write: Dr John C Stevenson raised some interesting points on the role ofthe vitamin D endocrine system in hypercalcaemia of malignancy (17 August, p 421). May we draw attention to the results of recent studies in patients with lymphoma, which suggest that these tumours may indeed be capable of providing an ectopic source of 1 ,25-dihydroxyvitamin D (1,25(0H)2D3) by converting precursor 25-hydroxyvitamin D3 to the active metabolite. 3 Moreover, with regard to his suggestion that humoral factors

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... eleased by the tumour may theoretically stimulate renal lahydroxylase activity, we have recently published data showing concentrations of circulating 1,25(OH)2D3 (or a similar substance) to be raised or "inappropriately detectable" in about 40% of patients with solid tumour hypercalcaemia.4 Most of these subjects exhibited other aspects of "parathyroid hormone like" activity on renal phosphate and calcium handling but invariably had suppressed immunoreactive parathyroid hormone concentrations. Like Dr Stevenson, we have speculated that the most likely mechanism of continued 1 ,25(OH)2D3 production is ectopic humoral stimulation of renal 1,25(OH)2D3 production. Accordingly, we would contend that this is a common rather than a rare occurrence in hypercalcaemic patients with cancer. None the less, we agree that in general the combination of bone resorption and decreased renal excretion of calcium appears to play the predominant part in such hypercalcaemia rather than hyperabsorption of dietary calcium. It is interesting to note, however, that in the only formal study of calcium absorption in patients with cancer Coombes et al found raised values in a few cases.5 It would be interesting if further research showed this subgroup to have also the highest circulating concentrations of 1,25(OH)2D3.