Parathyroid disorders

See also Hyper/hypocalcaemia for the acute calcium-disturbance work-up.

Calcium physiology (the PTH loop)

A fall in serum calcium triggers the parathyroids to release PTH, which:

1. makes the kidney retain calcium and excrete phosphate,
2. drives bone to release calcium, and
3. (via activated vitamin D) increases gut calcium absorption.

Interpreting results turns on measuring PTH alongside calcium:

• High calcium + high (or inappropriately normal) PTH → a parathyroid problem (primary hyperparathyroidism).
• High calcium + low PTH → PTH-independent hypercalcaemia (look elsewhere — commonly malignancy).
• Normal calcium + high PTH → secondary hyperparathyroidism (the parathyroid is compensating for low calcium availability, e.g. vitamin D deficiency).

Primary hyperparathyroidism

Usually a single parathyroid adenoma. Suspect in any patient with hypercalcaemia (“bones, moans, stones and abdominal groans”): fatigue, cognitive change, renal calculi. Calcium is elevated but rises slowly; PTH is high or inappropriately high-normal; fasting phosphate is low/low-normal.

Investigations: corrected calcium (CMP), UEC, albumin/creatinine ratio, vitamin D, PTH, and a bone density scan. Imaging is not needed for diagnosis — only for surgical planning, on specialist advice.

Management — definitive therapy is surgery (parathyroidectomy). Refer for surgery with renal calculi, renal impairment, or corrected calcium >0.25 mmol/L above the reference range. A watch-and-wait approach suits patients over 50 with all of: corrected calcium <2.9 mmol/L, normal kidney function, no nephrolithiasis/nephrocalcinosis, BMD T-score > −2.5, and no symptoms — about 50% avoid surgery over 10 years. For conservative management:

• monitor calcium and kidney function every 6–12 months, BMD every 2 years;
• avoid high calcium intake; limit vitamin D supplementation to 1000 IU (25 microgram)/day if needed for deficiency; keep water intake high (~2.5 L/day).

Refer patients younger than 40 for genetic testing.

Secondary and tertiary hyperparathyroidism

• Secondary — normal calcium, high PTH; typically from vitamin D deficiency or chronic kidney disease. Much more common than primary — treat the underlying cause and correct vitamin D first. Thiazides increase calcium retention and can unmask/worsen hypercalcaemia.
• Tertiary — prolonged secondary stimulation (usually CKD or post-transplant) becomes autonomous, producing hypercalcaemia; often needs partial parathyroidectomy.

Familial hypocalciuric hypercalcaemia (FHH)

Benign, familial, not dangerous. Only needs diagnosing if surgery is being considered (to avoid a futile parathyroidectomy) — urinary calcium is used to identify it. Otherwise don’t chase it.

Hypoparathyroidism

The commonest cause of hypocalcaemia. Causes: postoperative (thyroidectomy/ parathyroidectomy), congenital (DiGeorge syndrome), and idiopathic autoimmune. Features: neuromuscular hyperexcitability, tetany, and neuropsychiatric manifestations — see Hyper/hypocalcaemia.

Practical pearls

• Vitamin D toxicity is possible from oral colecalciferol, and more readily from calcitriol (acts directly on the gut).
• Calcium citrate is absorbed independent of gastric acidity — useful on a PPI.
• Emergency hypercalcaemia: calcium >3.5 mmol/L (or >3 with symptoms) needs urgent management.
• If PTH-independent hypercalcaemia has no obvious cause, look for malignancy; if still unclear, seek specialist advice.