Pathophysiology: UV Light

When calcium levels increase in a person with normal regulatory mechanisms, the hypercalcaemia suppresses the secretion of PTH. Normally, PTH stimulates release of calcium from bone by direct osteolytic action and via osteoclast upregulation. Therefore, a decline in serum PTH concentration decreases the flux of calcium from bone to extracellular fluid. PTH also acts to reabsorb calcium in the loop of Henle and distal tubule in the kidney. When PTH levels decrease, much of the filtered calcium is excreted in the urine. Finally, PTH stimulates enzymatic conversion of 25-hydroxyvitamin D to the active metabolite 1,25-dihydroxyvitamin D.

Ultraviolet light

Ultraviolet (UV) light converts 7-dehydrocholesterol in the skin to cholecalciferol (vitamin D3). Alternatively, previtamin D is directly ingested and transported by proteins to the liver, where it is converted to 25-hydroxyvitamin D. In the kidney, 25-hydroxyvitamin D (calcidiol) is converted to the active metabolite 1,25-dihydroxyvitamin D by a PTH-stimulated process. 1,25-dihydroxyvitamin D (calcitriol) serves to promote intestinal absorption of calcium. When PTH is suppressed because of hypercalcaemia, levels of 1,25-dihydroxyvitamin D decline, and thus intestinal calcium absorption declines.


Bone resorption, local bone destruction and enhanced intestinal absorption of calcium are believed to be responsible for hypercalcaemia associated with malignancy.