Horiguchi Hyogo
Division of Environmental Medicine, Center for Community Medicine, Jichi Medical University, Shimotsuke, Tochigi, Japan.
Nihon Eiseigaku Zasshi. 2007 May;62(3):888-904. doi: 10.1265/jjh.62.888.
Anemia is commonly induced by chronic cadmium (Cd) intoxication. Three main factors are involved in the development of Cd-induced anemia: hemolytic, iron-deficiency, and renal. Intravascular hemolysis can occur at the early stage of Cd exposure owing to the direct damaging effect on erythrocytes. In addition, Cd that accumulates in erythrocytes affects membrane cytoskeletons and decreases cell deformability, and these cells are then trapped and destroyed in the spleen. Iron deficiency can be detected in animals after an oral exposure to Cd, which competes with iron for absorption in the intestines, leading to anemia. However, an increase in body iron content along with anemia is often observed in cases of parenteral exposure or itai-itai disease. Therefore, it is estimated that Cd disrupts the efficient usage of iron in hemoglobin synthesis in the body. Renal anemia is observed during the very last phase of chronic, severe Cd intoxication, such as itai-itai disease, showing a decrease in the production of erythropoietin from renal tubular cells. Because the renal anemia is based on the same pathophysiology as Cd-induced osteomalacia, which is derived from the disturbance of mineral metabolism due to renal tubular dysfunction, it is reasonable to include renal anemia in the criteria for the diagnosis of itai-itai disease. Hemodilution could also contribute to the development of Cd-induced anemia. Bone marrow hypoplasia or the inhibition of heme synthesis might only be involved in Cd-induced anemia in severe cases of Cd intoxication.
贫血通常由慢性镉(Cd)中毒引起。镉诱导的贫血发展涉及三个主要因素:溶血、缺铁和肾脏因素。在镉暴露的早期,由于对红细胞的直接损伤作用,可发生血管内溶血。此外,积聚在红细胞中的镉会影响膜细胞骨架并降低细胞变形能力,这些细胞随后会被困在脾脏中并被破坏。口服镉后,动物体内可检测到缺铁,镉与铁在肠道吸收中竞争,导致贫血。然而,在肠胃外接触或痛痛病病例中,常观察到体内铁含量增加伴随贫血的情况。因此,据估计镉会干扰体内血红蛋白合成中铁的有效利用。在慢性重度镉中毒的最后阶段,如痛痛病,会出现肾性贫血,表现为肾小管细胞产生促红细胞生成素减少。由于肾性贫血与镉诱导的骨软化症具有相同的病理生理学基础,后者源于肾小管功能障碍导致的矿物质代谢紊乱,因此将肾性贫血纳入痛痛病的诊断标准是合理的。血液稀释也可能导致镉诱导的贫血。骨髓发育不全或血红素合成抑制可能仅在严重镉中毒病例中参与镉诱导的贫血。