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Last updated: December 14, 2019


Hyperparathyroidism (HPT) is characterized by abnormally high parathyroid hormone (PTH) levels in the blood due to overactivity of the parathyroid glands. It is differentiated into three types based on the underlying cause: primary HPT (pHPT), secondary hyperparathyroidism (sHPT), and tertiary hyperparathyroidism (tHPT). pHPT is characterized by elevated parathyroid hormone and calcium levels and is usually caused by parathyroid adenomas (or, in rare cases, by parathyroid carcinomas). Although often asymptomatic, symptoms such as bone pain, gastric ulcers, and/or kidney stones may emerge in severe cases. sHPT is characterized by high parathyroid hormone and low calcium levels and may be caused by kidney failure, vitamin D deficiency, or malabsorption. sHPT is also called reactive HPT, as the increase in (parathyroid) hormone production is a physiological response to hypocalcemia and not caused by an abnormality of the parathyroid glands. If sHPT and elevated parathyroid hormone blood levels persist, tHPT may develop, resulting in a shift from low to high calcium blood levels. Hyperparathyroidism is diagnosed and classified by evaluating calcium, phosphorus, and parathyroid hormone levels and, in the case of sHPT, evaluating the underlying disease (e.g., creatinine in chronic kidney disease). Surgery is the primary treatment option for symptomatic patients and asymptomatic patients who meet certain criteria. Patients who are not surgical candidates are managed with either calcimimetics or, if osteoporosis is present, bisphosphonates. In sHPT, treatment of the underlying disease is the focus.


All forms of hyperparathyroidism are characterized by elevated PTH levels.



Primary hyperparathyroidism

Epidemiological data refers to the US, unless otherwise specified.


Primary hyperparathyroidism

Secondary hyperparathyroidism

Tertiary hyperparathyroidism

  • Caused by persistent sHPT



Physiological secretion of PTH

Pathologically increased secretion of PTH

pHPT develops due to hyperplasia of the parathyroid glands. sHPT develops due to decreased levels of calcium in the blood (reactive HPT)!


Clinical features

Primary hyperparathyroidism

The majority of patients are asymptomatic!

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

Secondary hyperparathyroidism



Laboratory studies of hyperparathyroidism

Hypercalcemic crises may occur in primary and tertiary HPT!


  • Ultrasound/nuclear imaging (Tc99m-sestamibi scan): only performed prior to surgery to determine the exact location of the abnormal glands
  • Skeletal x-ray: decreased bone mineral density, but usually an incidental finding, as x-ray is not a routine diagnostic tool
    • Cortical thinning: especially prominent in the phalanges of the hand (acroosteolysis)
    • Salt-and-pepper skull
    • Rugger-jersey spine sign: Alternating low and high density in the vertebrae produces a banded pattern, similar to a striped rugby jersey.



Primary hyperparathyroidism

Secondary hyperparathyroidism

Tertiary hyperparathyroidism



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