyperparathyroidism is a persistent autonomous hypercalcaemic hyperparathyroidism occurring after kidney transplantation. A number of proposed factors may prevent involution of the hyperplastic parathyroid glands following resolution of the underlying renal impairment. These include impaired graft function, non-suppressible PTH secretion, slow involution of enlarged glands or insu ffi cient calcitriol conver - sion by the transplanted kidney . The biochemical diagnosis is confirmed by an elevated - total or ionised calcium, with an associated elevated or unsup - pressed PTH and a reduced phosphate occurring at least 1 year post renal transplantation. Di ff erentiation from PHPT can be di ffi cult. Few er than 1% of patients with tertiary hyperpara - thyroidism will require sur gical intervention ( Table 56.5 ). The only new evidence for intervention is the presence of nodular hyperplasia of the glands themselv es. Traditionally , localisa - tion studies or imaging of the neck was not indicated in tertiary hyperparathyroidism. However, increasing knowledge of the clonal nature of gland h yperplasia suggests that where there is a nodule within the parathyroid with a volume of tissue greater 3 than 500 /uni00A0 mm , then resolution of electrolyte abnormalities is unlikely . /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF /uni25CF The use of calcimimetics in tertiary hyperparathyroidism remains controversial and has not been approved for this indication. However, isolated reports have documented control of hypercalcaemia with minimal side e ff ects in individual patients. Surgical intervention remains the definitive management strategy . Subtotal parathyroidectomy or total

TABLE 56.5 Indications for surgical intervention in tertiary hyperparathyroidism. Subacute severe hypercalcaemia (>3 /uni00A0 mmol/L) Impaired graft function Nodular hyperplasia of the parathyroid gland(s) Progressive symptoms (>2 years following transplantation) Worsening bone disease (pain, fracture, bone loss) Renal stones/nephrocalcinosis Soft-tissue or vascular calci /f_i cations

surgical options. The majority of endocrine surgeons will opt for a subtotal parathyroidectomy in this setting, leaving a gland approximately four times normal in volume to minimise postoperative complications. Total parathyroidectomy without an autograft is not a treatment option because of the postoperative and persistent di ffi culties in managing the associated hypocalcaemia. Summary box 56.3 Tertiary hyperparathyroidism /uni25CF /uni25CF /uni25CF /uni25CF

Persistent autonomous hypercalcaemic hyperparathyroidism occurring after kidney transplantation Diagnosis is made by demonstrating an elevated total or ionised calcium with an associated elevated or unsuppressed PTH and a reduced phosphate occurring at least 1 year post renal transplantation Localisation studies are not required but a focused neck ultrasonography may con /f_i rm the presence of nodular enlargement Surgical intervention remains the mainstay of treatment and involves a subtotal parathyroidectomy