Semantics aside, Dr. Sterkel raises some important issues regarding the range of calcium pathophysiology, from symptomless hypercalciuria to complicated hypercalcemia, that can be observed in patients taking too much vitamin D [1]. First, this continuum is described by the degree to which and length of time that the glomerular filtration rate of calcium is increased and normal renal tubular function is maintained. Second, dysregulated calcium balance is supported by the presence of low parathyroid hormone levels, which further diminishes the clearance of filtered calcium. Third, as we documented in our patients, hypercalciuria can occur independently of food (calcium) consumption, indicating that the skeleton must contribute calcium to the extracellular fluid.

As pointed out by Dr. Sterkel and by Drs. McKenna and Freaney, we did not monitor markers of bone resorption. Instead, we monitored bone mineral density, the outcome most crucial to risk for fracture [2]. We monitored bone mineral density both at the hips and lumbar spine before and after supplement therapy was discontinued to confirm that the change in bone mineral density was generalized, which it was. No serial change in the vertebral height scores was seen; this finding excludes lumbar vertebral compression as a cause of increased bone mineral density. Contrary to Dr. Sterkel's conclusions, estrogen replacement therapy was already long-term (>5 years' duration) at the initiation of the study in two of our patients. Therefore, we doubt that an estrogen-induced change in the activation frequency of skeletal remodeling can explain this change in bone mineral density.

The most crucial point raised is the importance of detecting the opposite condition, vitamin D deficiency. We agree with the recommendation [3] to increase the current recommended daily allowance for oral vitamin D consumption by 50% to 100% (from 400 to 600 or 800 IU daily), particularly in elderly persons who have limited sunlight exposure and cutaneous vitamin D synthetic capacity [4]. This intake level is safe and will not cause hypercalciuria. What is not always safe and reliable is the label of a food supplement not regulated by the U.S. Food and Drug Administration. In our patients, the vitamin D content of the supplement was at least one order of magnitude greater than that advertised on the label. It is fortunate that the serum 25(OH)D level is the best screen for both hypervitaminosis D and hypovitaminosis D. Physicians should take better advantage of this versatile screening tool.