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Letters to the Editor |
IMVS, Royal Adelaide Hospital Adelaide 5000, South Australia
The article by Ghazali et al. (1) entitled "Low Bone Mineral Density and Peripheral Blood Monocyte Activation Profile in Calcium Stone Formers with Idiopathic Hypercalciuria" evokes substantial interest in relation to mechanisms that induce osteoporosis.
Secondary hyperparathyroidism has been described in patients with idiopathic hypercalciuria of renal origin (2). The authors have stated that they have excluded patients with hyperparathyroidism from their study. It would be of interest to know if those patients with renal hypercalciuria had borderline elevations in serum PTH or had serum PTH levels in the upper limits of the reference range as compared to those patients with dietary dependent hypercalciuria or the normal controls.
PTH acts on cells other than those of bone and kidney, and mitosis of lymphocytes has been described (3, 4). It may be interesting to note if there is a positive correlation between the PTH levels and the cytokines of patients with renal hypercalciuria, and whether this was responsible for the reduction in bone density.
Footnotes
Address correspondence to: Dr. Nihal Thomas, Department of Endocrinology and Biochemistry, Royal Adelaide Hospital, IMVS, Adelaide 5000, Australia.
Received July 11, 1997.
References
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