Mejia Luis A, Erdman John W
Department of Food Science and Human Nutrition, University of Illinois Urbana-Champaign, Urbana, IL 61801, United States.
Nutr Rev. 2025 Mar 1;83(3):577-585. doi: 10.1093/nutrit/nuae183.
Vitamin A deficiency (VAD) and iron deficiency anemia coexist around the world, particularly in children and women of reproductive age in low- and middle-income countries. Within this scenario, there is a known interaction between vitamin A and iron, and it has been postulated that lack of vitamin A impairs iron metabolism, leading to vitamin A deficiency anemia (VADA). Current animal, epidemiological, and clinical studies support this notion. The objective of this study was to review the current literature on proposed metabolic mechanisms regarding how VAD modulates iron metabolism leading to anemia. To attain this objective, a literature search was conducted of research publications in the related field, without date restriction, using PubMed, Scopus, Google Scholar, and the University of Illinois's reference system. The data support the essentiality of vitamin A for normal erythropoiesis. It indicates that, in VAD, iron mobilization is impaired, and that this mineral accumulates in the liver and spleen, making it less available for erythropoiesis. A triggering factor for the development of VADA seems to be inflammation and systemic infection, which release cytokines that upregulate the production of hepcidin by the liver. VAD may also increase hepcidin directly without the involvement of inflammation or infection. The elevated hepcidin, in turn, lowers circulating iron and sequesters iron in storage depots, downregulating erythropoietin, leading to inefficient erythropoiesis, decreased hemoglobin (Hb) production, and (subsequently) anemia. VAD may also impact the expression of iron regulatory protein 2 (IRP2), and thus affect intracellular iron metabolism gene expression. VADA is not due to iron deficiency, but to a redistribution of iron in the body. Understanding the mechanism of VADA will assist in designing more effective strategies for combating anemia worldwide.
维生素A缺乏症（VAD）和缺铁性贫血在全球范围内并存，尤其是在低收入和中等收入国家的儿童及育龄妇女中。在这种情况下，维生素A与铁之间存在已知的相互作用，据推测，维生素A缺乏会损害铁代谢，导致维生素A缺乏性贫血（VADA）。目前的动物、流行病学和临床研究支持这一观点。本研究的目的是回顾当前关于VAD如何调节铁代谢导致贫血的代谢机制的文献。为实现这一目标，我们使用PubMed、Scopus、谷歌学术和伊利诺伊大学的参考系统，对相关领域无日期限制的研究出版物进行了文献检索。数据支持维生素A对正常红细胞生成的必要性。这表明，在VAD中，铁的动员受损，这种矿物质在肝脏和脾脏中积累，使其较少可用于红细胞生成。VADA发生的一个触发因素似乎是炎症和全身感染，它们会释放细胞因子，上调肝脏中血浆铁调素的产生。VAD也可能在没有炎症或感染参与的情况下直接增加血浆铁调素。升高的血浆铁调素反过来会降低循环铁水平，并将铁隔离在储存库中，下调促红细胞生成素，导致红细胞生成效率低下、血红蛋白（Hb）生成减少，进而导致贫血。VAD还可能影响铁调节蛋白2（IRP2）的表达，从而影响细胞内铁代谢基因的表达。VADA不是由于缺铁，而是由于体内铁的重新分布。了解VADA的机制将有助于设计更有效的全球抗贫血策略。
