Hyperparathyroidism

Last updated: March 10, 2022

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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.

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).

Primary hyperparathyroidism

The majority of patients are asymptomatic.

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

Secondary and tertiary hyperparathyroidism

Laboratory studies of hyperparathyroidism

Overview of laboratory parameters in hyperparathyroidism
Calcium Phosphorus Alkaline phosphatase Parathyroid hormone (PTH)
Primary hyperparathyroidism
  • Low
  • High
  • High

Secondary hyperparathyroidism

  • Normal or low
  • High
  • High
Tertiary hyperparathyroidism
  • High
  • High
  • High
  • Very high

Hypercalcemic crises may occur in primary and tertiary HPT.

Imaging

  • X-ray: decreased bone mineral density, but usually an incidental finding, as x-ray is not a routine diagnostic tool ; [5]
    • Cortical thinning: especially prominent in the phalanges of the hand (acroosteolysis)
    • Salt-and-pepper skull: granular decalcification [6]
    • Rugger-jersey spine sign: Alternating low and high density in the vertebrae produces a banded pattern, similar to a striped rugby jersey. [7]
    • Osteitis fibrosa cystica (OFC): a rare skeletal disorder seen in advanced hyperparathyroidism characterized by replacement of calcified bone with fibrous tissue
  • Ultrasound/nuclear imaging (Tc99m-sestamibi scan): only performed prior to surgery to determine the exact location of the abnormal glands

Primary hyperparathyroidism

Surgical

Pharmacotherapy [9]

Secondary hyperparathyroidism [4]

Phosphate binders

Tertiary hyperparathyroidism

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  2. Bandeira L, Bilezikian J. Primary Hyperparathyroidism.. F1000Research. 2016; 5 . doi: 10.12688/f1000research.7039.1 . | Open in Read by QxMD
  3. Aksakal N, Erçetin C, Özçınar B, Aral F, Erbil Y. Lithium-associated primary hyperparathyroidism complicated by nephrogenic diabetes insipidus.. Ulusal cerrahi dergisi. 2015; 31 (3): p.166-9. doi: 10.5152/UCD.2014.2859 . | Open in Read by QxMD
  4. 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
  5. 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
  6. Salt and pepper sign (skull). https://radiopaedia.org/articles/salt-and-pepper-sign-skull-1. Updated: February 13, 2017. Accessed: February 13, 2017.
  7. Rugger-jersey spine. https://radiopaedia.org/articles/rugger-jersey-spine. Updated: February 13, 2017. Accessed: February 13, 2017.
  8. Naik A, Wani M, Wani K, Laway B, Malik A, Shah Z. Intraoperative parathyroid hormone monitoring in guiding adequate parathyroidectomy. Indian Journal of Endocrinology and Metabolism. 2018; 22 (3): p.410. doi: 10.4103/ijem.ijem_678_17 . | Open in Read by QxMD
  9. Farford B, Presutti RJ, Moraghan TJ. Nonsurgical Management of Primary Hyperparathyroidism. Mayo Clin Proc. 2007; 82 (3): p.351-355 . doi: 10.4065/82.3.351 . | Open in Read by QxMD

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