Dysregulated Iron Homeostasis in Ulcerative Colitis

• Published in: Indian journal of clinical biochemistry Vol. 34; no. S1; p. S77
• Main Authors: Jacob, M, Ramaswamy, J, Sukumaran, A, Jagadish, C, Varghese, J, Joseph, A.J, Simon, E.G, Jeyaseelan, V
• Format: Journal Article
• Language: English
• Published: Springer 24.05.2022
• Subjects: Anemia; Homeostasis; Ulcerative colitis
• ISSN: 0970-1915; 0974-0422

Hepcidin is the central hormone involved in systemic iron homeostasis. It is known to be regulated by a number of factors. For example, anemia and erythroid factors (such as erythroferrone [ERFE] and growth differentiation factor 15, both of which are released from the bone marrow during erythropoiesis) down-regulate it. On the other hand, inflammation up-regulates it. So, when anemia and inflammation are both present, which of these opposing factors has a predominant influence on hepcidin? To attempt to answer this question, we studied patients with ulcerative colitis (UC), an inflammatory bowel disease, in which anemia often co-exists with inflammation. Hemoglobin and serum iron levels were significantly lower and C-reactive protein levels (a marker of inflammation) significantly higher in patients with UC, than in those without. Despite the presence of systemic inflammation, however, serum hepcidin concentrations were found to be significantly lower in these patients; they also had significantly higher levels of serum ERFE, when compared to control subjects. When patients with UC were stratified into those with and without anemia, it was found that anemic patients had significantly lower hepcidin and higher erythroferrone levels than non-anemic subjects. These results indicate that, when anemia and inflammation co-exist, the effect of anemia on hepcidin appears to dominate over that of inflammation. This effect is possibly mediated through increased ERFE levels.