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S6238 Anorexia Nervosa Presenting With Severe Iron Overload and Hepatocellular Injury in a Young Man: Complete Resolution Without Iron-Directed Therapy
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S6238 Anorexia Nervosa Presenting With Severe Iron Overload and Hepatocellular Injury in a Young Man: Complete Resolution Without Iron-Directed Therapy

Nikkida T Bundrant, Alexander Garza, Lois W Sayrs, Marta Bravo and Kyle Brown
The American journal of gastroenterology, Vol.121(10S1), pp.S1341-S1342
10/01/2026
DOI: 10.14309/01.ajg.0001234204.40608.d1

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Abstract

Introduction: Anorexia nervosa (AN) in men remains underrecognized despite increasing incidence. Signs of iron overload with hepatic hemosiderosis is an uncommon manifestation of malnutrition and may mimic hereditary hemochromatosis. We report a young man with severe AN, MRI-confirmed hepatic hemosiderosis, marked hyperferritinemia and transferrin saturation elevation, and negative HFE testing who achieved complete normalization of iron indices following nutritional rehabilitation alone. Case Description/Methods: A 22-year-old man presented with 1 year of progressive weight loss due to dietary restriction. He denied excessive exercise, binge eating, purging behaviors, or use of weight-loss medications. Weight decreased from 253 lb to 108 lb over 12 months (body mass index 13.24 kg/m²). On admission, he was bradycardic, hypothermic, hypotensive, and cachectic with temporal wasting and marked muscle loss. Hemoglobin was 14.8 g/dL. He was admitted for severe AN complicated by refeeding syndrome (phosphorus nadir 1.7 mg/dL). On hospital day 6, hepatology was consulted for severe hepatocellular injury with peak ALT 1,460 U/L and AST 446 U/L. Iron studies demonstrated ferritin 1,346 ng/mL, transferrin saturation >99%, transferrin 131 mg/dL, and TIBC 142 µg/dL. Liver MRI revealed hepatic hemosiderosis, while HFE mutation testing was negative. Discussion: Severe malnutrition may modulate iron metabolism through various means including transferrin deficiency, non-transferrin-bound iron accumulation, hepatocyte autophagy, and inflammatory signaling. Iron overload in young men commonly prompts evaluation for hereditary hemochromatosis, whereas AN may be overlooked because of persistent gender-related diagnostic bias. The patient underwent a structured 1,600 kcal/day refeeding protocol without phlebotomy or chelation. Over 16 weeks, ALT decreased by 96%, AST by 91%, ferritin by 88%, transferrin saturation normalized from >99% to 23%, and hemoglobin increased to 15.3 g/dL, demonstrating complete biochemical resolution. This case highlights marked elevations in serum iron studies and hepatic hemosiderosis as reversible complications of AN. Recognition of malnutrition-associated iron dysregulation may prevent unnecessary iron-directed therapies and broaden the differential diagnosis of iron overload in young men. Increased awareness of AN in male patients and further research into sex-specific manifestations of iron metabolism in eating disorders are warranted.
 Metabolism Anorexia Hemoglobin Malnutrition Men

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