Physiological Mechanisms of Anaemia of Inflammation in Children with Severe Acute Malnutrition Undergoing Therapeutic Feeding in Katsina State, North West Nigeria

Background: Severe acute malnutrition carries a high burden of anaemia driven by both nutritional deficiency and inflammatory suppression of erythropoiesis through hepcidin-mediated iron sequestration. The relative contributions of iron deficiency, folate deficiency, erythropoietin insufficiency, and inflammation-induced hepcidin to anaemia in Nigerian children with severe acute malnutrition are poorly delineated, limiting the rational design of treatment protocols. Objectives: This study aims to characterise the pathophysiological contributions to anaemia in children with severe acute malnutrition at a therapeutic feeding centre in Katsina State by quantifying erythropoietin, hepcidin, soluble transferrin receptor, ferritin, serum folate, vitamin B12, and interleukin-6 at admission, week 4 of treatment, and discharge, and to model their dynamics in relation to haematological recovery. Methods: Eighty children aged 6 to 59 months with severe acute malnutrition and anaemia will be enrolled at the Katsina General Hospital therapeutic feeding unit. Venous blood will be collected at three time points. Erythropoietin and hepcidin will be quantified by ELISA. Full blood count and reticulocyte count will track erythropoietic response. Linear mixed-effects models will characterise biomarker trajectories and their predictors of haemoglobin recovery. Expected Outcomes: Hepcidin elevation driven by interleukin-6 is hypothesised to be the dominant mechanism at admission, with functional iron deficiency persisting despite nutritional repletion until inflammatory resolution. Conclusion: Results will generate original mechanistic insights enabling improved anaemia treatment protocols for severe acute malnutrition in Nigeria. Keywords: severe acute malnutrition, anaemia of inflammation, hepcidin, erythropoietin, Katsina.