Hypocalcaemia

Definition: corrected serum calcium below 8.5 mg/dL (normal range 8.5–10.5 mg/dL). Always correct for albumin or measure ionised calcium — hypoalbuminaemia is very common in the frail elderly and causes pseudo-hypocalcaemia. Corrected Ca (mg/dL) = measured Ca + 0.8 × (4.0 − serum albumin in g/dL)

Causes with LOW or inappropriately normal PTH (hypoparathyroidism): post-surgical after thyroidectomy or parathyroidectomy (the commonest, ~75–90% of chronic cases), autoimmune, infiltrative (haemochromatosis, Wilson's, metastasis), radiation, and hypomagnesaemia, which impairs both PTH secretion and PTH action.

Causes with HIGH PTH (secondary hyperparathyroidism): vitamin D deficiency — extremely common in Indian older adults; chronic kidney disease; malabsorption; hungry bone syndrome after parathyroidectomy; acute pancreatitis; rhabdomyolysis and tumour lysis syndrome (hyperphosphataemia); massive blood transfusion (citrate chelation); and drugs — bisphosphonates, denosumab, cinacalcet, phenytoin, foscarnet, proton pump inhibitors.

Clinical clue: suspect vitamin D deficiency in any older person with a borderline-low calcium and a raised alkaline phosphatase.

Clinical features — neuromuscular irritability: perioral and acral paraesthesia, muscle cramps, carpopedal spasm, tetany, laryngospasm and bronchospasm, seizures, confusion. Chronic hypocalcaemia causes cataract, basal ganglia calcification, papilloedema, dry skin, brittle nails and extrapyramidal features.

Signs and ECG: Chvostek's sign (facial twitch on tapping the facial nerve — falsely positive in up to 10% of normals) and Trousseau's sign (carpal spasm after cuff inflation above systolic pressure for 3 minutes) — Trousseau's is the more specific. ECG shows a prolonged QTc with risk of torsades de pointes.

Investigations: corrected and/or ionised calcium, magnesium, phosphate, creatinine, alkaline phosphatase, intact PTH, 25(OH) vitamin D, and 24-hour urinary calcium. High phosphate + low PTH = hypoparathyroidism; low phosphate + high PTH = vitamin D deficiency.

Acute symptomatic hypocalcaemia (tetany, seizure, laryngospasm, prolonged QT): IV 10% calcium gluconate 10– 20 mL diluted, over 10–20 minutes with cardiac monitoring, followed by an infusion delivering roughly 1 mg/kg/hour of elemental calcium. Correct magnesium first — calcium will not respond while the patient is hypomagnesaemic. Prefer gluconate to chloride peripherally (chloride is sclerosant).

Chronic management: oral elemental calcium 1–2 g/day in divided doses plus active vitamin D (calcitriol 0.25–1 µg/day) in hypoparathyroidism, or plain cholecalciferol where the problem is simple vitamin D deficiency. Target calcium at the LOW end of normal (8.0–8.5 mg/dL) — chasing a normal calcium in hypoparathyroidism produces hypercalciuria, nephrocalcinosis and renal failure, because PTH-driven renal calcium reabsorption is absent. A thiazide with a low-salt diet reduces hypercalciuria.

In the older patient specifically: stop the offending drug, treat malabsorption and renal disease, and ensure 800– 1000 IU/day vitamin D with 700–1200 mg calcium (target 25(OH)D ≥30 ng/mL) — the same regimen that reduces hip fracture and falls. Monitor calcium, phosphate, creatinine and urinary calcium on treatment. Latest Updates & Current Practice (2023–Present) — 3 Points Palopegteriparatide (TransCon PTH, Yorvipath) — the first long-acting once-daily PTH(1-34) prodrug, giving continuous physiological PTH exposure over 24 hours (released hormone half-life ≈60 hours). EMA-approved November 2023 and FDA-approved August 2024 for chronic hypoparathyroidism. The phase 3 PaTHway trial normalised serum calcium, phosphate and 24-hour urinary calcium with withdrawal of conventional therapy in the majority, sustained to 3 years, and normalised bone remodelling. rhPTH(1-84) (Natpara) manufacture was discontinued worldwide at the end of 2024. Revised ESE guideline (2025) and the Parathyroid Summit best-practice recommendations (2024/2025) retain calcium plus active vitamin D as first-line therapy, and reserve PTH replacement for patients with inadequate control, an unacceptable pill burden, persistent hypercalciuria, or declining renal function. Diagnosis of chronic hypoparathyroidism requires hypocalcaemia with an inappropriately low or normal PTH, and DNA analysis is now recommended in non-surgical cases. Emerging agents: eneboparatide (selective PTHR1 agonist), an oral PTH analogue, and encaleret (a calcilytic for autosomal dominant hypocalcaemia type 1) are in phase 2/3 development — the field is moving from calcium supplementation towards true hormone replacement.