• Alice Fanin, Lucia Miele, Emanuela Bertolini, Alessia Giorgini, Antonio Ettore Pontiroli, and Alberto Benetti.
• Dipartimento di Scienze della Salute, Ospedale San Paolo, Università degli Studi di Milano, via A. Di Rudinì 8, Milan, Italy. alice.fanin@hotmail.it.
• Intern Emerg Med. 2020 Mar 1; 15 (2): 337-339.

BackgroundLiver dysfunction has been widely reported in connection with anorexia nervosa (AN) but the pathogenesis of these alterations has never been fully understood despite reported theories about the presence of insulin resistance (IR) and non-alcoholic fatty liver disease (NAFLD). The aim of this study is to investigate if hypertransaminasemia in AN is linked to IR and NAFLD.MethodsAnthropometric data and laboratory exams of 34 patients and 34 controls were analyzed, including alanine-aminotransferase, aspartate-aminotransferase and homeostatic model assessment of insulin resistance (HOMA-IR) index. All subjects also underwent magnetic resonance imaging (MRI), ultrasonography (US), and transient elastography (TE).ResultsEvidence of increased alanine aminotransferase in AN patients was confirmed in our sample together with a lower HOMA-IR index compared to controls. Positive results in US appeared in 16 patients vs none in controls (p = 0.0007); patients with liver parenchyma abnormalities in US were not different than normal-US patients in any of the studied variables. Only one patient showed non-alcoholic fatty liver disease in MRI while abnormal TE was found in four patients and never in controls.ConclusionsLiver damage suggested by increased serum liver enzymes cannot be due to liver steatosis but potentially to a different liver disease (not identified by MRI) or to an early liver fibrosis not associated with an insulin-resistant status.

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