The development of a precise measure of the scale of weight loss could be beneficial. Screening for vitamin and minerals levels could also help to distinguish symptoms resembling depression or anxiety, such as irritability, moodiness, restlessness, etc, associated with malnutrition. These could mediate the effect of malnutrition on psychological symptoms more markedly than the variables explored in this study. Clinicians and the treating team of AN, should be aware that there could be confusion in the aetiology of certain malnutrition symptoms that appear as depression and anxiety symptoms. The cornerstone of treating AN is still nutrition rehabilitation which should be initiated immediately. Nutrition rehabilitation should start first in order to decrease immediately physical complications and psychological well-being. In practice managing co-occurent anxiety or depression symptoms in ED patients will include the specific treatment of ED, that could lower a part of anxiety and depressive symptoms by nutrition rehabilitation, withdrawal from binges and purges, specific psychotherapy and work on the social impact of the illness. Future studies with a longitudinal design and a follow up on the evolution during treatment are needed to explore variations in nutritional status in relation to psychological symptoms using more heterogeneous samples. For instance, future research should consider including a group of healthy controls or a group of recovered subjects, and the use of further assessment scales for psychological symptoms. More studies are needed to confirm our results. Drug-induced liver injury is the leading cause of acute liver failure and remains difficult to predict due to the lack of adequate biomarkers. These enzymes are not accurately predictive for DILI, because they can be detected only after damage has been instigated. In addition, some drugs can increase plasma liver enzymes without actually causing liver damage, such as diclofenac and methotrexate. Therefore, there is a need for SJN 2511 ALK inhibitor biomarkers that can detect DILI at the onset and can be used as a tool during drug development and monitoring of patients. Biomarkers predictive for DILI that can be detected in urine could be of great value to monitor patients on a regular basis in a non-invasive way. The urinary proteome mirrors the protein pool present in blood, and proteins related to pathologies, such as acute liver injury, can be detected in urine. Compared to blood, urine is well suited for proteomic profiling as it contains less high abundant proteins that can hamper biomarker detection. Nevertheless, human sample collection for biomarker assessment is difficult, because the overall incidence of DILI is 10–15 cases in 100 000 patient years and the incidence for any particular drug can range from 1 case in 10.000 to 1.000.000 patient years. Acetaminophen is an interesting model compound for searching biomarkers related to acute DILI. APAP is metabolized to its reactive metabolite N-acetyl-p-benzoquinone imine, which is detoxified by conjugation to GSH. With high dosages of APAP, the GSH pool is depleted allowing NAPQI to bind to cellular macromolecules. Binding of NAPQI to mitochondrial proteins initiates the formation of reactive oxygen species and peroxynitrite. It has been demonstrated that oxidative stress leads to lipid peroxidation, mitochondrial dysfunction, disruption of calcium homeostasis and eventually necrotic cell death. Previous proteomics studies using rodent plasma and liver tissue showed marked changes in the expression levels of various proteins as a result of APAP-induced hepatotoxicity.