Division of Psychological and Social Medicine and Developmental Neurosciences, Faculty of Medicine, Technische Universität Dresden, Dresden, Germany; Eating Disorder Treatment and Research Center, Department of Child and Adolescent Psychiatry, Faculty of Medicine, Technische Universität Dresden, Dresden, Germany.
University Hospital Carl Gustav Carus, Institute of Clinical Chemistry and Laboratory Medicine, Technische Universität Dresden, Dresden, Germany.
Psychiatry Res. 2022 Aug;314:114673. doi: 10.1016/j.psychres.2022.114673. Epub 2022 Jun 9.
Hepatic involvement in anorexia nervosa (AN) has been previously reported, but a link to elevated vitamin B concentrations, which can be a sign for liver damage, has not been thoroughly examined. We measured liver enzymes (alanine aminotransferase, aspartate aminotransferase, gamma-glutamyltransferase) and vitamin B parameters (total B, holotranscobalamin, methylmalonic acid) in the plasma of young female patients with acute AN (n=77) and after short-term weight restoration (n=58, median body mass increase=25%), in comparison to healthy control participants (n=63). For a comprehensive assessment of vitamin B status, the combined marker cB was calculated. In acute AN, activities of alanine aminotransferase and gamma-glutamyltransferase as well as holotranscobalamin concentrations were elevated, and alanine aminotransferase activities positively correlated with total B, holotranscobalamin and cB in patients with elevated liver enzyme activities. After weight restoration, alanine aminotransferase activities and holotranscobalamin concentrations were elevated, and cB increased above the level of the healthy control group. The present study provides further evidence for a hepatic involvement in acute AN in concert with vitamin B parameters and points to refeeding-associated alterations of liver and vitamin B parameters. Future studies should include non-invasive methods to characterize hepatic involvement and evaluate vitamin B status as a potential marker of liver damage/irritation.
目前已有报道称神经性厌食症 (AN) 可导致肝脏损伤,但尚未对导致维生素 B 浓度升高的原因进行深入研究,而维生素 B 浓度升高可能是肝脏损伤的一个迹象。我们测量了急性 AN 患者(n=77)和短期体重恢复后(n=58,体重中位数增加 25%)以及健康对照组(n=63)血浆中的肝酶(丙氨酸氨基转移酶、天冬氨酸氨基转移酶、γ-谷氨酰转肽酶)和维生素 B 参数(总 B、全钴胺素、甲基丙二酸)。为了全面评估维生素 B 状态,我们计算了综合标志物 cB。在急性 AN 中,丙氨酸氨基转移酶和γ-谷氨酰转肽酶的活性以及全钴胺素浓度升高,并且丙氨酸氨基转移酶活性与总 B、全钴胺素和 cB 在肝酶活性升高的患者中呈正相关。体重恢复后,丙氨酸氨基转移酶活性和全钴胺素浓度升高,cB 升高至高于健康对照组的水平。本研究进一步证明了肝脏在急性 AN 中的参与与维生素 B 参数有关,并提示与再喂养相关的肝脏和维生素 B 参数的改变。未来的研究应包括使用非侵入性方法来描述肝脏损伤,并评估维生素 B 状态作为肝脏损伤/刺激的潜在标志物。