Failure of alphacalcidol (1α-hydroxyvitamin D3) in treating nutritional rickets and the biochemical response to ergocalciferol

It has been previously documented that alphacalcidol (1α-hydroxyvitamin D3) is inefficient in healing rickets, partly because it results in a suboptimal rise in 1,25-dihydroxyvitamin D (1,25-(OH)2D) and partly because it fails to replenish the store of 25-hydroxyvitamin D (25-OHD). However, very few studies have actually documented this outcome. The aim was to document biochemically the response to alphacalcidol and subsequently the change in response to ergocalciferol. This study was conducted at our institution from January 2005 till December 2008. We included all patients referred to our clinic with active rickets after a failed course of alphacalcidol. At baseline the median (IQR) for PTH l7.1 (4.5–35.3) pmol/L, 25-OHD 29.0 (18–66.2) nmol/L, 1,25-(OH)2D 205 (158.2–311.2) pmol/L and ALP 676 (462.5–1101.7) IU/L. After 3 months treatment with ergocalciferol the concentrations changed markedly with biochemical healing: PTH 4.5 (3.9–7.5), 25-OHD 143.5 (101.5–206.5), 1,25-(OH)2D 277 (221.0–572.7), ALP 369 (302.2–438.0). The results confirm the biochemical and physiological basis for using ergocalciferol (or cholecalciferol) in nutritional rickets. Unfortunately these forms are not readily available in many geographic areas. This supply problem together with marketing strategies forces physicians to make an incorrect choice of medication. Treatment with ergocalciferol was either with intramuscular stosstherapy or drops for 3 months. The former ensures compliance and is associated with higher 25-OHD and 1,25-(OH)2D concentrations.