Circulating vitamin D metabolites and hypercalcaemia of malignancy

Abstract

Plasma concentrations of 1.25 dihvdroxvcholecalciferol were measured in 44 patients with malignancy associated hvpercalcaemia and related to other hormonal regulators of calcium metabolism. Immunoreactive PTH concentrations were suppressed in all but 2 patients and, as a group, patients with hvpercalcaemia of malignancy had lower 1,25 dihydroxycholecalciferol concentrations than normocalcaemic cancer patients.1,25 dihydroxycholecalciferol concentrations were clearly detectable in a significant proportion (43%) of hypercalcaemia cases however, suggesting that in these patients the active vitamin D metabolite may contribute to the pathogenesis and maintenance of the hypercalcaemia by stimulating bone resorption, and/or by increasing absorption of calcium from the intestine. Measurement of plasma 1,25 dihydroxycholecalciferol concentration does not provide a wholly reliable method for distinguishing the hypercalcaemia of malignancy from primary hyperparathyroidism.It has recently been established that in many pa¬ tients with malignancy associated hypercalcaemia, evidence can be found for a humoral aetiology, whether or not bone métastases are present

Intravenous pamidronate in the treatment of osteoporosis associated with corticosteroid dependent lung disease: an open pilot study.

“…After treatment there was a significant fall in serum alkaline phosphatase activity from (mean (SEM)) 220 (16) UII to 174 (9) U/l (normal 80-280 Ul1) and in the fasting urinary hydroxyproline:creatinine ratio from (mean (SEM) 0-040 (0-006) to 0-024 (0-003) (normal <0-033). A significant rise was noted in L2-4 density to 0-927 (0 047) g/ cm2; mean rise of 3-4%).…”

Parathyroid Hormone‐like Bioactivity in Tumours From Patients With Oncogenic Osteomalacia

“…The major differences between the three syndromes relate to serum calcium concentrations and serum concentrations of 1,25-dihydroxyvitamin D (1,25(OH)?D). This metabolite is frequently elevated in sera of patients with hyperparathyroidism (Stewart et a/., 1980), it is normal or low in HHM (Stewart et a/., 1980;Ralston et al, 1984) and clearly low in oncogenic osteomalacia (Drezner et al, 1982).…”

Comparison of Intestinal Calcium Absorption and Circulating 1,25‐dihydroxyvitamin D Levels in Malignancy‐associated Hypercalcaemia and Primary Hyperparathyroidism

“…In malignancy-associated hypercalcaemia intestinal calcium absorption is generally low (Coombes et al, 1976) and serum 1,25-dihydroxyvitamin D (1,25(OH)zD) levels depressed when compared with primary hyperparathyroidism (Stewart et al, 1980;Ralston et al, 1984a).…”

“…In some hypercalcaemic cancer patients, however, 1 ,25(OH)2D levels may be 'inappropriately' detectable or even raised (Stewart et al, 1980;Ralston et al, 1984a). When hypercalcaemia is due to lymphoreticular cancer, the elevated 1,25(OH)zD levels may be explained by 1 a-hydroxylation of precursor 25-hydroxycholecalciferol by tumour cells (Breslau et af., 1984;Davies et al, 1985;Rosenthal et al, 1985).…”

“…When hypercalcaemia is due to lymphoreticular cancer, the elevated 1,25(OH)zD levels may be explained by 1 a-hydroxylation of precursor 25-hydroxycholecalciferol by tumour cells (Breslau et af., 1984;Davies et al, 1985;Rosenthal et al, 1985). In the case of solid tumours, the cause of continued 1 ,25(OH)2D synthesis is less clear but has been attributed to the stimulatory effect of a parathyroid hormone (PTH)-like humoral mediator on renal la-hydroxylase activity (Ralston et al, 1984a).…”