Calcium Disorders

Hypercalcaemia

Hypercalcaemia is defined as serum adjusted calcium above the local reference range, typically >2.60 mmol/L for albumin-adjusted total calcium, or ionised calcium >1.32 mmol/L. In MRCP-style questions, always distinguish true hypercalcaemia from artefact due to dehydration, venous stasis, high albumin, paraproteinaemia, or sampling error. Albumin correction is conventionally: adjusted calcium = measured calcium + 0.02 × (40 − albumin g/L), although correction formulae perform poorly in critical illness, hypoalbuminaemia, CKD and acid–base disturbance; ionised calcium is preferred where clinical severity and total calcium are discordant.

Severity	Adjusted calcium	Typical clinical implication
Mild	2.60–2.99 mmol/L	Often asymptomatic; outpatient evaluation if stable
Moderate	3.00–3.49 mmol/L	Symptoms common; urgent investigation and treatment if acute
Severe	≥3.50 mmol/L	Medical emergency; high risk of arrhythmia, coma, renal failure

Pathophysiological classification

The pivotal discriminator is PTH-mediated versus PTH-suppressed hypercalcaemia. PTH increases renal distal tubular calcium reabsorption, phosphaturia, and 1α-hydroxylase activity, increasing calcitriol and intestinal calcium absorption. Malignancy causes hypercalcaemia via PTH-related peptide, osteolytic cytokines, or ectopic calcitriol production. A low phosphate supports PTH/PTHrP physiology; high or normal phosphate suggests vitamin D excess, renal failure, thyrotoxicosis or bone destruction, although overlap is common.

Biochemical pattern	Key causes	Exam clues
High or inappropriately normal PTH	Primary hyperparathyroidism, tertiary hyperparathyroidism, lithium-associated disease, familial hypocalciuric hypercalcaemia	Chronic mild hypercalcaemia; renal stones; osteoporosis; low urinary calcium in FHH
Suppressed PTH, high PTHrP	Squamous carcinoma, renal, bladder, ovarian, breast cancers	Rapid onset, marked calcium elevation, weight loss; phosphate often low
Suppressed PTH, high 1,25-dihydroxyvitamin D	Sarcoidosis, tuberculosis, lymphoma	Granulomatous disease; steroid responsive
Suppressed PTH, high 25-hydroxyvitamin D	Vitamin D intoxication	Supplement history; hyperphosphataemia may occur
Suppressed PTH, other mechanisms	Thiazides, thyrotoxicosis, adrenal insufficiency, immobilisation, milk-alkali syndrome, vitamin A excess	Medication/endocrine context; metabolic alkalosis in milk-alkali

Clinical features and complications

Symptoms correlate better with rate of rise than absolute calcium. Classical manifestations include polyuria, polydipsia, dehydration, constipation, anorexia, nausea, pancreatitis, proximal myopathy, neurocognitive impairment, depression, confusion and coma. Renal effects include nephrogenic diabetes insipidus, nephrolithiasis, nephrocalcinosis and acute kidney injury. ECG changes include shortened QT interval, PR prolongation, bradyarrhythmias and, in severe cases, ventricular arrhythmias. Hypercalcaemia potentiates digoxin toxicity.

Investigation strategy

Confirm the result with repeat adjusted calcium or ionised calcium, and assess U&Es/eGFR, phosphate, magnesium, ALP, bicarbonate, FBC, ESR/CRP and ECG. The first-line endocrine test is intact PTH, interpreted against the calcium concentration: a “normal” PTH is abnormal if calcium is high. If PTH is suppressed, investigate malignancy and non-PTH causes with targeted imaging, myeloma screen, 25-hydroxyvitamin D, 1,25-dihydroxyvitamin D where granulomatous disease/lymphoma is suspected, TFTs and cortisol when clinically indicated. In suspected FHH, calculate calcium–creatinine clearance ratio: <0.01 strongly supports FHH, whereas >0.02 favours primary hyperparathyroidism, though vitamin D deficiency and CKD confound interpretation.

Acute management

UK Society for Endocrinology emergency guidance treats symptomatic hypercalcaemia, or calcium typically >3.0 mmol/L, urgently; ≥3.5 mmol/L is an emergency. Stop thiazides, lithium, calcium, vitamin D and vitamin A; treat the cause; monitor fluid balance, renal function and ECG.

Intervention	Dose and kinetics	Key points
0.9% sodium chloride	Usually 4–6 L over 24 h, adjusted to age, cardiac and renal status	Restores GFR and calciuresis; avoid loop diuretics unless fluid overloaded after rehydration
Zoledronic acid	4 mg IV over ≥15 min; onset 2–4 days; nadir 4–7 days	Preferred bisphosphonate in malignancy; reduce/avoid in severe renal impairment; risk of hypocalcaemia and osteonecrosis of jaw
Pamidronate	30–90 mg IV over 2–4 h	Alternative when slower infusion preferred; renal caution
Calcitonin	4 IU/kg SC/IM every 12 h, may increase to 8 IU/kg 6–12-hourly	Onset 4–6 h; tachyphylaxis after 48–72 h; useful bridge in severe symptomatic disease
Denosumab	120 mg SC, repeated on days 8 and 15 then 4-weekly in malignancy regimens	Useful in bisphosphonate-refractory hypercalcaemia or renal impairment; monitor for profound hypocalcaemia
Glucocorticoids	Prednisolone 40 mg daily or hydrocortisone 100 mg IV 6-hourly	Indicated for calcitriol-mediated disease: lymphoma, sarcoidosis, vitamin D excess; response over 2–5 days

Haemodialysis with low-calcium dialysate is reserved for life-threatening hypercalcaemia with renal failure, refractory fluid overload, severe neurological compromise or arrhythmia. Avoid routine furosemide-driven “forced diuresis”; it worsens volume depletion and is not recommended except to manage iatrogenic overload after adequate rehydration.

Hypocalcaemia

Definition, physiology and clinical significance

Hypocalcaemia is defined as a serum adjusted calcium below the local reference range, typically <2.15 mmol/L, or an ionised calcium <1.10 mmol/L. Severe hypocalcaemia is commonly taken as adjusted calcium <1.90 mmol/L or symptomatic hypocalcaemia at any level. Approximately 40% of circulating calcium is albumin-bound, 10% complexed, and 50% ionised; only ionised calcium is biologically active. Albumin correction is approximate: corrected calcium = measured calcium + 0.02 × (40 − albumin g/L). In critical illness, renal failure, acid-base disturbance, citrate exposure or major transfusion, ionised calcium is preferable; alkalosis increases albumin binding and may produce symptomatic hypocalcaemia despite normal total calcium.

Mechanistic classification

Mechanism	Typical causes	Biochemical pattern
Reduced PTH secretion	Post-thyroidectomy/parathyroidectomy, autoimmune hypoparathyroidism, DiGeorge syndrome, infiltrative disease, activating CaSR mutation	Low calcium, low or inappropriately normal PTH, high phosphate
PTH resistance	Pseudohypoparathyroidism, severe hypomagnesaemia, chronic kidney disease	Low calcium, high PTH; phosphate often high
Vitamin D deficiency or impaired activation	Malabsorption, low sunlight, anticonvulsants, cholestasis, CKD, severe liver disease	Low/normal calcium, low phosphate in nutritional deficiency, high PTH, low 25-OH vitamin D
Calcium sequestration or loss	Acute pancreatitis, rhabdomyolysis, tumour lysis, hungry bone syndrome, massive transfusion citrate, bisphosphonates/denosumab	Variable PTH; phosphate high in tumour lysis/rhabdomyolysis, low in hungry bone
Magnesium-related	Alcohol excess, PPIs, diarrhoea, aminoglycosides, cisplatin, loop diuretics	Low Mg; impaired PTH secretion and end-organ response

Clinical features and severity

Neuromuscular irritability predominates: perioral paraesthesia, distal paraesthesia, cramps, carpopedal spasm, tetany, laryngospasm and seizures. Chronic hypocalcaemia may cause cataracts, basal ganglia calcification, extrapyramidal features, dry skin, brittle nails and dental abnormalities. Cardiac manifestations include QT prolongation, torsades de pointes, heart failure and reduced myocardial contractility. Chvostek’s sign is neither sensitive nor specific; Trousseau’s sign is more specific but not diagnostic. Symptoms correlate better with rate of fall and ionised calcium than with total calcium.

Investigation: exam approach

Confirm true hypocalcaemia with albumin-adjusted and, if acutely unwell, ionised calcium. Initial tests should include phosphate, magnesium, creatinine/eGFR, alkaline phosphatase, PTH, 25-hydroxyvitamin D, ECG and medication review. Interpret PTH in context: in genuine hypocalcaemia, PTH should be elevated; a “normal” PTH is therefore abnormal and suggests hypoparathyroidism or magnesium deficiency. A low magnesium, particularly <0.4 mmol/L, may render hypocalcaemia refractory until corrected. In suspected hypoparathyroidism, urinary calcium is important once treated because conventional therapy predisposes to hypercalciuria and nephrocalcinosis; target 24-hour urinary calcium is usually <7.5 mmol/day in women and <10 mmol/day in men.

Acute management

Emergency treatment is indicated for seizures, tetany, laryngospasm, arrhythmia, marked QT prolongation, or adjusted calcium <1.90 mmol/L. UK Society for Endocrinology emergency guidance recommends intravenous calcium gluconate rather than calcium chloride for peripheral administration.

Situation	Treatment	Key cautions
Severe symptomatic hypocalcaemia	10 mL of 10% calcium gluconate contains approximately 2.25 mmol calcium; give 10–20 mL IV over 10 minutes with ECG monitoring. Repeat until symptoms improve.	Extravasation injury; avoid rapid bolus in digoxin toxicity unless life-threatening.
Persistent hypocalcaemia	Infuse 100 mL of 10% calcium gluconate in 1 L 0.9% saline or 5% glucose at 50–100 mL/hour, titrated to calcium and symptoms.	Check calcium every 4–6 hours initially; avoid overtreatment.
Hypomagnesaemia	Magnesium sulfate 20 mmol IV over 12–24 hours, or faster if severe arrhythmia/seizure under monitoring.	Reduce dose in renal impairment; monitor reflexes and respiratory status.

Chronic management and prevention

Treatment depends on mechanism. Nutritional vitamin D deficiency is treated with colecalciferol loading, commonly total 300,000 IU over 6–10 weeks, followed by maintenance 800–2,000 IU/day, with calcium supplementation if dietary intake is inadequate. In hypoparathyroidism, native vitamin D alone is insufficient because renal 1α-hydroxylation is PTH-dependent; use activated vitamin D: alfacalcidol 0.25–1 microgram/day or calcitriol 0.25–1 microgram twice daily, plus oral elemental calcium typically 1–2 g/day in divided doses. Calcitriol has a short biological half-life of approximately 4–6 hours, permitting rapid titration, whereas colecalciferol has prolonged tissue storage.

The therapeutic target in chronic hypoparathyroidism is not a high-normal calcium but a low-normal or just-below-normal adjusted calcium that abolishes symptoms while minimising hypercalciuria. Monitor calcium, phosphate, magnesium, creatinine/eGFR and urinary calcium; hyperphosphataemia increases calcium-phosphate product and ectopic calcification risk. Thiazide diuretics with low-salt diet may reduce hypercalciuria. Recombinant human PTH therapy is reserved for selected refractory cases in specialist practice where available, particularly with poor biochemical control, renal complications or high calcium/calcitriol requirements.

Hyperparathyroidism

Hyperparathyroidism is defined by inappropriate excess parathyroid hormone (PTH) activity relative to extracellular calcium. For MRCP purposes, the key diagnostic act is to interpret PTH in context: in hypercalcaemia, a PTH within the laboratory reference range is abnormal because physiological suppression should be near-complete. Typical reference ranges are adjusted calcium 2.20–2.60 mmol/L, phosphate 0.8–1.5 mmol/L, and intact PTH approximately 15–65 pg/mL or 1.6–6.9 pmol/L, assay-dependent.

Classification and pathophysiology

Type	Biochemistry	Mechanism	Common causes
Primary hyperparathyroidism	High or inappropriately normal PTH; high calcium; low-normal phosphate; raised or high-normal urine calcium	Autonomous PTH secretion, usually from a single adenoma	Solitary adenoma 80–85%; multigland hyperplasia 10–15%; carcinoma <1%; MEN1, MEN2A, CDC73-related disease
Secondary hyperparathyroidism	High PTH; calcium low/normal; phosphate variable, often high in CKD	Appropriate chronic PTH drive due to hypocalcaemia, phosphate retention or reduced calcitriol	CKD stages 3–5, vitamin D deficiency, malabsorption, bariatric surgery, anticonvulsants
Tertiary hyperparathyroidism	Very high PTH; high calcium; often high phosphate in CKD	Autonomous nodular parathyroid hyperplasia after prolonged secondary disease	Long-term dialysis; post-renal transplantation
Normocalcaemic primary hyperparathyroidism	Repeatedly normal calcium with elevated PTH	Early primary disease after exclusion of secondary causes	Diagnosis requires vitamin D repletion and eGFR usually >60 mL/min/1.73 m2

PTH increases serum calcium via osteoblast-mediated RANKL expression with osteoclast activation, renal distal tubular calcium reabsorption, proximal tubular phosphate wasting, and stimulation of 1α-hydroxylase to increase 1,25-dihydroxyvitamin D. Primary disease therefore classically causes hypercalcaemia, hypophosphataemia, hypercalciuria, cortical bone loss and nephrolithiasis. In CKD, phosphate retention, reduced calcitriol synthesis and skeletal PTH resistance produce diffuse gland hyperplasia; prolonged stimulation may become clonal and autonomous.

Diagnosis and exclusion of mimics

Initial evaluation should include repeated adjusted or ionised calcium, PTH, phosphate, creatinine/eGFR, 25-hydroxyvitamin D, alkaline phosphatase, urinary calcium excretion and renal imaging if stone disease is suspected. Vitamin D deficiency should be corrected cautiously because it may unmask hypercalcaemia but also exaggerates PTH elevation. Familial hypocalciuric hypercalcaemia is the principal mimic of primary hyperparathyroidism: calculate the calcium-to-creatinine clearance ratio, with <0.01 supporting FHH and >0.02 favouring primary hyperparathyroidism; intermediate results occur with vitamin D deficiency, CKD, thiazides and lithium. FHH is usually due to heterozygous CASR variants and parathyroidectomy is ineffective.

Parathyroid imaging is for localisation before surgery, not diagnosis. Neck ultrasound has operator-dependent sensitivity of roughly 55–85% for solitary adenoma. ^99mTc-sestamibi SPECT/CT has sensitivity around 70–80% for single adenomas but much lower for multigland disease. 4D-CT may improve localisation in re-operative or discordant cases but adds radiation. Bilateral neck exploration remains appropriate when localisation is negative or multigland disease is suspected.

Management of primary hyperparathyroidism

Parathyroidectomy is definitive, with biochemical cure in >95% in expert hands for sporadic solitary adenoma. Intra-operative PTH monitoring exploits the short PTH half-life of approximately 3–5 minutes; a fall of >50% from the highest pre-excision level at 10 minutes, into or towards the normal range, supports cure.

Current international workshop criteria for surgery in asymptomatic primary hyperparathyroidism include any of the following:

• Serum calcium >0.25 mmol/L or >1.0 mg/dL above the upper limit of normal.
• Skeletal disease: fragility fracture, vertebral fracture on imaging, or DXA T-score ≤ -2.5 at lumbar spine, total hip, femoral neck or distal one-third radius.
• Renal involvement: eGFR or creatinine clearance <60 mL/min, nephrolithiasis or nephrocalcinosis, or 24-hour urine calcium >250 mg/day in women or >300 mg/day in men, particularly with stone-risk abnormalities.
• Age <50 years.
• Patient preference or inability to ensure surveillance.

Medical management is appropriate for non-operative candidates or those awaiting surgery. Maintain hydration, avoid thiazides and lithium where feasible, and do not impose severe calcium restriction; usual calcium intake of about 1,000 mg/day is acceptable. Replete 25-hydroxyvitamin D to at least 50 nmol/L, often 75 nmol/L, using cautious cholecalciferol regimens with calcium monitoring. Cinacalcet, a calcimimetic allosteric activator of the calcium-sensing receptor, lowers calcium but does not reliably improve bone mineral density; typical starting dose is 30 mg twice daily, titrated every 2–4 weeks to 60–90 mg twice daily or three times daily. Nausea and hypocalcaemia are limiting. Oral bisphosphonates, especially alendronate 70 mg weekly, improve BMD but have little effect on serum calcium; denosumab may be used in severe renal impairment but requires vigilance for hypocalcaemia.

Secondary and tertiary hyperparathyroidism

Management of CKD-related hyperparathyroidism follows KDIGO principles: interpret serial calcium, phosphate, PTH and alkaline phosphatase trends rather than isolated values; lower phosphate with dietary restriction and binders; correct vitamin D deficiency; and avoid hypercalcaemia. In dialysis patients, PTH is often maintained at approximately 2–9 times the assay upper limit rather than normalised. Active vitamin D analogues such as calcitriol 0.25 micrograms daily or alfacalcidol 0.25–1 microgram daily suppress PTH but may raise calcium and phosphate. Cinacalcet is commonly started at 30 mg daily in dialysis patients and titrated; the EVOLVE trial did not meet its unadjusted primary composite cardiovascular endpoint, but secondary and adjusted analyses supported reduced parathyroidectomy and severe hyperparathyroidism. Tertiary hyperparathyroidism with persistent hypercalcaemia after transplantation or refractory dialysis disease, especially PTH persistently >800 pg/mL with hypercalcaemia, hyperphosphataemia, bone pain, pruritus or calciphylaxis, generally requires subtotal or total parathyroidectomy with autotransplantation. Post-operatively, anticipate hungry bone syndrome requiring aggressive calcium and calcitriol replacement.

Parathyroid Disease

Applied physiology and anatomical considerations

Parathyroid disease is best understood through the calcium–PTH–vitamin D axis. PTH is an 84-amino-acid peptide with a plasma half-life of approximately 2–4 minutes; intact PTH assays measure full-length PTH and large fragments, with typical reference ranges around 1.6–6.9 pmol/L or 15–65 pg/mL, depending on assay. PTH secretion is regulated by the calcium-sensing receptor (CaSR) on chief cells: reduced ionised calcium rapidly increases PTH secretion, whereas hypercalcaemia suppresses it. PTH increases renal calcium reabsorption in the distal nephron, reduces proximal tubular phosphate reabsorption, and stimulates renal 1α-hydroxylase, increasing 1,25-dihydroxyvitamin D and intestinal calcium absorption.

Most individuals have four parathyroid glands, each approximately 30–50 mg. Superior glands are relatively constant, usually posterior to the upper thyroid; inferior glands migrate with the thymus and are more variable, including intrathyroidal, mediastinal, carotid sheath and thymic locations. This embryology is clinically important in persistent or recurrent disease after surgery.

Classification of parathyroid disorders

Disorder	Biochemical pattern	Typical mechanism	Key clinical point
Primary hyperparathyroidism	High or inappropriately normal PTH with hypercalcaemia; low-normal phosphate	Single adenoma 80–85%; multigland hyperplasia 10–15%; carcinoma <1%	Common outpatient cause of hypercalcaemia; often asymptomatic
Secondary hyperparathyroidism	High PTH with low/normal calcium; phosphate variable, high in CKD	Appropriate response to hypocalcaemia, vitamin D deficiency, CKD, malabsorption	Treat driver; parathyroidectomy rarely needed except refractory renal disease
Tertiary hyperparathyroidism	High PTH with hypercalcaemia, usually after longstanding CKD	Autonomous nodular parathyroid hyperplasia	Often post-transplant or dialysis-associated; may require surgery
Hypoparathyroidism	Low or inappropriately normal PTH with hypocalcaemia and hyperphosphataemia	Post-thyroidectomy, autoimmune, infiltrative, genetic	Conventional therapy aims low-normal calcium, avoiding hypercalciuria
Pseudohypoparathyroidism	High PTH with hypocalcaemia and hyperphosphataemia	End-organ PTH resistance, commonly GNAS-related	Albright hereditary osteodystrophy in type 1a

Primary hyperparathyroidism: sporadic and familial disease

Primary hyperparathyroidism (PHPT) is usually sporadic, with female predominance and peak incidence after 50 years. The hallmark is hypercalcaemia with non-suppressed PTH; PTH within the laboratory reference range is abnormal if calcium is elevated. Familial syndromes are disproportionately represented in younger patients, multigland disease, recurrent disease, or a family history of endocrine tumours.

• MEN1: MEN1 mutation; parathyroid hyperplasia is the commonest and earliest manifestation, often multiglandular. Associated pancreatic neuroendocrine tumours and pituitary adenomas.
• MEN2A: RET mutation; medullary thyroid carcinoma, phaeochromocytoma, and PHPT, usually milder than MEN1.
• Hyperparathyroidism-jaw tumour syndrome: CDC73 mutation; ossifying jaw fibromas, renal/uterine lesions, and increased parathyroid carcinoma risk.
• Familial isolated hyperparathyroidism: genetically heterogeneous; consider MEN1, CDC73, CASR and GCM2 testing in selected cases.
• Familial hypocalciuric hypercalcaemia: CaSR-pathway disorder mimicking PHPT; calcium–creatinine clearance ratio typically <0.01, though overlap exists. Parathyroidectomy is ineffective.

Diagnosis, localisation and operative strategy

Diagnosis is biochemical, not radiological. Initial assessment should include adjusted and/or ionised calcium, phosphate, creatinine/eGFR, 25-hydroxyvitamin D, PTH, urinary calcium excretion, renal imaging where indicated, and bone mineral density at lumbar spine, hip and distal one-third radius. Vitamin D deficiency should be corrected cautiously because it can exaggerate PTH elevation and obscure interpretation.

Localisation imaging is performed only after a decision for surgery. Neck ultrasonography and ^99mTc-sestamibi scintigraphy are first-line in many centres. Sestamibi sensitivity is approximately 70–90% for solitary adenomas but substantially lower in multigland disease. 4D-CT improves localisation, particularly after negative or discordant first-line imaging, but increases radiation exposure. Selective venous sampling is reserved for re-operative or complex cases.

Indication for parathyroidectomy in asymptomatic PHPT	Guideline threshold commonly used
Serum calcium	>0.25 mmol/L, or >1.0 mg/dL, above upper limit of normal
Skeletal disease	T-score ≤ −2.5 at lumbar spine, total hip, femoral neck or distal radius; or fragility/vertebral fracture
Renal impairment	eGFR <60 mL/min/1.73 m²
Renal stone risk	Nephrolithiasis/nephrocalcinosis or marked hypercalciuria, commonly >250 mg/day in women or >300 mg/day in men
Age	<50 years

Focused minimally invasive parathyroidectomy is appropriate for concordant single-gland localisation. Bilateral neck exploration is preferred for suspected multigland disease, hereditary syndromes, lithium-associated disease, or non-localising imaging. Intra-operative PTH monitoring exploits the short PTH half-life: the Miami criterion defines cure as a fall of >50% from the highest pre-excision or pre-incision value at 10 minutes. Cure rates in expert hands exceed 95% for sporadic single adenoma.

Parathyroid carcinoma and renal hyperparathyroidism

Parathyroid carcinoma is rare but exam-relevant. Clues include calcium often >3.5 mmol/L, PTH several-fold above the upper limit, palpable neck mass, recurrent laryngeal nerve palsy, severe bone/renal disease, and CDC73 association. Fine-needle aspiration is generally avoided because of seeding risk and limited diagnostic utility. Management is en bloc surgical excision; recurrence is common, and cinacalcet is useful for controlling hypercalcaemia when unresectable.

In CKD-mineral bone disorder, secondary hyperparathyroidism reflects phosphate retention, reduced calcitriol, hypocalcaemia and parathyroid hyperplasia. KDIGO guidance emphasises trends rather than isolated values; in dialysis, PTH is often targeted to approximately 2–9 times the assay upper limit. Therapy includes dietary phosphate restriction, phosphate binders, vitamin D analogues, and calcimimetics such as cinacalcet 30 mg once daily titrated every 2–4 weeks. Parathyroidectomy is considered for severe refractory disease, calciphylaxis, bone pain, pruritus, or tertiary autonomous hypercalcaemia.

Hypoparathyroidism and post-operative complications

Postsurgical hypoparathyroidism is the commonest cause in developed practice. Acute symptomatic hypocalcaemia requires intravenous calcium gluconate, while chronic therapy uses oral calcium, typically 1–3 g/day elemental calcium in divided doses, plus alfacalcidol 0.25–2 micrograms/day or calcitriol 0.25–2 micrograms/day. Monitoring should include serum calcium, phosphate, magnesium, creatinine and 24-hour urinary calcium; the therapeutic aim is low-normal or slightly below-normal calcium with symptom control, avoiding nephrolithiasis and nephrocalcinosis. Recombinant PTH therapy is reserved for selected refractory cases, availability permitting.

After parathyroidectomy for severe hyperparathyroidism, hungry bone syndrome causes prolonged hypocalcaemia due to rapid skeletal remineralisation, especially with high pre-operative alkaline phosphatase, radiological bone disease, vitamin D deficiency and renal disease. It requires aggressive calcium and active vitamin D replacement, with magnesium repletion where necessary.