About This Page
This is a clinician-written, evidence-based summary aligned to the 2026 MLA Content Map. It is intended for medical students and junior doctors preparing for the UKMLA. Always cross-reference with NICE guidance, local protocols, and clinical judgement.
The Bottom Line
- Most common cause: iatrogenic — post-thyroidectomy or parathyroidectomy (transient or permanent)
- Other causes: autoimmune (isolated or APS type 1), congenital (DiGeorge syndrome — 22q11 deletion), hypomagnesaemia
- Biochemistry: low calcium, high phosphate, low/absent PTH (unlike pseudohypoparathyroidism where PTH is high)
- Clinical features: neuromuscular excitability — tetany, paraesthesiae, Chvostek sign, Trousseau sign, seizures
- Treatment: oral calcium supplements + alfacalcidol/calcitriol (active vitamin D). Aim for low-normal calcium
- Recombinant PTH (teriparatide) considered for refractory cases
Overview
Hypoparathyroidism is characterised by deficient parathyroid hormone (PTH) secretion or action, resulting in hypocalcaemia and hyperphosphataemia. The most common cause is surgical damage to or inadvertent removal of the parathyroid glands during thyroidectomy or parathyroidectomy (post-surgical hypoparathyroidism). It may be transient (resolves within weeks) or permanent (lasts >6 months). Autoimmune hypoparathyroidism occurs in isolation or as part of autoimmune polyglandular syndrome type 1 (APS1: hypoparathyroidism + Addison disease + chronic mucocutaneous candidiasis). Congenital causes include DiGeorge syndrome (22q11.2 microdeletion — absent/hypoplastic parathyroid and thymus). Functional hypoparathyroidism can result from severe hypomagnesaemia, which impairs PTH secretion and action.
Epidemiology
Post-surgical hypoparathyroidism is the most common form. Transient hypocalcaemia occurs in up to 30% of patients after total thyroidectomy; permanent hypoparathyroidism in 1–3%. Prevalence of chronic hypoparathyroidism is approximately 20–40 per 100,000. Autoimmune hypoparathyroidism is rare. DiGeorge syndrome occurs in approximately 1 in 4,000 births. Hypomagnesaemia-related functional hypoparathyroidism is important to recognise as it is reversible with magnesium replacement.
Clinical Features
Symptoms
Perioral and digital paraesthesiae (tingling around mouth, fingers, toes)
Muscle cramps and spasms
Tetany (carpopedal spasm)
Seizures (due to hypocalcaemia-induced neuronal excitability)
Laryngospasm (stridor — can be life-threatening)
Fatigue, anxiety, depression, cognitive impairment
Signs
Chvostek sign: tapping over facial nerve (anterior to ear) → ipsilateral facial muscle twitch
Trousseau sign: inflate BP cuff above systolic for 3 min → carpopedal spasm (main d'accoucheur). More specific than Chvostek
Prolonged QT interval on ECG (risk of arrhythmias)
Papilloedema (chronic hypocalcaemia, rare)
Dry skin, brittle nails, dental enamel hypoplasia (chronic disease)
Cataracts (chronic hypocalcaemia → lens calcification)
Investigations
First-line
Albumin-adjusted serum calciumLow (<2.2 mmol/L). Severity of symptoms correlates with rapidity of fall rather than absolute level
Serum phosphateElevated (loss of PTH-mediated renal phosphate excretion)
Serum PTHLow or undetectable = hypoparathyroidism. Elevated PTH with hypocalcaemia = vitamin D deficiency or pseudohypoparathyroidism
Second-line
Serum magnesiumLow magnesium impairs PTH secretion and action — must correct before calcium will respond
Vitamin D (25-OH)Exclude coexistent vitamin D deficiency
ECGProlonged QT interval — risk of Torsades de Pointes. Important in acute setting
Renal functionChronic hypocalcaemia treatment with calcium/vitamin D can cause hypercalciuria → nephrocalcinosis
Specialist
24 h urinary calciumMonitor during treatment — aim to keep below upper limit to avoid nephrocalcinosis
Genetic testingIf congenital suspected (DiGeorge: FISH/microarray for 22q11.2 deletion), APS1 (AIRE gene mutations)
1
Acute symptomatic hypocalcaemia (EMERGENCY)
- IV calcium gluconate 10% — 10 mL (2.2 mmol Ca²⁺) over 10 min with cardiac monitoring
- Can repeat if needed. Follow with IV infusion: 40 mL of 10% calcium gluconate in 1 L 0.9% NaCl over 8–12 h
- Check and replace magnesium (IV magnesium sulphate 8 mmol over 15 min if low)
- DO NOT mix calcium with bicarbonate in same line (precipitates)
- Monitor ECG continuously (risk of arrhythmia if calcium given too fast)
2
Chronic replacement
- Oral calcium: calcium carbonate or calcium citrate 1–3 g/day in divided doses
- Active vitamin D: alfacalcidol 0.5–2 mcg daily or calcitriol 0.25–1 mcg daily (conventional vitamin D is ineffective without PTH to activate it)
- Target: albumin-adjusted calcium in low-normal range (2.0–2.25 mmol/L) — avoid hypercalcaemia
- Monitor: serum calcium, phosphate, renal function, urinary calcium every 3–6 months
3
Refractory cases
- Recombinant PTH (teriparatide): off-label for refractory hypoparathyroidism requiring high calcium/calcitriol doses
- TransCon PTH: long-acting PTH prodrug — licensed in some countries for chronic hypoparathyroidism
- Thiazide diuretic: reduces urinary calcium excretion, useful if hypercalciuria develops on treatment
- Low-phosphate diet may help reduce hyperphosphataemia
Complications
- Seizures: From severe hypocalcaemia — important differential diagnosis of new-onset seizures
- Cardiac arrhythmias: Prolonged QT → Torsades de Pointes. ECG monitoring essential in acute setting
- Laryngospasm: Can cause airway obstruction — life-threatening
- Basal ganglia calcification: Chronic hypoparathyroidism → bilateral symmetrical calcification (Fahr syndrome) — may cause movement disorders
- Cataracts: Posterior subcapsular cataracts from chronic hypocalcaemia
- Nephrocalcinosis/renal stones: Paradoxically from treatment — calcium + vitamin D → hypercalciuria. Monitor urinary calcium
UKMLA Exam Tips
- 1Post-thyroidectomy day 1: patient develops tingling, cramping → check calcium URGENTLY. This is hypoparathyroidism until proven otherwise
- 2Chvostek sign (facial twitch) is sensitive but not specific. Trousseau sign (carpopedal spasm) is more specific
- 3Low calcium + high phosphate + LOW PTH = hypoparathyroidism. Low calcium + high phosphate + HIGH PTH = pseudohypoparathyroidism (PTH resistance)
- 4Always check magnesium — hypomagnesaemia causes functional hypoparathyroidism. Calcium won't correct until Mg is replaced
- 5IV calcium gluconate is SAFE peripherally. Calcium chloride is for central lines only (causes tissue necrosis if extravasated)
- 6Prolonged QT on ECG = check calcium. Short QT = check calcium (hypercalcaemia). Calcium affects QT interval bidirectionally
practicetest your knowledge on hypoparathyroidismApply what you've learnt with UKMLA-style questions from the iatroX Q-Bank — endocrine and beyond.
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