Primary and Secondary Hypoparathyroidism ✅

Related Subjects: |PTH Physiology |Calcium Physiology |Magnesium Physiology |Calcitonin |Hypocalcaemia |Hypercalcaemia |Hypomagnesaemia |Hypermagnesaemia |Primary Hyperparathyroidism |Familial hypocalciuric hypercalcaemia (FHH) |Sarcoidosis

🧑‍⚕️ Hypoparathyroidism is most commonly iatrogenic after anterior neck surgery (~75% of cases). It results in low PTH, hypocalcaemia, and hyperphosphataemia, which can cause neuromuscular excitability, cardiac arrhythmias, and long-term renal/bone complications. Always check serum calcium, phosphate, and PTH in post-thyroidectomy patients with symptoms.

📖 About

• Rare endocrine disorder due to inadequate parathyroid hormone (PTH) secretion.
• Classical manifestations are of hypocalcaemia (tetany, seizures, paraesthesia).
• May be primary (autoimmune, genetic) or secondary (surgical, radiation, magnesium deficiency).

🧾 Aetiology

• Primary: Autoimmune destruction (APS1), DiGeorge syndrome, idiopathic congenital absence.
• Secondary: Anterior neck surgery (thyroidectomy, parathyroidectomy), neck irradiation, hypomagnesaemia (impairs PTH secretion).
• Biochemistry: Low PTH → low calcium, high phosphate, normal alkaline phosphatase.

🧬 Definition (per guidelines)

• Albumin-corrected hypocalcaemia confirmed on ≥2 occasions, ≥2 weeks apart.
• PTH undetectable or inappropriately low (<20 pg/mL) in presence of hypocalcaemia.
• Phosphate often high or upper-normal.
• Post-neck surgery: chronic hypoparathyroidism defined after 6 months.

🩺 Clinical Features

• Neuromuscular irritability: perioral tingling, carpopedal spasm, cramps, tetany, seizures, laryngospasm/stridor.
• Chronic complications: basal ganglia calcification, nephrocalcinosis, ectopic calcium deposits in skin/joints/eyes.
• Cardiac: prolonged QT → arrhythmias.
• Long-term: impaired renal function and skeletal health if poorly controlled.

🔍 Investigations

• Bloods: Ca²⁺ low, phosphate high, PTH low, Mg²⁺ (correct if low), vitamin D metabolites, U&E.
• ECG: QT prolongation, arrhythmia risk.
• Urine: 24-hour calcium, creatinine clearance, nephrolithiasis risk.
• Imaging: Renal US/CT (nephrocalcinosis), skull X-ray (calcifications).
• BMD: DXA scan to monitor bone health.

💊 Management

• Correct magnesium first if deficient (Mg²⁺ needed for PTH secretion).
• Calcium replacement: oral calcium carbonate/citrate; IV calcium gluconate for acute symptomatic hypocalcaemia.
• Activated vitamin D analogues (calcitriol, alfacalcidol) to enhance calcium absorption.
• Thiazide diuretics + low-salt diet → reduce urinary calcium loss in patients with hypercalciuria.
• Phosphate binders + dietary phosphate restriction if hyperphosphataemia persists.
• Recombinant PTH (e.g. Natpara) – for refractory/chronic hypoparathyroidism under specialist supervision.
• Regular monitoring: serum Ca²⁺, phosphate, magnesium, renal function, and urine calcium.
• Patient education: hypocalcaemia symptoms, emergency management with rapid calcium if needed.

📚 References

• Management of Hypoparathyroidism: Guidelines, JCEM
• Review of Hypoparathyroidism (NCBI)

Cases - Hypoparathyroidism

• Case 1 - Post-Thyroidectomy Hypocalcaemia ⚠️: 52F post-total thyroidectomy for multinodular goitre develops perioral tingling & hand cramps. Trousseau’s positive. Labs: Ca²⁺ 1.75 mmol/L, PO₄³⁻ ↑, PTH low. Management: IV calcium gluconate acutely; long-term oral calcium + calcitriol/alfacalcidol; monitor electrolytes & renal function.
• Case 2 - Autoimmune Primary Hypoparathyroidism 🧬: 30F with Addison’s disease, muscle cramps, cataracts, seizures. Labs: low Ca²⁺, high phosphate, low PTH. Management: Oral calcium + active vitamin D; monitor Ca²⁺ & renal function; educate patient on symptom recognition.
• Case 3 - CKD-Related Secondary Hypoparathyroidism 💧: 65M, CKD5 on haemodialysis, bone pain & pruritus. Labs: Ca²⁺ low–normal, PO₄³⁻ high, PTH ↑. Management: Phosphate binders, alfacalcidol, optimise dialysis, consider calcimimetics.
• Case 4 - Vitamin D Deficiency Secondary Hypocalcaemia 🌥️: 45M with coeliac disease, bone pain, proximal weakness. Labs: low Ca²⁺, low phosphate, high PTH, vitamin D deficient. Management: Oral vitamin D + calcium, treat malabsorption; monitor response.

Teaching Commentary 🧠

- Primary hypoparathyroidism: low PTH → hypocalcaemia, hyperphosphataemia (post-surgical or autoimmune). - Secondary hypoparathyroidism: compensatory ↑PTH due to chronic hypocalcaemia (CKD, vitamin D deficiency, malabsorption). - Clinical features: paraesthesia, tetany, seizures, psychiatric changes, prolonged QT. - Management is cause-directed: replace calcium & active vitamin D in primary; treat underlying disorder in secondary. ⚠️ Key lab distinction: PTH low in primary, high in secondary hypocalcaemia.