Parathyroid hormone (PTH)
- Secreted from chief cells when serum calcium (Ca) is low
- 3 actions
- Increase osteoclastic bone reabsorption
- Increase intestinal reabsorption
- Increase calcitriol (D3), tubular reabsorption, phosphate excretion
Etiology
- Excessive PTH due to primary/tertiary hyperPTH
- If low PTH levels – malignant disease – myeloma
- Excessive Vitamin D action – iatrogenic/systemic disease/lymphoma
- Endocrine disorders – thyrotoxicosis, addisons
- Drugs – thiazides, vitamin D analogues, lithium, vitamin A
Primary hyperPTH – adenomas (MEN II if > 1 gland affected) (primary = MCC 90%)
Secondary hyperPTH – compensatory response to hypocalcemia (chronic kidney failure, vitimin D deficiency)
Tertiary hyperPTH – autonomous PTH gland after chronic hypocalcemia
Clinical features
- Mild hypercalcemia (<3.0mmol/L)
- General – malaise, tiredness, dehydration, depression
- Renal – stones, polyuria, nocturia, hematuria, HT
- Bones – cortical bones, pain, cysts, brown tumours, Osteitis fibrosa
- Chondrocalcinosis, corneal calcification
- Malignant diseases – breast, lungs, bones, myeloma
- Severe hypercalcemia (>3.0mmol/L)
- Nausea, vomit, dehydration, nocturia, polyuria
Diagnosis
- Serum PTH – increased PTH is the hallmark for primary hyperPTH
- Renal tests, 24hr urinary calcium
- If undetectable levels of PTH
- Protein electrophoresis – exclude myeloma
- Serum TSH – exclude hyperthyroidism
- Serum ACTH/cortisol – exclude addisons
- Hydrocortisone suppression tests – exclude sarcoidosis
- Urinary calcium – exclude familial hypocalciuric hypercalcemia
- CXR, DXA bone density scans, US, CT, scintigraphy
Treatment
- Fluids, cinacalcet (Ca sensor receptors)
- Surgical removal of one or more lobes
- Post-surgery – alfacalcidiol for hypocalcemia
- Chvoskek and Trousseau signs
- Severe hypercalcemia(>3.0mmol/L)
- Pamidronate [60-90mg], prednisolone, fluids [4-6L]