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PRIMARY CARE PATHWAY: HYPERPARATHYROIDISM V7 27.3.13 JS Hyperparathyroidism (HPT) is due to overactivity of the parathyroid glands, and can be primary (due to an adenoma or hyperplasia), or secondary (due to lowered calcium levels), such as in vitamin D deficiency or CKD. Common symptoms of hypercalcaemia are thirst, polyuria and polydipsia, constipation, general malaise and depression (NOTE: similar to diabetes). Primary hyperparathyroidism is being identified more frequently in asymptomatic individuals with the widespread use of biochemical autoanalysers. Diagnosis: In primary HPT (1HPT), the calcium is usually raised, and PTH (Parathyroid Hormone) raised or high-normal, and the phosphate may be low. In secondary HPT, the calcium is usually low or normal and PTH elevated. Hypercalcaemia with a low PTH suggests hypercalcaemia of malignancy or other causes of hypercalcaemia (eg vitamin D toxicity, sarcoidosis) Minor degrees of hypercalcaemia may be seen if the blood is taken after prolonged application of the tourniquet. This is due to increased albumin to which calcium is bound. The corrected serum calcium is therefore more reliable. Investigation: Calcium and corrected calcium and phosphate Vitamin D level Urinary calcium (to exclude Familial Hypocalciuric Hypercalcaemia) Other investigation as thought clinically relevant – such as Thyroid function, glucose, U&E Complications of Primary HPT: Osteoporosis Urolithiasis (calcium renal stones and their own complications of infection, pain, renal damage) Renal failure Severe hypercalcaemia can cause CNS effects including confusion Indications for surgical treatment: Symptoms related to hypercalcaemia Adjusted calcium > 2.80 mmol/L Age under 50 years Osteoporosis Urolithiasis Renal impairment Treatment: Usually surgical, with removal of the parathyroid adenoma or (in cases of parathyroid hyperplasia) subtotal parathyroidectomy In patients in whom treatment is indicated, but surgery not possible, medical therapy under the Endocrine clinic with cinacalcet may be considered for those with symptomatic hypercalcaemia. Patients with osteoporosis may require bisphosphonate treatment – which prevents bone loss and may decrease, but not normalise, serum calcium. Monitoring: For patients not requiring surgery or for whom it is unsuitable, monitoring is necessary, with referral to Endocrinology if any of the criteria for surgical treatment are met. Similarly, patients seen in the Endocrine Clinic may be referred back to Primary Care for monitoring if there are no current indications for intervention (see below). Monitoring should include: Annual clinical assessment for symptoms Annual assessment of calcium, PTH, vitamin D and renal function Patients with 1HPT are at increased risk of vitamin D deficiency and this cannot be identified from calcium and PTH levels. Vitamin D need not continue to be monitored in patients who are found to be deficient and who are treated successfully and continue taking maintenance vitamin D regularly. Periodic DXA scans - guidelines advise scanning every 24 months but this may be reduced based on clinical judgement, eg in patients with stable BMD and those on bisphosphonate therapy in whom a good response to treatment has already been confirmed. P1NP cannot be used in place of DXA scanning to diagnose osteoporosis and cannot be used to monitor the effects of 1HPT in patients who are not receiving bisphosphonate therapy. P1NP may however be useful to monitor bisphosphonate response in these patients and thereby reduce the frequency of DXA assessment. Referral Pointers: Symptomatic hypercalcaemia Any complications which would indicate surgery Write for advice if needed. Discharge and Ongoing Monitoring: Suitable patients will be discharged and the calcium, Vitamin D and U&E will need monitoring annually, unless the letter states anything different.