top of page

Hyperparathyroidism

Hyperparathyroidism is a condition in which one or more of the parathyroid glands produce excessive amounts of parathyroid hormone (PTH). This hormone plays a key role in regulating the body’s calcium and phosphate balance, and overproduction can negatively affect the skeleton, kidney function, and nervous system¹.


The parathyroid glands are small endocrine organs located on the posterior surface of each thyroid lobe² ³. Each of the four glands is about the size of a grain of rice³. Despite the name, hyperparathyroidism has no functional relationship with thyroid disorders such as hypothyroidism or hyperthyroidism².

Parathyroid glands

Types

Thyroid gland

Hyperparathyroidism is categorized into three clinical forms: primary, secondary, and tertiary¹.

  • Primary hyperparathyroidismThe most common form, usually caused by a benign adenoma in one gland⁴. It is characterized by excessive secretion of PTH despite normal or elevated serum calcium levels.

  • Secondary hyperparathyroidismDevelops when the glands are chronically stimulated due to another underlying condition¹. The most frequent causes include severe vitamin D deficiency, calcium deficiency, and especially chronic kidney disease⁵.

  • Tertiary hyperparathyroidismSeen in patients with long-standing secondary hyperparathyroidism, particularly those undergoing dialysis. Impaired conversion and absorption of vitamin D leads to reduced calcium uptake and persistent stimulation of the parathyroid glands⁵.


Epidemiology

Hyperparathyroidism affects approximately 2–3 women per 1000, most frequently in postmenopausal women over 65 years of age⁴. While it can occur in both sexes and across all age groups, it is strongly associated with aging. Today, about 80% of cases are detected incidentally during routine blood tests⁶.


Symptoms and Clinical Presentation

Hyperparathyroidism symptoms

The biochemical hallmark of hyperparathyroidism is an elevated PTH level, or an inappropriately high-normal PTH in the presence of hypercalcemia.

Many patients remain asymptomatic, but others may experience:

  • Fatigue and muscle weakness

  • Anxiety, depression, or irritability

  • Loss of appetite, nausea, or vomiting

  • Abdominal pain and constipation

  • Excessive thirst and frequent urination

  • Bone pain

  • Rarely, cardiac arrhythmias


Symptoms of complications include:

  • Osteoporosis and fracture risk – due to chronic bone resorption

  • Kidney stones – caused by hypercalciuria and elevated calcium levels⁴


Diagnosis

Diagnosis is confirmed through blood tests measuring calcium, phosphate, magnesium, and PTH levels. Hypercalcemia with elevated or inappropriately normal PTH is characteristic. Additional investigations may include:

  • Skeletal X-rays – to detect bone loss or subperiosteal resorption

  • Kidney imaging – to evaluate nephrolithiasis or nephrocalcinosis

  • Bone density scans (DEXA) – to assess osteoporosis risk

  • Biopsy – in selected cases, to clarify etiology or tissue involvement


Medical Treatment

Primary hyperparathyroidism

The treatment of choice is surgical removal of the affected parathyroid gland (parathyroidectomy)¹. If surgery is not feasible, medications are prescribed to protect the skeleton and control hypercalcemia.


Secondary hyperparathyroidism

Management targets the underlying cause. In cases linked to chronic kidney disease, nephrologists may recommend:

  • Calcimimetics – drugs that mimic calcium, reducing PTH secretion

  • Calcium supplementation and sometimes protein restriction⁷

Other underlying conditions require specific treatment:

  • Celiac disease → strict gluten-free diet

  • Vitamin D deficiency → vitamin D supplementation⁴


Physiotherapy

Patients with hyperparathyroidism may develop skeletal, joint, and neuromuscular changes due to prolonged hormone excess. These include muscle weakness, bone pain, reduced balance, and increased fracture risk¹ ³.

Key considerations:

  • Acute phase or severe hypercalcemia: Physiotherapists must be cautious, as patients are more prone to osteoporosis and low-energy fractures¹. This applies especially to elderly individuals and those with long-term elevated PTH.

  • Post-surgery: Early mobilization after parathyroidectomy is essential. Patients should be encouraged to resume walking and daily activities as soon as medically safe to counteract bone demineralization¹.

  • Fall prevention: Physiotherapists should provide practical advice on reducing home hazards (removing rugs, improving lighting, mobility aids) to minimize fall and fracture risk in older patients.

The goal of physiotherapy is to promote safe activity, preserve independence, and maintain skeletal health without exposing patients to unnecessary fracture risk.


References

  1. Goodman C, Fuller K. Pathology: Implications for the Physical Therapist. 3rd ed. St. Louis, Missouri: Saunders Elsevier; 2007.

  2. Goodman C, Snyder T. Differential Diagnosis for Physical Therapists: Screening for Referral. 5th ed. St. Louis, Missouri: Saunders Elsevier; 2013.

  3. Mayo Clinic. Diseases and Conditions – Hyperparathyroidism: Symptoms. Available from: http://www.mayoclinic.org

  4. Verywell Health. Hyperparathyroidism – Symptoms, Causes, Diagnosis and Treatment. Available from: https://www.verywellhealth.com/hyperparathyroidism-symptoms-causes-diagnosis-and-treatment-4688580

  5. Mayo Clinic. Diseases and Conditions – Hyperparathyroidism: Causes. Available from: http://www.mayoclinic.org

  6. Skugor M, Milas M. Hypercalcemia. Available from: http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/endocrinology/hypercalcemia/

  7. Mayo Clinic. Diseases and Conditions – Hyperparathyroidism: Treatment. Available from: http://www.mayoclinic.org

  8. Hamdy N. A patient with persistent primary hyperparathyroidism due to a second ectopic adenoma. Nature Clinical Practice Endocrinology and Metabolism. 2007;3:311–315. Available from: http://www.nature.com/nrendo/journal/v3/n3/full/ncpendmet0448.html

  9. Forman BH, Ciardiello K, Landau SJ, Freedman JK. Diplopia associated with hyperparathyroidism: report of a case. Yale Journal of Biology and Medicine. 1995;68(5–6):215–217. Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2588946/

Tip: Use Ctrl + F to search on the page.

Help us keep PhysioDock free

All content on PhysioDock is free – but it costs to keep it running.

PhysioDock is built to be an open and accessible platform for physiotherapists, students, and patients alike. Here you’ll find articles, measurement tools, exercise libraries, diagnostic resources, and professional materials – all completely free.

Behind the scenes, however, there are hundreds of hours of work: research, writing, development, design, maintenance, testing, and updates. We do this because we believe in open knowledge and better health information.

If you’d like to support our work and help us continue developing and improving PhysioDock, we truly appreciate everyone who:
– subscribes to a PhysioDock+ membership
– uses and recommends PhysioDock in their work or studies
– shares PhysioDock with others

Every contribution makes a difference – and helps us keep the platform open to everyone.
Thank you for supporting PhysioDock!

Best value

PhysioDock+

NOK 199

199

Every month

PhysioDock+ gives you exclusive benefits such as discounts, AI tools, and professional resources. The membership helps you work more efficiently, stay updated, and save time and money in your daily practice.

Valid until canceled

Access to Fysio-Open

Physionews+

Quizzes

10% discount on all purchases

5% discount on "Website for Your Clinic"

50% discount on shipping

Access to PhysioDock-AI (Under development)

Partner discounts

Exclusive product discounts

Contact us

Is something incorrect?

Something missing?
Something you’d like to see added?
More recent literature?

Feel free to get in touch and let us know which article it concerns and what could be improved.
We truly appreciate your feedback!

  • Facebook
  • Twitter
  • LinkedIn
  • Instagram

Thanks for contributing!

bottom of page