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Iron overload may be critical for liver dysfunction in anorexia nervosa, and the role of haematocrit-adjusted albumin in assessing nutritional status: a case report

BACKGROUND: Anorexia nervosa (AN) is frequently associated with liver dysfunction, but the precise mechanism remains undefined. Since the nutritional marker albumin has a low correlation with changes in body weight in AN, and patients with AN often have dehydration as a complication, we also examine...

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Detalles Bibliográficos
Autores principales: Yoshida, Tomohiko, Namiki, Toshiki, Yamaga, Masaya, Onishi, Shunichiro, Takemoto, Minoru
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10617211/
https://www.ncbi.nlm.nih.gov/pubmed/37907890
http://dx.doi.org/10.1186/s12887-023-04367-6
Descripción
Sumario:BACKGROUND: Anorexia nervosa (AN) is frequently associated with liver dysfunction, but the precise mechanism remains undefined. Since the nutritional marker albumin has a low correlation with changes in body weight in AN, and patients with AN often have dehydration as a complication, we also examined whether haematocrit (HCT)-adjusted serum albumin could be a better nutritional marker in AN. CASE PRESENTATION: We describe a 15-year-old girl with severe weight loss and liver damage whose liver enzymes normalized after 1.5 months of hospitalization and weight gain. We found a significant correlation between body weight (BW) and HCT-adjusted serum albumin (Spearman’s rank correlation coefficient (r(s)) = 0.66, P = 5.28 × 10(−3)) and between BW and alanine aminotransferase (ALT) (r(s) = -0.825, P = 8.45 × 10(−5)). After division by HCT, correlations between serum albumin and ALT (r(s) = -0.835, P = 5.24 × 10(−5)) and between the iron-storage protein ferritin and the liver enzyme gamma-glutamyl transferase (r(s) = 1.0, P = 0.017) were also statistically significant. CONCLUSION: These results suggest that improvement of the nutritional status in AN could relieve liver dysfunction and facilitate iron transport. Since a decrease in the iron-transport protein transferrin presumably increases labile non-transferrin-bound iron, resulting in excess reactive oxygen species production, a defect in iron transport due to malnutrition could be one of the causes of liver injury in AN. In addition, HCT-adjusted albumin could be a better marker than its raw data to assess changes in nutritional status in AN.