Among the calcium regulating hormones investigated, 25(OH)D did not change in either the eldecalcitol or alfacalcidol treatment groups without vitamin D supplementation. Serum 1,25(OH)2D increased by approximately 20% in the alfacalcidol treatment group but decreased by approximately 50% in the eldecalcitol treatment group, regardless of the value of 25(OH)D at 6 months. In regard to the mechanism whereby eldecalcitol reduces serum 1,25(OH)2D concentration, eldecalcitol is shown to drastically induce CYP24A1 and suppress CYP27B1 in the kidney [4]. In contrast, because alfacalcidol itself is converted to calcitriol, the net effect is a slight increase in serum

1,25(OH)2D concentration. On the other hand, the effect of eldecalcitol in suppressing intact PTH tends to be slightly weaker than that of alfacalcidol. Previous basic and clinical studies have shown that the effect Cilengitide of eldecalcitol in suppressing PTH is lower than that of

calcitriol or alfacalcidol [9] and [10]. As a result, we speculate that eldecalcitol decreases serum 1,25(OH)2D concentration without much changes in serum PTH level. The present study has limitations. In this study, supplementation with native vitamin D3 was given if the patient’s serum 25(OH)D was below 20 ng/mL. Therefore, serum 25(OH)D at 6 months was relatively high. According to the result of a previous study by eldecalcitol, in which native vitamin D3 supplementation was not given, there was no correlation Anti-cancer Compound Library between serum 25(OH)D concentration and the increase in lumbar BMD [11]. almost However, because there was a large variation in the change in BMD by eldecalcitol among subjects with serum 25(OH)D below 20 ng/mL, prospective studies with and without vitamin D supplementation are necessary to investigate its influence on the efficacy of eldecalcitol. “
“Calcitriol (1α,25-dihydroxyvitamin D3, 1α,25(OH)2D3) exerts a wide variety of biological actions in many target organs. Calcitriol regulates calcium and phosphorus homeostasis, mineral metabolism, and bone metabolism. Through the action of calcitriol, in cooperation

with parathyroid hormone (PTH) and fibroblast growth factor-23 (FGF-23), the absorption of intestinal calcium and phosphorus, resorption of bone phosphorus and calcium, and reabsorption of renal calcium and phosphorus are increased, resulting in a rise in the serum calcium and phosphorus available for bone mineralization [1], [2] and [3]. Vitamin D3 is first metabolized to 25-hydroxyvitamin D3 [25(OH)D3] in the liver, then to calcitriol (1α,25(OH)2D3) in the kidneys. In this pathway, renal 1α-hydroxylation (by 25-OHD-1α-hydroxylase, CYP27B1) is a rate-limiting step in the production of calcitriol. Degradation of 25(OH)D3 and calcitriol is mediated by renal 24-hydroxylase (CYP24A1). The concentration of calcitriol in the blood is tightly regulated by a feedback loop controlling expression of renal CYP27B1 and CYP24A1.