Demontis R, Reissi D, Noel C, Boudailliez B, Westeel P F, Leflon P, Brasseur J, Coevoet B, Fournier A
Nephrology Service, Centre hospitalier, St. Quentin, France.
Clin Nephrol. 1989 Mar;31(3):123-7.
In a previous study we showed that 1 alpha OH vitamin D3 [1 alpha (OH)3] given to 16 hemodialyzed patients taking Al(OH)3 at a constant dose increased their plasma concentrations of aluminum [Demontis et al. 1986]. In order to choose between 2 possible mechanisms explaining this increase (increased intestinal absorption or decreased tissue storage of aluminum), we gave, in the present study, 1 alpha (OH)3 the same dose (6 micrograms per week) for the same period (4 weeks) to 15 stable hemodialyzed patients after their Al(OH)3 had been discontinued for 6 weeks. Under Al(OH)3 treatment they had a mean plasma aluminum (2.33 +/- 2.36 mumol/l) which was not significantly different from that of the patients in our former study (1.23 +/- 0.25 mumol/l). After Al(OH)3 discontinuation, plasma aluminum (measured by inductively coupled plasma emission spectrometry) decreased significantly as early as the 2nd week of the control period (1.39 mumol/l). The decrease was maintained at a plateau throughout the 5 weeks of the control period (1.38 mumol/l), the 4 weeks of 1 alpha OH vitamin (vit) D3 administration (1.40 mumol/l) and the 8 weeks of the post 1 alpha (OH)3 period (1.22 mumol/l). Plasma calcium and phosphate concentrations increased significantly with 1 alpha (OH)3 and decreased thereafter whereas plasma PTH concentrations decreased during 1 alpha (OH)2 D3 and increased after its discontinuation suggesting biological activity of 1 alpha (OH)3. Since 1 alpha (OH)3 increases plasma aluminum in hemodialyzed patients only when they are simultaneously taking Al(OH)3, it is suggested that this increase is explained by an increase of intestinal absorption of aluminum and not by a tissue redistribution of aluminum.
在之前的一项研究中，我们发现，给予16名持续服用恒定剂量氢氧化铝的血液透析患者1α-羟基维生素D3[1α(OH)3]后，他们血浆中的铝浓度升高了[德蒙蒂斯等人，1986年]。为了在解释这种升高的两种可能机制（铝的肠道吸收增加或组织储存减少）之间做出选择，在本研究中，我们在15名稳定的血液透析患者停用氢氧化铝6周后，给予他们相同剂量（每周6微克）的1α(OH)3，持续相同时间（4周）。在接受氢氧化铝治疗期间，他们的平均血浆铝浓度为(2.33±2.36微摩尔/升)，与我们之前研究中的患者（1.23±0.25微摩尔/升）相比，没有显著差异。停用氢氧化铝后，血浆铝（通过电感耦合等离子体发射光谱法测量）早在对照期的第2周就显著下降（1.39微摩尔/升）。在整个5周的对照期（1.38微摩尔/升）、4周的1α-羟基维生素（维生素）D3给药期（1.40微摩尔/升）和1α(OH)3给药后的8周（1.22微摩尔/升）内，这种下降一直维持在一个平稳水平。血浆钙和磷浓度在给予1α(OH)3后显著升高，此后下降，而血浆甲状旁腺激素浓度在1α(OH)2 D3给药期间下降，停药后升高，这表明1α(OH)3具有生物活性。由于1α(OH)3仅在血液透析患者同时服用氢氧化铝时才会使其血浆铝升高，因此表明这种升高是由铝的肠道吸收增加所致，而非铝的组织重新分布。
