MacFarlane I A, Mawer E B, Berry J, Hann J
Clin Endocrinol (Oxf). 1982 Jul 1;17(1):51-9. doi: 10.1111/j.1365-2265.1982.tb02633.x.
The serum concentrations of 25-hydroxycholecalciferol (25 OH D3), 24,25-dihydroxycholecalciferol [24,25(OH)-2D3] and 1,25-dihydroxycholecalciferol [1,25(OH)2D3] were measured in twenty-one patients with untreated hyperthyroidism. Compared with control subjects, 25 OH D3 concentrations were not altered, 24,25(OH)2D3 concentrations were increased, although not significantly and 1,25(OH)2D3 concentrations were decreased (P = 0.01). Following oral carbimazole therapy, 24,25(OH)2D3 concentrations fell (P less than 0.01), 1,25(OH)2D3 concentrations increased (P less than 0.01) and 25 OH D3 concentrations were unchanged. The altered 1,25(OH)2D3 and 24,25(OH)2D3 concentrations found in hyperthyroidism are probably due to the effects of thyroid hormone on bone and mineral metabolism. Increased serum calcium and phosphate concentrations with secondary hypoparathyroidism result in stimulation of the renal 24-hydroxylase and suppression of the 1-hydroxylase enzymes. In addition, serum 24,25(OH)2D3 concentrations were significantly correlated with serum triiodothyronine levels (T3) (r = 0.66, P less than 0.002) before treatment. This may indicate a direct stimulatory effect of T3 on 24-hydroxylase activity. No relationship was found between serum 1,25(OH)2D3 concentrations before therapy and serum T3.
对21例未经治疗的甲状腺功能亢进患者测定了血清25-羟胆钙化醇(25-OH D3)、24,25-二羟胆钙化醇[24,25(OH)-2D3]和1,25-二羟胆钙化醇[1,25(OH)2D3]的浓度。与对照组相比,25-OH D3浓度未改变,24,25(OH)2D3浓度升高,虽不显著,而1,25(OH)2D3浓度降低(P = 0.01)。口服卡比马唑治疗后,24,25(OH)2D3浓度下降(P<0.01),1,25(OH)2D3浓度升高(P<0.01),25-OH D3浓度未变。甲状腺功能亢进时1,25(OH)2D3和24,25(OH)2D3浓度的改变可能是由于甲状腺激素对骨和矿物质代谢的影响。继发性甲状旁腺功能减退导致血清钙和磷浓度升高,从而刺激肾脏24-羟化酶并抑制1-羟化酶。此外,治疗前血清24,25(OH)2D3浓度与血清三碘甲状腺原氨酸水平(T3)显著相关(r = 0.66,P<0.002)。这可能表明T3对24-羟化酶活性有直接刺激作用。治疗前血清1,25(OH)2D3浓度与血清T3之间未发现相关性。