Definition
Hypoparathyroidism is defined as a disorder characterised by inadequate secretion or action of PTH
Causes and Risk Factors
Important causes: [Ref1][Ref2]
- Surgery – leading overall cause
- Parathyroidectomy
- Unintended injury from thyroidectomy
- Autoimmune destruction – leading non-surgical cause
- Genetic cause (e.g. DiGeorge syndrome)
- Infiltrative diseases (e.g. haemochromatosis, Wilson’s disease)
- Neck irradiation
- Hypomagnesaemia (causes functional hypoparathyroidism; therefore it’s important to correct any underlying hypomagnesaemia before correcting hypocalcaemia)
Clinical Features
Clinical features are typically secondary to hypocalcaemia [Ref]
| Early / mild hypocalcaemia features [Ref] |
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| Features of more severe hypocalcaemia: [Ref] |
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Hypocalcaemia increases neuromuscular excitability because ionised calcium normally stabilises voltage-gated sodium channels. When calcium levels fall, these channels open more easily, leading to spontaneous depolarisation.
Rare features typically only seen in chronic hypoparathyroidism: [Ref]
- Neuropsychiatric symptoms (e.g. confusion, depression, irritability, cognitive dysfunction)
- Basal ganglia calcification (→ secondary Parkinsonism)
- Ophthalmologic
- Cataracts
- Papilloedema
Investigation and Diagnosis
Biochemical changes: [Ref]
- ↓ PTH
- ↓ Calcium
- ↑ Phosphate
- ↓ / normal 1,25 dihydroxyvitamin D (due to lack of PTH-stimulated renal conversion)
Rationalising the biochemical changes:
- Actions of PTH
- ↑ Serum calcium (via ↑ bone resorption, ↑ renal calcium reabsorption, ↑ intestinal calcium absorption)
- ↓ Serum phosphate (via ↑ renal phosphate excretion)
The initiating event is low PTH, which results in the subsequent biochemical changes (opposite of PTH’s action).
Management
Conventional therapy: [Ref1][Ref2]
- Oral calcium supplements
- Oral activated vitamin D supplements
- Manage other secondary complications
- Prevent hypercalciuria by reducing calcium supplement dose, sodium-restricted diet, and/or thiazide diuretic
- Manage hyperphosphataemia with phosphate-restricted diet and/or increase calcium supplement dose (as calcium acts as a phosphate binder in the gut)
- Manage any hypomagnesaemia with magnesium supplements
Do not routinely use PTH replacement therapy (e.g. teriparatide), only consider in those where hypocalcaemia cannot be controlled with conventional therapy.
Therapeutic goal in hypoparathyroidism is to:
- Maintain serum calcium in the low-normal range
- Avoid hypercalcaemia and hypercalciuria
- Maintain serum phosphate in the high-normal range