Davies M, Heys S E, Selby P L, Berry J L, Mawer E B
University Department of Medicine, Manchester Royal Infirmary, United Kingdom.
J Clin Endocrinol Metab. 1997 Jan;82(1):209-12. doi: 10.1210/jcem.82.1.3644.
Serum vitamin D metabolites and PTH were measured in seven subjects with a history of previous partial gastrectomy (PGX) and metabolic bone disease. The elimination t1/2 of [3H]25-hydroxyvitamin D3 ([3H]25OHD3) in serum was assessed after an iv pulse dose of 5 microCi [26,27-3H]25OHD3. Median serum 25OHD3 was 37.5 (27.5-101.3) nmol/L, [normal range (NR) 10.8-58.5 nmol/L], mean serum 1,25-dihydroxyvitamin D [1, 25-(OH)2D3] was raised at 175 +/- 72 pmol/L, (NR 48-120 pmol/L) and mean PTH was also high, 67 +/- 27 ng/L, (NR 10-60 ng/L). Serum t1/2 [3H]25OHD3 ranged from 10.9-21.2 days. A strong negative correlation existed between t1/2 [3H]25OHD3 and serum 1,25-(OH)2D3 [Spearman's rank correlation coefficient (r = -0.82, P = 0.002)] and PTH [Spearman's rank correlation coefficient (r = -0.81, P = 0.001)]. Four subjects who had high initial PTH concentrations (60-115 ng/L) and elevated 1,25-(OH)2D levels (162-300 pmol/L) were reassessed after calcium supplementation to suppress secondary hyperparathyroidism (2 degrees HPT). In this subgroup, after-treatment PTH fell from 82 +/- 24 to 52 +/- 24 ng/L (mean +/- SD), not significant; 1,25-(OH)2D fell from 210 +/- 61 to 116 +/- 28 pmol/L, P = 0.015; and t1/2 [3H]25OHD3 increased from 13.2 +/- 1.9 to 18.9 +/- 3.1 days, P = 0.012. Patients with PGX and evidence of 2 degrees HPT with elevated 1,25-(OH)2D have a reduced t1/2 [3H]25OHD3, and this may explain the increased susceptibility of the subjects to osteomalacia. Calcium supplementation suppresses 2 degrees HPT, increases t1/2 [3H]25OHD3 and may protect against PGX osteoporosis and osteomalacia.
对7名有既往部分胃切除术（PGX）病史且患有代谢性骨病的受试者进行了血清维生素D代谢产物和甲状旁腺激素（PTH）检测。静脉注射5微居里[26,27 - 3H]25 - 羟基维生素D3（[3H]25OHD3）脉冲剂量后，评估血清中[3H]25 - 羟基维生素D3（[3H]25OHD3）的消除半衰期（t1/2）。血清25OHD3中位数为37.5（27.5 - 101.3）nmol/L，[正常范围（NR）10.8 - 58.5 nmol/L]，血清1,25 - 二羟基维生素D[1,25 - (OH)2D3]平均升高至175±72 pmol/L，（NR 48 - 120 pmol/L），且平均PTH也较高，为67±27 ng/L，（NR 10 - 60 ng/L）。血清[3H]25OHD3的t1/2范围为10.9 - 21.2天。t1/2[3H]25OHD3与血清1,25 - (OH)2D3之间存在强负相关[斯皮尔曼等级相关系数（r = - 0.82，P = 0.002）]以及与PTH之间也存在强负相关[斯皮尔曼等级相关系数（r = - 0.81，P = 0.001）]。对4名初始PTH浓度较高（60 - 115 ng/L）且1,25 - (OH)2D水平升高（162 - 300 pmol/L）的受试者补充钙剂以抑制继发性甲状旁腺功能亢进（2°HPT）后进行了重新评估。在该亚组中，治疗后PTH从82±24降至52±24 ng/L（平均值±标准差），无显著差异；1,25 - (OH)2D从210±61降至116±28 pmol/L，P = 0.015；且t1/2[3H]25OHD3从13.2±1.9增加至18.9±3.1天，P = 0.012。患有PGX且有2°HPT证据且1,25 - (OH)2D升高的患者，其[3H]25OHD3的t1/2降低，这可能解释了这些受试者对骨软化症易感性增加的原因。补充钙剂可抑制2°HPT，增加t1/2[3H]25OHD3，并可能预防PGX骨质疏松症和骨软化症。
