Pathogenesis of hypercalcaemia of malignancy. NLM AIDSLINE Important note: Information in this article was accurate in 1986. The state of the art may have changed since the publication date.

Click here to return to AIDSLINE main menu
DonateNow
Print this Article


Pathogenesis of hypercalcaemia of malignancy.

Clin Endocrinol (Oxf). 1985 Dec;23(6):705-14. Unique Identifier : AIDSLINE MED/86162216
Mundy GR

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 decreased 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.
Keywords: Bone Resorption Breast Neoplasms/METABOLISM Calcium/METABOLISM Extracellular Space/METABOLISM Growth Substances/BIOSYNTHESIS Human Hypercalcemia/*ETIOLOGY/METABOLISM HTLV-BLV Viruses Kidney/METABOLISM Lung Neoplasms/METABOLISM Lymphoma/METABOLISM Multiple Myeloma/METABOLISM Neoplasms/*COMPLICATIONS/METABOLISM Parathyroid Hormones/METABOLISM Peptides/BIOSYNTHESIS Receptors, Cell Surface/METABOLISM Support, U.S. Gov't, P.H.S. JOURNAL ARTICLE REVIEW

KWDboneresorptionbreastneoplasms/metabolismcalcium/metabolismextracellularspace/metabolismgrowthsubstances/biosynthesishumanhypercalcemia/KWDetiology/metabolismhtlv-blvviruseskidney/metabolismlungneoplasms/metabolismlymphoma/metabolismmultiplemyeloma/metabolismneoplasms/KWDcomplications/metabolismparathyroidhormones/metabolismpeptides/biosynthesisreceptors,cellsurface/metabolismsupport,uKWDsKWDgov't,pKWDhKWDsKWDjournalarticlereview
860730
M8670140

Copyright © 1986 - National Library of Medicine. Reproduced under license with the National Library of Medicine, Bethesda, MD.

AEGiS is a 501(c)3, not-for-profit, tax-exempt, educational corporation. AEGiS is made possible through unrestricted funding from Boehringer Ingelheim, Bridgestone/Firestone Charitable Trust, Bristol-Myers Squibb Company, Elton John AIDS Foundation, Gill Foundation, the National Library of Medicine, Quest Diagnostics, Roche and Trimeris, and donations from users like you. Always watch for outdated information. This article first appeared in 1986. This material is designed to support, not replace, the relationship that exists between you and your doctor.

AEGiS presents published material, reprinted with permission and neither endorses nor opposes any material. All information contained on this website, including information relating to health conditions, products, and treatments, is for informational purposes only. It is often presented in summary or aggregate form. It is not meant to be a substitute for the advice provided by your own physician or other medical professionals. Always discuss treatment options with a doctor who specializes in treating HIV.

Copyright ©1980, 1986. AEGiS. All materials appearing on AEGiS are protected by copyright as a collective work or compilation under U.S. copyright and other laws and are the property of AEGiS, or the party credited as the provider of the content. .