eMedicine Specialties > Endocrinology > Parathyroid Gland

Hypoparathyroidism: Differential Diagnoses & Workup

Author: J Michael Gonzalez-Campoy, MD, PhD, FACE, Medical Director and CEO, MN Center for Obesity, Metabolism, and Endocrinology
Contributor Information and Disclosures

Updated: Jul 17, 2009

Differential Diagnoses

Hypocalcemia
Pseudohypoparathyroidism

Workup

Laboratory Studies

  • Parathyroid hormone
    • Primary hypoparathyroidism is defined by a low concentration of PTH with a concomitant low calcium level.
    • In pseudohypoparathyroidism, the serum PTH concentration is elevated as a result of resistance to PTH caused by mutations in the PTH receptor system.
    • In secondary hypoparathyroidism, the serum PTH concentration is low and the serum calcium concentration is elevated.
  • Calcium
    • The calcium ion is highly bound to protein. A total calcium level cannot be interpreted without a total protein or albumin level.
    • Hypoalbuminemia causes a drop in total calcium concentration, but the ionized fraction may be within the reference range. Elevated protein states, such as multiple myeloma and paraproteinemias, may cause an elevation of the total calcium concentration, but the ionized fraction may be within the reference range.
    • Conversely, in the presence of albumin or protein excess, low ionized calcium levels with reference range levels of total calcium are possible. Likewise, if the patient is hypoalbuminemic, high ionized calcium levels with a reference range level of total calcium are possible.
    • Measurement of ionized calcium concentration in the plasma is ideal; however, it is not readily available in many places.
    • The relationship between total serum calcium and albumin is defined by the following simple rule: the serum total calcium concentration falls by 0.8 mg/dL for every 1-g/dL fall in serum albumin concentration. This rule assumes that normal albumin equals 4.0 g/dL and normal calcium is 10.0 mg/dL.
    • Alkalosis causes ionized calcium to bind to albumin more strongly. This causes a decrease in the ionized calcium and may trigger symptoms of hypocalcemia.
  • Measurement of 25-hydroxy vitamin D: This measurement is important to exclude vitamin D deficiency as a cause of hypocalcemia.
  • Serum magnesium: Hypomagnesemia may cause PTH deficiency and subsequent hypocalcemia. Exclude it in any patient with primary hypoparathyroidism.
  • Serum phosphorus: PTH is a phosphaturic hormone. In its absence, phosphorus levels in the blood rise.

More on Hypoparathyroidism

Overview: Hypoparathyroidism
Differential Diagnoses & Workup: Hypoparathyroidism
Treatment & Medication: Hypoparathyroidism
Follow-up: Hypoparathyroidism
References
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References

  1. Goswami R, Goel S, Tomar N, et al. Prevalence of clinical remission in patients with sporadic idiopathic hypoparathyroidism. Clin Endocrinol (Oxf). Jun 22 2009;[Medline].

  2. Rubin MR, Dempster DW, Zhou H, et al. Dynamic and structural properties of the skeleton in hypoparathyroidism. J Bone Miner Res. Dec 2008;23(12):2018-24. [Medline].

  3. Ebrahimi H, Edhouse P, Lundgren CI, et al. Does autoimmune thyroid disease affect parathyroid autotransplantation and survival?. ANZ J Surg. May 2009;79(5):383-5. [Medline].

  4. Brown EM. Anti-parathyroid and anti-calcium sensing receptor antibodies in autoimmune hypoparathyroidism. Endocrinol Metab Clin North Am. Jun 2009;38(2):437-45, x. [Medline].

  5. Goltzman D, Cole DEC. Hypoparathyroidism. In: Favus MJ, ed. Primer on the Metabolic Bone Diseases and Disorders of Mineral Metabolism. Philadelphia, Pa: Lippincott-Raven; 1996:220-3.

  6. Cheung M. Drugs used in paediatric bone and calcium disorders. Endocr Dev. 2009;16:218-232. [Medline].

  7. Brown EM, Harris HW, Vassilev PM. The biology of the extracellular Ca2+-sensing receptor. In: Bilezikian JP, ed. Principles of Bone Biology. San Diego, Calif: Academic Press; 1996:243-62.

  8. Cole DEC, Hendy GN. Hypoparathyroidism and pseudohypoparathyroidism. Endotext.com. 2005, Available at. [Full Text].

  9. Marx SJ. Hyperparathyroid and hypoparathyroid disorders. N Engl J Med. Dec 21 2000;343(25):1863-75. [Medline].

  10. Thakker RV. Molecular basis of PTH underexpression. In: Bilezikian JP, et al, eds. Principles of Bone Biology. San Diego, Calif: Academic Press; 1996:837-51.

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Further Reading

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Keywords

hypoparathyroidism, parathyroid, PTH, hyperparathyroidism, hypocalcemia, parathyroid hormone, tetany, parathyroid glands, parathyroid gland, surgery parathyroid, parathyroid surgery, parathyroidectomy, hypoparathyroid, parathyroid hormone deficiency, PTH deficiency, primary hypoparathyroidism, inadequate PTH activity, secondary hypoparathyroidism, hypercalcemia

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Contributor Information and Disclosures

Author

J Michael Gonzalez-Campoy, MD, PhD, FACE, Medical Director and CEO, MN Center for Obesity, Metabolism, and Endocrinology
J Michael Gonzalez-Campoy, MD, PhD, FACE is a member of the following medical societies: American Association of Clinical Endocrinologists, American Medical Association, and Minnesota Medical Association
Disclosure: Nothing to disclose.

Medical Editor

David S Schade, MD, Chief, Division of Endocrinology and Metabolism, Professor, Department of Internal Medicine, University of New Mexico School of Medicine and Health Sciences Center
David S Schade, MD is a member of the following medical societies: American College of Physicians, American Diabetes Association, American Federation for Medical Research, Endocrine Society, New Mexico Medical Society, New York Academy of Sciences, and Society for Experimental Biology and Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Yoram Shenker, MD, Chief of Endocrinology Section, Veterans Affairs Medical Center of Madison; Interim Chief, Associate Professor, Department of Internal Medicine, Section of Endocrinology, Diabetes and Metabolism, University of Wisconsin at Madison
Yoram Shenker, MD is a member of the following medical societies: American Heart Association, Central Society for Clinical Research, and Endocrine Society
Disclosure: Nothing to disclose.

CME Editor

Mark Cooper, MBBS, PhD, FRACP, Head, Diabetes & Metabolism Division, Baker Heart Research Institute, Professor of Medicine, Monash University
Disclosure: Nothing to disclose.

Chief Editor

George T Griffing, MD, Professor of Medicine, St Louis University School of Medicine
George T Griffing, MD is a member of the following medical societies: American Association for the Advancement of Science, American College of Medical Practice Executives, American College of Physician Executives, American College of Physicians, American Diabetes Association, American Federation for Medical Research, American Heart Association, Central Society for Clinical Research, Endocrine Society, International Society for Clinical Densitometry, and Southern Society for Clinical Investigation
Disclosure: Nothing to disclose.

 
 
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