Liver Test at Hospital Admission Predicts Dangerous Refeeding Complication in Anorexia

When patients with severe anorexia nervosa are admitted to hospital and clinicians begin the delicate process of restoring nutrition, they face two complications that can strike in quick succession and each of which can be life-threatening. The first is starvation hepatitis, an injury to the liver caused by profound protein-energy malnutrition that shows up as sharply elevated liver enzymes in the blood. The second is refeeding syndrome, a potentially catastrophic shift in fluids and electrolytes that occurs when calories are reintroduced to a body that has adapted to surviving on almost nothing. A new retrospective cohort study from a French university hospital now suggests that these two complications are not merely neighbours on a timeline but are directly linked: patients who arrive with signs of starvation liver injury are dramatically more likely to develop refeeding syndrome once feeding starts.

The research, published in the Journal of Eating Disorders, analysed the medical records of 62 adults hospitalised for anorexia nervosa at a single French centre between January 2020 and December 2025. To be included, patients had to stay in hospital for more than five days, carry a diagnosis of anorexia nervosa, and have no pre-existing liver disease that could confound the interpretation of their liver enzymes. The overwhelming majority of participants, 95 percent, were female, with a mean age of 28.9 years. Their mean body mass index at admission was 13.47 kilograms per square metre, a figure that places most patients deep within the range of extreme, organ-threatening malnutrition.

The findings on the prevalence of starvation hepatitis were striking in their own right. Half of all patients, 31 of the 62 admitted, already had the condition when they arrived, defined by elevated transaminases, the enzymes alanine aminotransferase and aspartate aminotransferase, in the context of advanced protein-energy malnutrition. This liver injury is thought to arise because prolonged starvation depletes the liver of the substrates it needs to maintain its own cells, triggering autophagy, steatosis-like changes and hepatocyte dysfunction. Clinically, it matters because the liver sits at the centre of the metabolic machinery that must be revived when feeding resumes, and because severe transaminase elevations can themselves signal hepatic compromise that requires careful management.

Refeeding syndrome, the study’s second focus, is defined as a clinically significant decrease in plasma phosphate, potassium and/or magnesium within five days of resuming caloric intake. The mechanism is deceptively simple but physiologically profound. In starvation, insulin secretion falls to minimal levels and the body switches to burning fatty acids and ketone bodies, while intracellular stores of phosphate, potassium and magnesium are progressively depleted even though serum levels may look deceptively normal. When carbohydrates are suddenly reintroduced, insulin surges, driving glucose and electrolytes into cells and causing serum phosphate and other electrolytes to plummet. The consequences can include cardiac arrhythmia, respiratory failure, seizures, and death. Clinical guidelines from bodies such as NICE and the French Haute Autorité de Santé already recommend low initial caloric intake and close electrolyte monitoring in high-risk patients, but identifying who is truly high risk remains an inexact science.

In the new cohort, refeeding syndrome occurred in 19 patients, or 30.6 percent overall, within the first five days of nutritional rehabilitation. But the distribution was far from even. Among patients who had starvation hepatitis at admission, 48.4 percent went on to develop refeeding syndrome, compared with just 12.9 percent of those whose liver enzymes were normal when they arrived. That difference, statistically significant with a p-value of 0.006, hinted at a strong biological relationship between the two conditions, one that clinicians had long suspected but that had never before been formally tested in this population.

To confirm that the association was real and not merely a reflection of patients being sicker in general, the researchers performed a multivariate logistic regression, adjusting for body mass index and initial caloric intake, two factors that are themselves known to influence refeeding risk. The result held. Starvation hepatitis at admission was the only independent predictor of refeeding syndrome, with an adjusted odds ratio of 3.6 and a 95 percent confidence interval of 1.08 to 12.2, and a p-value of 0.038. In other words, even after accounting for how thin the patient was and how aggressively calories were reintroduced, the presence of liver injury on arrival more than tripled the odds of the electrolyte crisis that follows.

The biological plausibility of this link is a subject worth unpacking. The liver is the primary site of glycogen storage, gluconeogenesis, and phosphate-dependent ATP production, all of which are central to the pathophysiology of refeeding. A malnourished liver that is already injured may have diminished capacity to handle the sudden metabolic load of renewed nutrition, including the surge in insulin-driven intracellular uptake of phosphate that characterises refeeding syndrome. Hepatic depletion of adenosine triphosphate and phosphorus stores may leave patients with less reserve to buffer the shift, so serum phosphate falls faster and further. The authors propose that starvation hepatitis may therefore serve not just as a marker of extreme malnutrition but as a window into the functional state of the metabolic machinery that refeeding will stress.

What makes the finding clinically compelling is the simplicity of the marker involved. Transaminase measurements are a routine part of the standard blood panel drawn from virtually every hospitalised patient, requiring no specialised equipment, no imaging, and no additional cost. If a team knows that elevated liver enzymes on the admission screen flag a patient as being at especially high risk of refeeding syndrome, they can act on that information immediately: starting calories at a lower level, advancing the feeding plan more cautiously, and scheduling more frequent checks of phosphate, potassium and magnesium over the critical first five days. Electrolyte abnormalities detected early can often be corrected with supplementation before they progress to arrhythmia or organ failure, which is precisely the kind of preventable deterioration that structured monitoring is designed to avert.

The study does have limitations inherent to its design. It was retrospective, meaning the researchers relied on data collected in the course of routine clinical care rather than on a prospectively standardised protocol, and it was conducted at a single centre with a modest sample size of 62 patients. The confidence interval around the odds ratio, while excluding the null value, is wide, reflecting the small number of events involved. Residual confounding cannot be excluded, and the study population, overwhelmingly female and severely underweight, may not fully represent the broader spectrum of eating disorders seen in clinical practice. Nevertheless, the consistency of the effect with known physiology, and the fact that it persisted after adjustment for the most obvious confounders, lend the finding credibility and make it a candidate for confirmation in larger, prospective cohorts.

For clinicians working in eating disorder units, medical wards and intensive care settings, the study offers a practical rule of thumb grounded in evidence: check the liver panel before the first meal. For researchers, it opens a new line of inquiry into the hepatic mechanisms that connect starvation and refeeding, potentially identifying further biomarkers of metabolic reserve. And for patients and families, it is a reminder that recovery from severe anorexia nervosa is a medically intricate process, one in which the pace of renourishment can matter as much as the nutrition itself. A simple blood test, the study suggests, may help clinicians get that pace right for the patients who need caution most.

Subject of Research: The association between starvation hepatitis and refeeding syndrome in hospitalised patients with severe anorexia nervosa

Article Title: Starvation hepatitis and refeeding syndrome in anorexia nervosa: a retrospective cohort study

Article References: DEGLAIRE, J., ROULAND, A., GERSTER, T., BRINDISI, M.-C., BOUILLET, B., LUU, M., & MOUILLOT, T. (2026). Starvation hepatitis and refeeding syndrome in anorexia nervosa: a retrospective cohort study. Journal of Eating Disorders. https://doi.org/10.1186/s40337-026-01779-4

Image Credits: AI Generated

DOI: 10.1186/s40337-026-01779-4

Keywords: anorexia nervosa, starvation hepatitis, refeeding syndrome, malnutrition, liver enzymes, electrolytes, nutritional rehabilitation, hypophosphatemia, eating disorders, hospitalisation, risk prediction, transaminases