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Related Concept Videos

The Parathyroid Glands00:59

The Parathyroid Glands

The two pairs of parathyroid glands embedded within the posterior surface of the thyroid gland are restricted by a dense capsule around them. These glands comprise two distinct cell populations—parathyroid oxyphil and parathyroid principal cells- pivotal in calcium homeostasis.
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Related Experiment Video

Updated: Jul 10, 2026

Two Techniques to Create Hypoparathyroid Mice: Parathyroidectomy Using GFP Glands and Diphtheria-Toxin-Mediated Parathyroid Ablation
07:13

Two Techniques to Create Hypoparathyroid Mice: Parathyroidectomy Using GFP Glands and Diphtheria-Toxin-Mediated Parathyroid Ablation

Published on: March 14, 2017

Lethal hyperparathyroid crisis: hazards of phosphate administration.

A M Vernava1, L W O'Neal, V Palermo

  • 1Department of Surgery, St. John's Mercy Medical Center, St. Louis, Mo.

Surgery
|December 1, 1987
PubMed
Summary

Phosphate administration in hypercalcemia crisis may cause fatal pulmonary insufficiency due to metastatic calcification. This study discourages phosphate use for lowering calcium levels, highlighting risks associated with intravascular precipitation.

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Last Updated: Jul 10, 2026

Two Techniques to Create Hypoparathyroid Mice: Parathyroidectomy Using GFP Glands and Diphtheria-Toxin-Mediated Parathyroid Ablation
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Area of Science:

  • Nephrology
  • Endocrinology
  • Pathology

Background:

  • Hypercalcemia crisis, often linked to parathyroid adenoma, presents a critical medical condition requiring prompt management.
  • Traditional treatments for hypercalcemia aim to reduce serum calcium levels effectively and safely.

Observation:

  • Two patients with hypercalcemia crisis experienced fatal pulmonary insufficiency following phosphate administration.
  • Pulmonary complications arose concurrently with elevated serum calcium and phosphate (Ca x PO4) product.
  • Autopsy revealed extensive metastatic calcification within the pulmonary alveolar lining in both patients.

Findings:

  • Phosphate administration appears to have precipitated the fatal pulmonary complications in these hypercalcemia patients.
  • The mechanism involves a significant rise in the blood calcium-x-phosphate product, leading to widespread calcification.
  • Phosphate may lower serum calcium levels primarily through intravascular precipitation, not by addressing the underlying calcium dysregulation.

Implications:

  • The use of phosphates as a therapeutic agent for lowering calcium in hypercalcemia is strongly discouraged.
  • Clinicians should exercise extreme caution and consider alternative strategies for managing hypercalcemia to avoid iatrogenic harm.
  • This case highlights the critical importance of understanding the physiological consequences of therapeutic interventions in complex metabolic disorders.