Baker Joshua F, Ghio Andrew J
Division of Rheumatology, Department of Medicine, 5 Maloney Building, Suite 504, 3600 Spruce Street, Hospital of the University of Pennsylvania, Philadelphia, PA 19104, USA.
Rheumatology (Oxford). 2009 Nov;48(11):1339-44. doi: 10.1093/rheumatology/kep221. Epub 2009 Jul 23.
Iron is critical in nearly all cell functions and the ability of a cell, tissue and organism to procure this metal is obligatory for survival. Iron is necessary for normal immune function, and relative iron deficiency is associated with mild immunosuppression. Concentrations of this metal in excess of those required for function can present both an oxidative stress and elevate risks for infection. As a result, the human has evolved to have a complex mechanism of regulating iron and limiting its availability. This homoeostasis can be disrupted. Autoimmune diseases and gout often present with abnormal iron homoeostasis, thus supporting a participation of the metal in these injuries. We review the role of iron in normal immune function and discuss both clinical evidence of altered iron homoeostasis in autoimmune diseases and gout as well as possible implications of both depletion and supplementation of this metal in this patient population. We conclude that altered iron homoeostasis may represent a purposeful response to inflammation that could have theoretical anti-inflammatory benefits. We encourage physicians to avoid routine iron supplementation in those without depleted iron stores.
铁在几乎所有细胞功能中都至关重要，细胞、组织和生物体获取这种金属的能力是生存所必需的。铁对于正常免疫功能必不可少，相对铁缺乏与轻度免疫抑制相关。这种金属的浓度超过功能所需水平时，会产生氧化应激并增加感染风险。因此，人类进化出了复杂的机制来调节铁并限制其可用性。这种稳态可能会被破坏。自身免疫性疾病和痛风常伴有铁稳态异常，从而支持这种金属参与这些损伤。我们综述了铁在正常免疫功能中的作用，并讨论了自身免疫性疾病和痛风中铁稳态改变的临床证据，以及在该患者群体中消耗和补充这种金属的可能影响。我们得出结论，铁稳态改变可能代表了对炎症的一种有目的的反应，理论上可能具有抗炎益处。我们鼓励医生避免对铁储备未耗尽的患者进行常规补铁。
