Synopsis
Separate absent PTH from end-organ PTH resistance, manage chronic calcium safely, and recognise genetic and multi-hormone implications requiring specialist care.
- Hypoparathyroidism produces low calcium and high phosphate with PTH that is low or inappropriately normal, most often after anterior neck surgery.
- Pseudohypoparathyroidism produces a similar calcium-phosphate pattern but PTH is raised because target tissues resist its signal.
- Severe magnesium depletion can suppress PTH secretion and action, so it must be corrected before declaring permanent gland failure.
- Albright hereditary osteodystrophy features can include short stature, round face, brachydactyly and subcutaneous ossification, but their absence does not exclude a GNAS-related disorder.
- Some GNAS disorders cause resistance to TSH and other hormones as well as PTH, making thyroid and developmental assessment part of specialist care.
- Conventional hypoparathyroid therapy uses oral calcium plus activated vitamin D because absent PTH impairs renal activation of native vitamin D.
- Aim for symptom control with calcium in a safe low-normal range; normalising serum calcium aggressively can cause hypercalciuria, stones and nephrocalcinosis.
- Genetic testing is phenotype-led through an NHS genomic service, and inheritance can depend on parental origin because GNAS is an imprinted locus.
Investigation priorities
Distinguish inadequate PTH secretion from an appropriately raised but ineffective PTH response.
Management branches
Persistent hypocalcaemia and hyperphosphataemia suggest parathyroid-axis disease.
- Confirm true low calcium and measure PTH, phosphate, magnesium, kidney function and vitamin D from the same physiological period.
- Correct significant magnesium deficiency and review surgery, autoimmune history, CKD and medicines before concluding gland loss or resistance.
- If PTH is raised with preserved renal function, assess Albright and multi-hormone features and refer through a specialist genomic pathway.
Key medicines
Calcitriol or alfacalcidolBegin and adjust the activated vitamin D preparation in small specialist-guided increments according to symptoms, calcium, phosphate, kidney function and urine calcium, following the local product-specific regimen.The preparations differ and dosing errors can cause prolonged hypercalcaemia, hyperphosphataemia and kidney damage. Monitor closely after changes and during intercurrent illness; do not substitute nutritional vitamin D casually.
Oral calciumUse a divided elemental-calcium regimen selected for dietary intake, symptoms and activated vitamin D dose, with product and timing documented because different salts contain different elemental amounts.High doses cause constipation and hypercalciuria and interfere with levothyroxine, iron and some antibiotics. Serum calcium alone cannot detect renal calcium toxicity.