TY - JOUR
T1 - METABOLITES OF VITAMIN D IN HUMAN VITAMIN-D DEFICIENCY
T2 - EFFECT OF VITAMIN D3 OR 1,25-DIHYDROXYCHOLECALCIFEROL
AU - Papapoulos, S. E.
AU - Fraher, L. J.
AU - Clemens, T. L.
AU - Gleed, J.
AU - O'Riordan, J. L.H.
N1 - Funding Information:
supported in part by the Medical Research Service of the Veterans Administra- tion, the Clinical Research Center, NIH grant no. RR00287-12, of the Uni- versity of Missouri School of Medicine, and the Gastroenterology Research Foundation Inc. of Mid-Missouri.
Funding Information:
These studies were supported by a generous grant from the Wellcome Trust to J. L. H. O’R. We would like to thank the physicians who referred patients to us for investigation.
PY - 1980
Y1 - 1980
N2 - Circulating concentrations of hydroxylated metabolites of vitamin D were measured in seven Asian patients with histologically proven osteomalacia before and during treatment with either cholecalciferol (vitamin D3) or 1,25-dihydroxycholecalciferol. All patients showed an excellent clinical and biochemical response to treatment irrespective of type of vitamin D administered. Circulating concentrations of 25-hydroxycholecalciferol and 24,25, 25,26, and 1,25 dihydroxycholecalciferols were abnormally low in the untreated patients. In five patients treated with small doses of cholecalciferol (3000 units, 75 μg daily) the concentration of 1,25-dihydroxycholecalciferol rose rapidly to normal and reached supra-normal levels within 72 h. Raised concentrations (up to 200 pg/ml) were sustained for several months and then started falling to normal. Serum 24,25 and 25,26 dihydroxycholecalciferols rose on ly gradually, after circulating 25–hydroxycholecalciferol concetration had increased to normal. In contrast, in the two patients who received 1,25–dihydroxycholoecalciferol (1 μg daily) serum concentrations of this metabolite rose to normal. The highest concentration observed was 80 pg/ml. Healing of osteomalacia occured, however, in these two patients in the absence of any measurable increases in 25–hydroxycholecalciferol and 24,25 or 25,26 dihydroxycholecalciferols which all remained abnormally low. Thus, it seems that 1,25–dihydroxycholecalciferol is the most important factor for the healing of vitamin-D-deficient osteomalacia and that other hydroxy metabolites are unimportant.
AB - Circulating concentrations of hydroxylated metabolites of vitamin D were measured in seven Asian patients with histologically proven osteomalacia before and during treatment with either cholecalciferol (vitamin D3) or 1,25-dihydroxycholecalciferol. All patients showed an excellent clinical and biochemical response to treatment irrespective of type of vitamin D administered. Circulating concentrations of 25-hydroxycholecalciferol and 24,25, 25,26, and 1,25 dihydroxycholecalciferols were abnormally low in the untreated patients. In five patients treated with small doses of cholecalciferol (3000 units, 75 μg daily) the concentration of 1,25-dihydroxycholecalciferol rose rapidly to normal and reached supra-normal levels within 72 h. Raised concentrations (up to 200 pg/ml) were sustained for several months and then started falling to normal. Serum 24,25 and 25,26 dihydroxycholecalciferols rose on ly gradually, after circulating 25–hydroxycholecalciferol concetration had increased to normal. In contrast, in the two patients who received 1,25–dihydroxycholoecalciferol (1 μg daily) serum concentrations of this metabolite rose to normal. The highest concentration observed was 80 pg/ml. Healing of osteomalacia occured, however, in these two patients in the absence of any measurable increases in 25–hydroxycholecalciferol and 24,25 or 25,26 dihydroxycholecalciferols which all remained abnormally low. Thus, it seems that 1,25–dihydroxycholecalciferol is the most important factor for the healing of vitamin-D-deficient osteomalacia and that other hydroxy metabolites are unimportant.
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U2 - 10.1016/S0140-6736(80)90283-4
DO - 10.1016/S0140-6736(80)90283-4
M3 - Article
C2 - 6107407
AN - SCOPUS:0018856789
SN - 0140-6736
VL - 316
SP - 612
EP - 615
JO - The Lancet
JF - The Lancet
IS - 8195
ER -