PATHOGENESIS OF HYPERCALCAEMIA OF MALIGNANCY

G. R. MUNDY

Research output: Contribution to journalArticlepeer-review

38 Scopus citations

Abstract

The hypercalcaemia of malignancy is multi‐factorial, even within individual tumours. In most cases, hypercalcaemia is due to a combination of increased bone resorption associated with uecreased renal capacity to excrete the increased extracellular fluid calcium. In solid tumours such as carcinoma of the lung, tumour‐derived growth factors are probably primarily responsible for the increased bone resorption, and a separate family of factors which interact with some parathyroid hormone (PTH) receptors cause increased renal tubular calcium reabsorption. PTH production by non‐parathyroid tumours rarely if ever occurs. In contrast, haematological malignancies such as myeloma and T‐cell lymphomas produce locally acting bone resorbing lymphokines in excessive amounts. Some T‐cell lymphomas in addition have the capacity to metabolize 25‐hydroxyvitamin D to 1,25‐dihydroxyvitamin D. In myeloma, impaired glomerular filtration frequently contributes to the pathogenesis of hypercalcaemia by impairing renal compensatory mechanisms for maintaining normal serum calcium concentrations in the presence of increased bone resorption.

Original languageEnglish (US)
Pages (from-to)705-714
Number of pages10
JournalClinical Endocrinology
Volume23
Issue number6
DOIs
StatePublished - Dec 1985

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

Fingerprint

Dive into the research topics of 'PATHOGENESIS OF HYPERCALCAEMIA OF MALIGNANCY'. Together they form a unique fingerprint.

Cite this