Last updated: February 15, 2023

Summarytoggle arrow icon

Hyperparathyroidism (HPT) is characterized by abnormally high parathyroid hormone (PTH) levels in the blood due to parathyroid gland overactivity. HPT is further classified based on the underlying cause: primary HPT (pHPT), secondary HPT (sHPT), or tertiary HPT (tHPT). pHPT is characterized by elevated PTH and calcium levels and is usually caused by parathyroid adenomas or hyperplasia, or, in rare cases, parathyroid carcinomas. Although pHPT is often asymptomatic, symptoms such as bone pain, gastric ulcers, and kidney stones may be present in severe or untreated cases. sHPT is characterized by high PTH and low calcium levels and may be caused by chronic kidney disease (CKD), vitamin D deficiency, insufficient calcium intake, or malabsorption. sHPT is also called reactive HPT, as the increase in PTH production is a physiological response to hypocalcemia rather than an abnormality of the parathyroid glands. If sHPT and elevated serum PTH levels persist, tHPT may develop, resulting in a shift from low to high serum calcium levels. Diagnostics and classification involve evaluating calcium, PTH, and phosphate levels, and, in the case of sHPT, identifying the underlying cause (e.g., CKD). Surgery is the primary treatment option for most patients with pHPT or tHPT. Patients who do not undergo surgery can be managed with either calcimimetics or, if osteoporosis is present, bisphosphonates. In sHPT, management focuses on treating the underlying cause.

Overviewtoggle arrow icon

All forms of HPT are characterized by elevated PTH levels (or inappropriately normal levels ). See also “Calcium homeostasis.”

Overview of hyperparathyroidism [1][2][3]

Primary hyperparathyroidism (pHPT) Secondary hyperparathyroidism (sHPT) Tertiary hyperparathyroidism (tHPT)
Laboratory studies in hyperparathyroidism Calcium (ionized calcium or corrected calcium)
  • Normal or low

  • High


  • High (or inappropriately normal)
  • High
  • Very high
  • Low
  • Normal or high in CKD
  • Low with most other causes
  • High
Alkaline phosphatase
  • High
Treatment Surgical therapy
  • Indicated for symptomatic patients and certain asymptomatic patients [2]
  • Almost always curative
  • Not generally indicated
  • Consider for patients refractory to medical therapy if modifiable factors have been addressed (e.g., vitamin D deficiency). [3]
  • Usually first-line treatment [1]
  • May be curative
Medical management

pHPT develops as a result of hyperplasia of the parathyroid glands. sHPT develops as a result of decreased levels of calcium in the blood (reactive HPT).

Hypercalcemic crises can occur in primary and tertiary HPT.

Primary hyperparathyroidismtoggle arrow icon


Etiology [1]


Clinical features

Patients with pHPT are usually asymptomatic. Symptomatic patients often have clinical features of hypercalcemia.

The majority of patients are asymptomatic.

"Stones, bones, abdominal groans, thrones, and psychiatric overtones!"

Diagnostics [2][7]


Laboratory studies [2][7]

A normal PTH level does not exclude pHPT. PTH should be low in patients with hypercalcemia, therefore, a normal PTH level would suggest pHPT.

Routine imaging studies [2][7]

Obtain in all patients with confirmed pHPT to evaluate for renal and skeletal manifestations.

Additional imaging studies

  • Neck imaging [7]
    • For surgical planning to determine the location of the abnormal glands and evaluate for concomitant thyroid disease
    • Options include ultrasound neck and nuclear imaging, i.e., Tc-99m sestamibi scan.
  • X-ray is not routinely indicated; potential findings include:
    • Decreased BMD
    • Cortical thinning: especially prominent in the phalanges of the hand; manifests as acroosteolysis (a subperiosteal pattern of bone resorption) [9]
    • Salt and pepper skull: granular decalcification manifesting as diffusely distributed lytic foci on imaging of the calvarium [9]
    • Features of osteitis fibrosa cystica

Parathyroid imaging is used for surgical planning but is not indicated for initial diagnosis. [2][7]

Differential diagnoses

Management [2][7]


Management should be guided by a specialist.

  • Provide treatment for hypercalcemia.
  • Refer all symptomatic patients and eligible asymptomatic patients for surgical evaluation.
  • For patients who do not undergo surgery:
    • Start pharmacotherapy.
    • Monitor for complications.

Parathyroidectomy is curative in ∼ 98% of patients and therefore is indicated for most patients with pHPT. [2]

Start immediate hypercalcemia treatment (e.g., IV fluids, calcitonin, and bisphosphonates) for patients with a serum calcium level > 14 mg/dL (> 3.5 mmol/L).

Surgical therapy [2][7]

Pharmacotherapy [2]

Low vitamin D levels further stimulate the parathyroid glands, which increases PTH secretion, leading to an increased risk of complications from pHPT. [7]

Monitoring [2]


Secondary and tertiary hyperparathyroidismtoggle arrow icon



Clinical features

Diagnostics [3][12][13]


Laboratory studies [12]

Differential diagnoses

Treatment [11][12]

Referencestoggle arrow icon

  1. Jameson JL, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J. Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2). McGraw-Hill Education / Medical ; 2018
  2. Bilezikian JP, Khan AA, Silverberg SJ, et al. Evaluation and Management of Primary Hyperparathyroidism: Summary Statement and Guidelines from the Fifth International Workshop. J Bone Miner Res. 2022.doi: 10.1002/jbmr.4677 . | Open in Read by QxMD
  3. Taniegra ED. Hyperparathyroidism. Am Fam Physician. 2004; 69 (2): p.333-9.
  4. Abood A, Vestergaard P. Increasing incidence of primary hyperparathyroidism in Denmark. Danish medical journal. 2013; 60 (2): p.A4567.
  5. Bandeira L, Bilezikian J. Primary Hyperparathyroidism. F1000Research. 2016; 5.doi: 10.12688/f1000research.7039.1 . | Open in Read by QxMD
  6. Shapiro HI, Davis KA. Hypercalcemia and “Primary” Hyperparathyroidism During Lithium Therapy. Am J Psychiatry. 2015; 172 (1): p.12-15.doi: 10.1176/appi.ajp.2013.13081057 . | Open in Read by QxMD
  7. Wilhelm SM, Wang TS, Ruan DT, et al. The American Association of Endocrine Surgeons Guidelines for Definitive Management of Primary Hyperparathyroidism. JAMA Surgery. 2016; 151 (10): p.959.doi: 10.1001/jamasurg.2016.2310 . | Open in Read by QxMD
  8. Joseph SY, Nidhi GK, Michael GF et al. Osteoporosis and Bone Mineral Density. J Am Coll Radiol. 2022.
  9. Bennett J, Suliburk JW, Morón FE. Osseous Manifestations of Primary Hyperparathyroidism: Imaging Findings. Int J Endocrinol. 2020; 2020: p.1-10.doi: 10.1155/2020/3146535 . | Open in Read by QxMD
  10. Jain N, Reilly RF. Hungry bone syndrome. Curr Opin Nephrol Hypertens. 2017; 26 (4): p.250-255.doi: 10.1097/mnh.0000000000000327 . | Open in Read by QxMD
  11. Saliba W, El-Haddad B. Secondary Hyperparathyroidism: Pathophysiology and Treatment. J Am Board Fam Med. 2009; 22 (5): p.574-581.doi: 10.3122/jabfm.2009.05.090026 . | Open in Read by QxMD
  12. Kidney Disease: Improving Global Outcomes (KDIGO) CKD-MBD Update Work Group. KDIGO 2017 Clinical Practice Guideline Update for the Diagnosis, Evaluation, Prevention, and Treatment of Chronic Kidney Disease–Mineral and Bone Disorder (CKD-MBD). Kidney Int Suppl. 2017; 7 (1): p.1-59.doi: 10.1016/j.kisu.2017.04.001 . | Open in Read by QxMD
  13. Gilbert, SJ; Weiner, DE. National Kidney Foundation's Primer on Kidney Disease. Elsevier Health Sciences ; 2017
  14. Pitt SC, Sippel RS, Chen H. Secondary and Tertiary Hyperparathyroidism, State of the Art Surgical Management. Surg Clin North Am. 2009; 89 (5): p.1227-1239.doi: 10.1016/j.suc.2009.06.011 . | Open in Read by QxMD

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