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Hypoparathyroidism

Definition and epidemiology

Hypoparathyroidism is most commonly caused by accidental injury to the glands during neck surgery. The second most common cause is autoimmune destruction. Hypoparathyroidism causes hypocalcaemia.

Postsurgical hypoparathyroidism can occur after thyroid, parathyroid, or radical neck surgery for head and neck cancer. It may be transient, intermittent, or permanent. Transient hypoparathyroidism occurs in up to 20% of cases. Because of the high risk for hypoparathyroidism, calcium levels should be monitored after thyroid surgery.

Clinical features

Manifestations depend on the severity and rate of development of the hypocalcaemia.

The most common acute manifestation is tetany (numbness, cramps, laryngospasm, seizures, etc.). Chronic hypoparathyroidism causes calcification of basal ganglia which leads to extrapyramidal symptoms, as well as skeletal abnormalities, cataracts, and abnormal skin.

Diagnosis and evaluation

Labs show hypocalcaemia, low or normal PTH, and hyperphosphataemia. Signs of hypocalcaemia, including Chvostek sign and Trousseau sign (see here), may be present.

If there is no history of neck surgery, the underlying cause should be sought.

Treatment

In case of acute, severe hypocalcaemia, IV calcium must be supplemented. In other cases, oral supplements of calcium and vitamin D are sufficient. Recombinant PTH exists and may be used, but it’s expensive, administered subcutaneously, and long-term safety is unknown.

Hyperparathyroidism

Introduction

For introduction, pathology, and etiology, see the corresponding pathology 2 topic.

Clinical features

Hyperparathyroidism is often asymptomatic (incidentally discovered hypercalcaemia), but it may cause severe features as well:

• Stones
  • Nephrolithiasis
  • Nephrocalcinosis
• Bones
  • Bone pain
  • Osteitis fibrosa cystica
• Abdominal groans (pain)
• Thrones
  • Polyuria
  • Constipation
• Psychiatric overtones
  • Lethargy
  • Depression
  • Psychosis
• Others
  • Peptic ulcers
  • Acute pancreatitis
  • Left ventricular hypertrophy

The symptoms of primary hyperparathyroidism are often remembered as “bones, stones, abdominal groans, thrones, and psychiatric overtones”.

Diagnosis and evaluation

For comparison of lab values in primary and secondary hyperparathyroidism, see the table:

	PTH level	Ca level	Phosphate level	ALP level
Primary PHT	Elevated	Elevated	Decreased	Elevated
Secondary PHT	Strongly elevated	Normal or decreased	Elevated	Elevated

X-ray is not performed for evaluation, but characteristic findings of PTH may be found incidentally on x-ray. Characteristic findings include cortical thinning of bone, especially prominent in the phalanges of the hand, salt-and-pepper skull (granular decalcification), and osteitis fibrosa cystica (bone cysts).

If primary PHT is evident on labs and surgery is indicated, studies should be performed to localise the pathology. This is important as the localisation of the glands shows a great variability between persons. This is done with ultrasonography or technetium-99m sestamibi scintigraphy.

Treatment

The treatment of primary hyperparathyroidism is surgery. For surgical treatment, see topic B2 of surgery-traumatology.

For patients with primary hyperparathyroidism and an indication for surgery but who are unable to have surgery, medical therapy is an option. The drug cinacalcet is used for this, which inhibits PTH release. Cinacalcet may also be used for parathyroid carcinoma.

Management for secondary hyperparathyroidism involves treating the underlying cause. Dietary restriction of phosphate and vitamin D supplements are also important. Phosphate binders may be used in case hyperphosphataemia remains despite dietary restriction. Cinacalcet may also be used.