Pathophysiology of primary hyperparathyroidism

Research output: Contribution to journalArticle

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Abstract

Primary hyperparathyroidism (PHPT) is characterized by hypersecretion of parathyroid hormone (PTH) leading to hypercalcemia and relative hypophosphatemia. PTH acts by binding to cell surface receptors coupled to G proteins. Cyclic AMP is the classic second messenger of PTH action, but substantial evidence indicates that PTH also acts to stimulate formation of the dual second messengers, inositol trisphosphate and diacylglycerol, thereby mobilizing intracellular calcium. The physiologic actions of PTH include (1) an increase in extracellular fluid ionized calcium through direct actions on kidney and bone, the classic target organs for PTH, and (2) a decrease in extracellular fluid phosphate primarily through renal action. The pathophysiologic effects of PTH arise from (1) direct actions of PTH on bone and kidney, and possibly on nonclassic target organs, and (2) indirect effects of altered mineral homeostasis. PTH hypersecretion in PHPT can lead to bony demineralization, nephrolithiasis, and hypercalcemic crisis. PHPT may also be associated with mental disturbances, neuromuscular disease, hypertension, and glucose intolerance.

Original languageEnglish (US)
JournalJournal of Bone and Mineral Research
Volume6
Issue numberSUPPL. 2
StatePublished - Oct 1991
Externally publishedYes

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Primary Hyperparathyroidism
Parathyroid Hormone
Extracellular Fluid
Second Messenger Systems
Kidney
Calcium
Hypophosphatemia
Bone and Bones
Nephrolithiasis
Neuromuscular Diseases
Glucose Intolerance
Diglycerides
Hypercalcemia
Cell Surface Receptors
Inositol
GTP-Binding Proteins
Cyclic AMP
Minerals
Homeostasis
Phosphates

ASJC Scopus subject areas

  • Surgery

Cite this

Pathophysiology of primary hyperparathyroidism. / Spiegel, Allen M.

In: Journal of Bone and Mineral Research, Vol. 6, No. SUPPL. 2, 10.1991.

Research output: Contribution to journalArticle

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