In this review article we discuss current knowledge about iron in the skin and the cutaneous wound healing process. Iron plays a key role in both oxidative stress and photo-induced skin damage. The main causes of oxidative stress in the skin include reactive oxygen species (ROS) generated in the skin by ultraviolet (UVA) 320–400 nm portion of the UVA spectrum and biologically available iron. We also discuss the relationships between iron deficiency, anemia and cutaneous wound healing. Studies looking at this fall into two distinct groups. Early studies investigated the effect of anemia on wound healing using a variety of experimental methodology to establish anemia or iron deficiency and focused on wound-strength rather than effect on macroscopic healing or re-epithelialization. More recent animal studies have investigated novel treatments aimed at correcting the effects of systemic iron deficiency and localized iron overload. Iron overload is associated with local cutaneous iron deposition, which has numerous deleterious effects in chronic venous disease and hereditary hemochromatosis. Iron plays a key role in chronic ulceration and conditions such as rheumatoid arthritis (RA) and Lupus Erythematosus are associated with both anemia of chronic disease and dysregulation of local cutaneous iron hemostasis. Iron is a potential therapeutic target in the skin by application of topical iron chelators and novel pharmacological agents, and in delayed cutaneous wound healing by treatment of iron deficiency or underlying systemic inflammation.

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Cell-to-cell interactions via gap junctional communication and connexon hemichannels are involved in the pathogenesis of diabetes. Gap junctions are highly specialized transmembrane structures that are formed by connexon hemichannels, which are further assembled from proteins called “connexins.” In this paper, we discuss current knowledge about connexins in diabetes. We also discuss mechanisms of connexin influence and the role of individual connexins in various tissues and how these are affected in diabetes. Connexins may be a future target by both genetic and pharmacological approaches to develop treatments for the treatment of diabetes and its complications.

Introduction. Diabetic foot ulceration (DFU) is the commonest cause of severe limb ischaemia in the western world. In diabetes mellitus, anaemia is frequently unrecognized, yet studies have shown that it is twice as common in diabetics compared with nondiabetics. We aimed to assess the incidence of anaemia and further classify the iron deficiency seen in a high-risk DFU patient group. Methods. An observational study was undertaken in a multidisciplinary diabetic foot clinic setting. All patients with DFU attending over a four-month period were included. Anaemia was defined as haemoglobin (Hb) levels <12 g/dL. Iron deficiency was classified according to definitions of AID (absolute iron deficiency) and FID (functional iron deficiency). Results. 27 patients had DFU; 14 (51.9%) were anaemic; two (7.41%) had severe anaemia (Hb < 10 g/dL). No patient had B12 or Folate deficiency. In patients with anaemia, there was significant spread of indices. Only one patient had “textbook” absolute iron deficiency (AID) defined as low Hb, MCV, MCH, and ferritin. Functional iron deficiency (FID) was seen in a further seven patients (25.5%). Conclusion. Anaemia and iron deficiency are a common problem in patients with DFU. With current clinical markers, it is incredibly difficult to determine causal relationships and further in-depth scientific study is required.

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