Related Subjects:
|PTH Physiology
|Calcium Physiology
|Magnesium Physiology
|Calcitonin
|Hypocalcaemia
|Hypercalcaemia
|Hypomagnesaemia
|Hypermagnesaemia
|Primary Hyperparathyroidism
|Familial hypocalciuric hypercalcaemia (FHH)
|Sarcoidosis
📖 About
- Tertiary hyperparathyroidism develops after prolonged secondary hyperparathyroidism 🌀 (usually from chronic kidney disease, CKD).
- Due to parathyroid hyperplasia becoming autonomous → PTH secretion continues even after correction of hypocalcaemia.
- Biochemically characterised by hypercalcaemia ⬆️ (unlike secondary HPT, which is usually normo- or hypocalcaemic).
🩺 Clinical Features
- Occurs in the context of advanced CKD or post-renal transplant.
- Features of hypercalcaemia: "stones, bones, abdominal groans, and psychiatric moans" 🪨🦴😖.
- Bone disease (renal osteodystrophy), pruritus, muscle weakness.
- Vascular and soft-tissue calcification → cardiovascular risk 💔.
🔬 Investigations
- CKD markers: ⬆️ Urea and Creatinine.
- Biochemical profile:
- ⬆️ Calcium
- ⬆️ Phosphate
- ⬆️ Alkaline phosphatase (ALP)
- ⬆️ PTH (markedly elevated)
- ⬇️ 1,25(OH)₂ Vitamin D (impaired renal activation)
- Imaging: Sestamibi parathyroid scan (for localisation if considering surgery).
- DEXA scanning may show low bone density.
⚖️ Management
- 🎯 Definitive therapy → Parathyroidectomy (subtotal or total with autotransplantation).
- 💊 Cinacalcet (calcimimetic) useful for patients unsuitable for surgery or awaiting transplant.
- Vitamin D analogues (e.g. alfacalcidol, calcitriol) may help suppress PTH.
- Phosphate binders and dietary phosphate restriction to control ⬆️ phosphate.
- Conservative management may be considered in frail/elderly patients if hypercalcaemia is controlled medically.
📚 References