'Oversaturation' of transferrin after intravenous ferric gluconate (Ferrlecit(R)) in haemodialysis patients

'Oversaturation' of transferrin after intravenous ferric gluconate (Ferrlecit(R)) in haemodialysis patients
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DOI:
10.1093/oxfordjournals.ndt.a027405
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发表时间:
1996-05-01
影响因子:
6.1
通讯作者:
deJong, GMT
deJong, GMT
中科院分区:
医学1区
文献类型:
--
作者:
Zanen, AL;Adriaansen, HJ;deJong, GMT

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背景。慢性血液透析会导致失血和缺铁。这可以通过静脉注射制剂来纠正,例如葡萄糖酸钠铁(FeGl)。两名患者在 FeG1 输注期间主诉低血压和不适,同时血清铁水平高且计算出的转铁蛋白铁饱和度高于 100%。铁毒性可能是这些投诉的原因,众所周知,游离铁会加剧体内不断形成的自由基和其他活性氧产物的毒性。我们比较了四种 FeGI 输注速率的铁参数。方法。 20 名透析患者总共接受了 36 次 FeGl 输注。在透析的最后30分钟期间快速输注125mg(方案A(n=10))或62.5mg(方案B(n=7))FeG1。在透析 4 或 4.5 小时期间缓慢输注 125 mg(方案 C(n=9))或 62.5 mg(方案 D(n=10))。透析前、透析期间和透析后定期采血,测定血清铁、转铁蛋白、铁蛋白、血细胞比容、总蛋白、白蛋白和乳酸脱氢酶(LDH)。根据转铁蛋白和血清铁计算转铁蛋白饱和度。结果。快速输注 A(125 mg)时,输注结束时血清铁水平最高(中位 120(范围 40-159)μmol/l)和转铁蛋白饱和度(207(84-331)%),显着高于 B、C 和 D 的峰值水平(P 小于或等于 0.03)。快速输注 B(62.5 mg)时,峰值水平中等偏高(血清铁 61 (50-96) mu mol/l;转铁蛋白饱和度 118 (91-174)%)。缓慢输注 C(125 mg)可观察到相似的峰值水平(血清铁 83 (43-106) mu mol/l;转铁蛋白饱和度 141 (88-172)%)。缓慢输注 D (62.5 mg) 时,出现最低峰值水平(血清铁 38 (31-55) mu mol/l;转铁蛋白饱和度 78 (43-92)%)。这些水平显着低于 A、B 和 C 的水平(P 小于或等于 0.002)。仅使用 D,所有患者的转铁蛋白饱和度均低于 100%。所有患者在下次透析前铁蛋白均升高。在任何输注过程中LDH均未显着升高。结论。常用的 FeGl 快速输注速率 (A) 会导致转铁蛋白“过饱和”。这与游离铁引起的铁中毒相一致,这可以解释我们患者的抱怨。游离铁不能直接测量。 LDH 作为细胞损伤的粗略衡量指标并未升高。目前还没有更好的测量方法来证明游离铁的毒性,例如脂质过氧化物。以较低剂量(D)进行较长时间的输注是有效的,并且消除了转铁蛋白的“过饱和”以及可能的铁中毒的危险。
Background. Chronic haemodialysis causes blood loss and iron-deficiency. This can be corrected with intravenous preparations, e.g. sodium ferric-gluconate (FeGl). In two patients complaints of hypotension and malaise during FeGl infusion coincided with high levels of serum iron and a calculated transferrin iron saturation above 100%. Iron toxicity could be the cause of these complaints, Free iron is known to aggravate the toxicity of free radicals and other reactive oxygen products that are constantly formed in the body. We compared four rates of FeGl infusion with regard to iron parameters.Methods. 20 dialysis patients received a total of 36 infusions of FeGl. A rapid infusion of 125 mg (Protocol A (n=10)) or 62.5 mg (Protocol B (n=7)) of FeGl was given during the last 30 min of dialysis. A slow infusion of 125 mg (Protocol C (n=9)) or 62.5 mg (Protocol D (n=10)) was given during 4 or 4.5 h of dialysis. Blood was taken at regular intervals before, during, and after dialysis for determination of serum iron, transferrin, ferritin, haematocrit, total protein, albumin, and lactate dehydrogenase (LDH). Transferrin saturation was calculated from transferrin and serum iron.Results. With rapid infusion A (125 mg) the highest levels of serum iron (median 120 (range 40-159) micromol/l) and transferrin saturation (207 (84-331)%) were seen at the end of the infusion, These were significantly higher than the peak levels with B, C, and D (P less than or equal to 0.03). With rapid infusion B (62.5 mg), peak levels were intermediately high (serum Iron 61 (50-96) mu mol/l; transferrin saturation 118 (91-174)%). With slow infusion C(125 mg) similar peak levels were seen (serum iron 83 (43-106) mu mol/l; transferrin saturation 141 (88-172)%). With slow infusion D (62.5 mg), the lowest peak levels were seen (serum iron 38 (31-55) mu mol/l; transferrin saturation 78 (43-92)%). These levels were significantly lower than those with A, B and C (P less than or equal to 0.002). Only with D all patients showed a transferrin saturation lower than 100%. Ferritin was increased before the next dialysis in all patients. LDH was not significantly elevated during any infusion.Conclusions. The commonly used rapid infusion rate (A) of FeGl causes 'oversaturation' of transferrin. This is compatible with iron toxicity due to free iron which may explain our patients' complaints. Free iron cannot be measured directly. LDH as a crude measure of cell damage was not elevated. Better measurements to prove free iron toxicity, like lipid peroxides, are not yet readily available. Infusion during a longer period at a lower dose (D) is effective and eliminates 'oversaturation' of transferrin and probably the danger of iron toxicity.