Related Subjects:
|PTH Physiology
|Calcium Physiology
|Magnesium Physiology
|Calcitonin
|Hypocalcaemia
|Hypercalcaemia
|Hypomagnesaemia
|Hypermagnesaemia
|Primary Hyperparathyroidism
|Familial hypocalciuric hypercalcaemia (FHH)
|Sarcoidosis
Hypoparathyroidism most commonly results from anterior neck surgery (≈75% of cases).
The condition leads to low PTH, hypocalcaemia, and hyperphosphataemia, with potentially life-threatening neuromuscular and systemic complications.
📖 About
- Rare endocrine disorder caused by inadequate secretion of parathyroid hormone (PTH).
- Classically presents with features of hypocalcaemia.
- See also: linked articles on calcium physiology & hypocalcaemia management.
🧾 Aetiology
- Primary: Autoimmune destruction, genetic syndromes (e.g. DiGeorge, Bartter’s), idiopathic.
- Secondary: Anterior neck surgery (thyroidectomy, parathyroidectomy), radiation injury, hypomagnesaemia (inhibits PTH secretion).
- Biochemistry: Low PTH, low calcium, high phosphate, normal ALP.
🧬 Definition (per guidelines)
- Albumin-adjusted hypocalcaemia confirmed on ≥2 occasions, ≥2 weeks apart.
- PTH undetectable or inappropriately low (<20 pg/mL) in the presence of hypocalcaemia.
- Phosphate usually high or upper-normal.
- After neck surgery, chronic hypoparathyroidism is defined after 6 months.
🩺 Clinical Features
- Neuromuscular irritability: tingling, cramps, carpopedal spasm, seizures, stridor.
- Chronic complications: basal ganglia calcification, nephrocalcinosis, ectopic calcium deposits (joints, eyes, skin, vasculature).
- Long-standing disease can lead to impaired renal and skeletal health.
🔍 Investigations
- Bloods: Ca²⁺ low, Phosphate high, PTH low, Mg²⁺ (exclude deficiency), U&E, vitamin D metabolites.
- ECG: Prolonged QTc interval.
- Urine: 24-hr calcium, creatinine clearance, stone risk profile.
- Imaging: Renal US/CT (nephrocalcinosis), skull X-ray (calcifications).
- BMD: DXA scan to assess bone mineral density.
💊 Management
- Correct Mg²⁺ first if deficient.
- Activated vitamin D analogues (e.g. Calcitriol 1,25(OH)₂D) ± oral calcium supplements.
- Thiazide diuretics with low salt diet → reduce urinary calcium loss.
- Phosphate binders + low phosphate diet if hyperphosphataemia persists.
- PTH replacement therapy (recombinant PTH) – emerging option in refractory/chronic cases.
- Regular monitoring for renal function, nephrocalcinosis, and calcium/phosphate balance.
📚 References
Cases — Primary & Secondary Hypoparathyroidism
- Case 1 — Post-Thyroidectomy Hypocalcaemia ⚠️ (Primary):
A 52-year-old woman undergoes total thyroidectomy for multinodular goitre. On day 2 post-op, she develops perioral tingling, hand cramps, and a positive Trousseau’s sign. Bloods: Ca²⁺ 1.75 mmol/L (low), PO₄³⁻ high, PTH low.
Diagnosis: Primary hypoparathyroidism due to surgical damage to parathyroid glands.
Management: IV calcium gluconate acutely; long-term oral calcium + alfacalcidol/calcitriol.
- Case 2 — Autoimmune Hypoparathyroidism 🧬 (Primary):
A 30-year-old woman with Addison’s disease presents with muscle cramps, cataracts, and seizures. Bloods: low Ca²⁺, high phosphate, low PTH.
Diagnosis: Autoimmune primary hypoparathyroidism (part of polyglandular autoimmune syndrome).
Management: Calcium + active vitamin D analogues; monitor renal function and Ca²⁺ levels closely.
- Case 3 — CKD-Related Secondary Hypoparathyroidism 💧 (Secondary):
A 65-year-old man with CKD stage 5 (on haemodialysis) develops bone pain and pruritus. Bloods: Ca²⁺ low–normal, phosphate high, PTH elevated.
Diagnosis: Secondary hyperparathyroidism due to CKD, causing hypocalcaemia.
Management: Phosphate binders, vitamin D analogues (alfacalcidol), optimise dialysis, consider calcimimetics.
- Case 4 — Vitamin D Deficiency 🌥️ (Secondary):
A 45-year-old man with coeliac disease and poor sunlight exposure presents with diffuse bone pain and proximal muscle weakness. Bloods: Ca²⁺ low, phosphate low, PTH elevated, Vit D low.
Diagnosis: Secondary hypoparathyroidism due to vitamin D deficiency.
Management: Oral vitamin D supplementation, calcium replacement, treat underlying malabsorption.
Teaching Commentary 🧠
- Primary hypoparathyroidism = low PTH → low Ca²⁺, high phosphate (classically after thyroid surgery or autoimmune).
- Secondary hypoparathyroidism = compensatory ↑PTH due to chronic hypocalcaemia (from CKD, Vit D deficiency, malabsorption).
- Symptoms: paraesthesia, tetany, seizures, psychiatric changes, prolonged QT.
- Management always targets the cause: replace calcium & vitamin D in primary; treat CKD or Vit D deficiency in secondary.
⚠️ Key distinction = **PTH levels** (low in primary, high in secondary).