Synopsis
Distinguish autonomous and compensatory PTH excess using calcium-phosphate-renal physiology, then choose surgery, renal management or surveillance appropriately.
- Primary hyperparathyroidism is autonomous PTH secretion, usually with hypercalcaemia and low or low-normal phosphate, from a single adenoma more often than multi-gland disease.
- Secondary hyperparathyroidism is an appropriate compensatory response to hypocalcaemic stimuli such as CKD, vitamin D deficiency, malabsorption or low calcium intake.
- Tertiary hyperparathyroidism is autonomous secretion after prolonged secondary stimulation, classically in advanced CKD or after transplantation, and usually produces hypercalcaemia.
Investigation priorities
Establish whether PTH response is appropriate at the time of confirmed calcium disturbance.
Management branches
Repeated hypercalcaemia has a non-suppressed PTH without advanced CKD.
- Review medicines and family history, correct relevant vitamin D deficiency carefully, and assess urinary calcium before labelling sporadic primary disease.
- Measure renal function, renal stone burden and DXA including the forearm, documenting symptoms and pregnancy or hereditary considerations.
Key medicines
CinacalcetInitiate and titrate through the relevant endocrine or renal specialist protocol according to the licensed indication, calcium, PTH response and tolerability; NICE commissioning criteria apply in refractory dialysis-associated secondary disease.
Activated vitamin D analogueUse alfacalcidol or calcitriol only within the renal or hypoparathyroid protocol, titrating small regimen changes against calcium, phosphate and PTH after native vitamin D deficiency has been addressed where appropriate.