Parathyroid conditions

Hypoparathyroidism

This is a condition characterised by low levels of parathyroid hormone.

Symptoms occur due to the hypocalcaemia raising excitability of nerve and muscle.

Primary hypoparathyroidism

This refers to low levels of PTH due to an impairment in PTH secretion.

It can primary due to autoimmune damage, congenital DiGeorge syndrome or secondary to other causes, e.g., surgery or low Mg2+ (needed for synthesis).

Symptoms

Muscle twitching, tetany, cramping and spasm

Numbness and tingling around mouth

Can lead to seizures

Chvostek sign – a clinical sign where tapping on the zygomatic bone causes twitching of facial muscles

Key tests

Blood tests show ↓ PTH and ↓ Ca2+, but ↑ PO4 3

Management

Vitamin D/calcium supplements to increase calcium levels

Pseudohypoparathyroidism

 This occurs due to a failure of the organs to respond to PTH

It can be autosomal dominant – characterized by short stature with short 4th and 5th digits, round face

An alternate form is pseudopseudohypoparathyroidism – same features but with normal biochemistry

Key tests

Blood test shows decreased Ca2+, but ­increased Phosphate and ­PTH

During infusion of PTH, urinary cAMP and Phosphate do not rise unlike in hypoparathyroidism.

Management

Calcium and vitamin D supplements

Hyperparathyroidism

This is a condition characterised by high levels of parathyroid hormone.

Symptoms occur due to the hypercalcaemia decreasing membrane excitability.

Symptoms

Bones – ectopic calcifications (e.g., cornea) and bone pain (due to bone resorption)

Stones – renal stones and kidney failure

Groans – abdominal pain, vomiting, constipation, and weakness

Psychic moans – confusion, irritability, depression

Primary Hyperparathyroidism

This refers to high levels of PTH due to an intrinsic disorder of the parathyroid gland.

Most cases are due to a parathyroid adenoma (benign PTH-secreting tumour), but it is also associated with parathyroid hyperplasia or parathyroid carcinoma.

Key tests

Blood test ­increased PTH (can be normal), ­increased Ca2+, increased ­urinary cAMP, increased ­ALP and decreased Phosphate

Urine Calcium: creatinine clearance ratio > 0.01

 X-ray – osteitis fibrosa cystica of phalanges + “pepper-pot” skull appearance

Management

Hypercalcaemia can be managed with fluids or medication (e.g., cinacalcet)

Definitive management is total parathyroidectomy

Secondary Hyperparathyroidism

This refers to excess PTH due to a disease extrinsic to gland.

The most common cause is chronic renal failure. This is because renal insufficiency leads to decreased phosphate excretion so PO43- binds serum Ca2+.

Less free circulating calcium stimulates the parathyroid glands to secrete PTH. 

Key tests

Blood test shows ↑ PTH, ↑ ALP, ↑ PO4 3-, ↓ Ca2+ and ↓ vitamin D Management

Management

Vitamin D supplements and effective renal replacement therapy (dialysis)

Tertiary hyperparathyroidism

This occurs after prolonged secondary hyperparathyroidism, causing the glands to act autonomously after undergoing hyperplasia, which is seen in chronic renal failure.

It leads to increased [Ca2+] as result from unlimited PTH secretion.

Key tests

Blood tests show ↑ PTH, ↑ Ca2+, ↑ urinary cAMP, ↑ ALP, ↓ PO4 3- and ↓ vitamin D

Malignant hyperparathyroidism

Parathyroid-related protein is produced by some squamous cell lung, breast, and renal carcinomas.

This protein mimics PTH resulting in increased calcium levels.

Management

Manage hypercalcaemia medically, and treat the underlying cancer if possible