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Pediatric Hyperparathyroidism Clinical Presentation

  • Author: Gordon L Klein, MD, MPH; Chief Editor: Stephen Kemp, MD, PhD  more...
 
Updated: Dec 03, 2014
 

History

Patients with primary hyperparathyroidism commonly present without symptoms. Hyperparathyroidism may be diagnosed in an otherwise asymptomatic patient by incidental discovery during routine blood chemistry analysis of hypercalcemia.

Symptoms of early disease, when present, are specific to hypercalcemia. They include muscle weakness, depression, increased sleepiness, nausea, vomiting, acute abdominal pain (which might be the result of pancreatitis), constipation, and polydipsia. Frequent and occasionally painful urination and dysuria and/or back pain may be observed, the latter from nephrolithiasis. The most common presenting symptoms of the 10 children reported by Libansky et al included urolithiasis, nephrolithiasis, nephrocalcinosis, and bone resorption, as well as fatigue and muscle weakness.[8] If multiple endocrine neoplasia type I (MEN 1) is present, peptic ulcer disease, hypertension, or both may be noted.[12]

Patients with secondary hyperparathyroidism usually present with a history of underlying disease such as renal or intestinal conditions. Symptoms are musculoskeletal in nature, including bone pain, muscle weakness, and previous fracture.

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Physical

Findings in primary hyperparathyroidism include the following:

  • Signs of dehydration due to hypercalcemia, such as tenting of skin, prolonged capillary refill time, and dry mucous membranes
  • Bradycardia, with or without irregular heartbeat
  • Decreased muscle tone and somnolence

Findings in secondary hyperparathyroidism include the following:

  • Skeletal deformity
  • Decreased muscle tone
  • Bone pain on palpation
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Causes

Primary hyperparathyroidism is caused by a genetic mutation.

Secondary hyperparathyroidism may develop as a response to hypocalcemia caused by intestinal disease resulting in calcium and vitamin D malabsorption.

  • Chronic renal insufficiency
  • Insufficient vitamin D and calcium intake: Insufficient intake in children may cause rickets. Although this is not as common in the United States, rickets are a major cause of secondary hyperparathyroidism in developing countries, especially those countries in which children are kept out of the sun while parents work. Moreover, a growing body of data suggest that many children and adolescents, especially in northern climates, are vitamin D insufficient and have a serum level of 25-hydroxyvitamin D between 20-30 ng/mL. Levels in this range are associated with increased circulating intact parathyroid hormone (PTH).
  • Cholestatic liver disease: Contrary to previous belief, not all children with chronic cholestatic liver disease have secondary hyperparathyroidism. Many of these patients, as well as adults with chronic liver disease, have levels of PTH within the reference range.
  • Iatrogenic causes: Iatrogenic causes, such as lithium administration, may decrease the ability of circulating levels of calcium that are within the reference range to suppress PTH secretion. The mechanism for this is not presently clear.
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Contributor Information and Disclosures
Author

Gordon L Klein, MD, MPH Clinical Professor of Orthopedic Surgery and Rehabilitation, University of Texas Medical Branch School of Medicine

Gordon L Klein, MD, MPH is a member of the following medical societies: American Academy of Pediatrics, American Society for Nutrition, American Gastroenterological Association, American Pediatric Society, American Society for Bone and Mineral Research, North American Society for Pediatric Gastroenterology, Hepatology and Nutrition, Society for Pediatric Research

Disclosure: Nothing to disclose.

Specialty Editor Board

Mary L Windle, PharmD Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

George P Chrousos, MD, FAAP, MACP, MACE, FRCP(London) Professor and Chair, First Department of Pediatrics, Athens University Medical School, Aghia Sophia Children's Hospital, Greece; UNESCO Chair on Adolescent Health Care, University of Athens, Greece

George P Chrousos, MD, FAAP, MACP, MACE, FRCP(London) is a member of the following medical societies: American Academy of Pediatrics, American College of Physicians, American Pediatric Society, American Society for Clinical Investigation, Association of American Physicians, Endocrine Society, Pediatric Endocrine Society, Society for Pediatric Research, American College of Endocrinology

Disclosure: Nothing to disclose.

Chief Editor

Stephen Kemp, MD, PhD Former Professor, Department of Pediatrics, Section of Pediatric Endocrinology, University of Arkansas for Medical Sciences College of Medicine, Arkansas Children's Hospital

Stephen Kemp, MD, PhD is a member of the following medical societies: American Academy of Pediatrics, American Association of Clinical Endocrinologists, American Pediatric Society, Endocrine Society, Phi Beta Kappa, Southern Medical Association, Southern Society for Pediatric Research

Disclosure: Nothing to disclose.

Additional Contributors

Phyllis W Speiser, MD Chief, Division of Pediatric Endocrinology, Steven and Alexandra Cohen Children's Medical Center of New York; Professor of Pediatrics, Hofstra-North Shore LIJ School of Medicine at Hofstra University

Phyllis W Speiser, MD is a member of the following medical societies: American Association of Clinical Endocrinologists, Endocrine Society, Pediatric Endocrine Society, Society for Pediatric Research

Disclosure: Nothing to disclose.

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Normal parathyroid glands as seen during a thyroidectomy. The large arrow points to the superior parathyroid. The thinner arrow points to the inferior parathyroid. The forceps points toward the recurrent laryngeal nerve. The patient's head is toward the right.
 
 
 
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