anorexia nervosa is a common eating disorder , particularly in women , with a lifetime prevalence estimated to be 0.30.9% . this disorder is associated with numerous medical complications ( cardiovascular problems , endocrine disorders , electrolyte and hematopoietic abnormalities , amenorrhea , and osteoporosis ) , among which changes in liver tests are frequent . a mild increase in serum aminotransferase levels is indeed observed in up to 60% of these patients [ 2 , 3 ] leading the american psychiatric association to recommend a systematic assessment of liver tests for these patients . conversely , severe liver damage with a significant decrease in coagulation factors appears to be uncommon in patients with anorexia nervosa , although some cases have been reported . even if the mechanisms of liver injury during anorexia nervosa remain unclear , a complex programmed cell death in response to starvation , called autophagy , has been suggested in few studies to play a pivotal role in yeast and animals   as well as in human beings . we report here the case of a 24-year - old woman with anorexia nervosa , who experienced acute liver injury in association with histological and electron microscopical evidence of liver autophagy that was slowly reversible following careful renutrition . a 24-year - old woman was admitted for severe malnutrition and dehydration in the context of anorexia nervosa that was diagnosed one year ago . during this time , she was treated with serotonin reuptake inhibitor and denied taking illicit drug or potentially harmful products . on admission , she presented hypotension ( 90/50  mmhg ) , sinus bradycardia ( 40  bpm ) , slight hypoglycemia ( 3.9  mmol / l ) , and hypothermia ( 35.7c ) . she measured 160  cm and her body weight was 36  kg , corresponding to a body mass index ( bmi ) of 14  kg / m . at physical examination laboratory data at admission demonstrated the following : glycemia ( 3.5  mmol / l ) , na 137  mmol / l ( n : 136144 ) , k 3.7  mmol / l ( 3.64.6 ) , total ca 2.34  mmol / l ( n : 2.22.52 ) , mg 1.10  mmol / l ( n : 0.651.05 ) , p 1.22 ( n : 0.81.5 ) , and osmolality 289  mosm / kg . platelets were at 144  g / l ( n : 150350 ) , hemoglobin was at 133  g / l ( n : 120160 ) , and leucocytes were at 6.6  g / l ( n : 411 ) . the liver function tests was abnormal with a factor v at 33% ( n : > 70% ) . serum aminotransferase levels were increased as follow : ast 208  u / l ( n : 1142 ) , alt 341 ( n : 942 ) , and total bilirubin 65  mol / l ( n : 725 ) . the vitamin c was normal at 78  umol / l ( n : 1785 ) as was the thiamine at 208  umol / she was treated with serotonin reuptake inhibitor and denied taking illicit drug or potentially harmful products . after one week , the laboratory routine tests revealed abnormal hematological tests with hemoglobin at 114  g / l , leucopenia at 2.5  g / l , and thrombocytopenia at 52 additional investigations included prealbumin : 121  mg / l ( n : 223380 ) and albumin : 36  g / l ( n : 3548 ) . liver tests were as follows : ast 1088  u / l , alt 1868  u / l , ggt  138  u / l , pa 102 hepatitis a , b , c , and e , cmv , and hiv tests were negative . autoantibodies were absent ; iron studies and ceruloplasmin were normal . at abdominal ultrasound the liver appeared normal with no ascites . thus , a diagnosis of acute liver injury associated with anorexia nervosa was considered the most plausible diagnosis . thus , 10 days after hospital admission , a liver biopsy was performed by the transjugular route . at histology , cytoplasm of hepatocytes was clarified and some acidophil bodies were found predominant in the centrilobular region . in addition , ceroid pigments at the apical pole of the hepatocytes were observed ( figure 1 ) . an electron microscopy study was also performed in a fragment of liver biopsy , which showed features that strongly suggested a phenomenon of autophagocytosis : the density of glycogen particles in the hepatocytes was very low , consistent with cytoplasm clarification on pas staining at the optical microscopy . in addition , the number of both mitochondria and rough endoplasmic reticulum appeared to be reduced . this observation contrasts with an increased number of golgi bodies and smooth endoplasmic reticulum as well as primary and secondary lysosomes containing digested material ( figure 1 ) . eight weeks after admission , with progressive refeeding the test returned back to normal ( figure 2 ) . this case of anorexia nervosa illustrates the consequences of severe malnutrition on the liver , with marked elevation of liver enzymes , profound glycogen depletion , and histological evidence of autophagocytosis . although mild liver injury is not rare and is reported in up to 60% of patients with anorexia nervosa , high levels of serum transaminases are rather uncommon [ 3 , 8 ] . a median peak value of alt of 56 times normal has been reported in a recent case series . this biological alteration has been found to inversely correlate with the body mass index , suggesting that severe starvation is involved in the pathogenic mechanism of anorexia nervosa associated liver injury . surprisingly , these biological signs of acute liver injury contrast with the absence of liver cell necrosis , which we would expect with such an elevation in liver enzymes . accordingly , rautou et al . have described in the majority of their cases histological alterations including swelling of hepatocytes with cytoplasmic clarification and ceroid pigments , in the absence of inflammatory changes and fibrosis . overall , these histological findings are consistent with severe glycogen depletion as the primary cause of liver injury . a more detailed examination of liver tissue using electron microscopy brings additional information on the consequences of severe starvation . in addition to low density of glycogen particles , we observed a decreased number of mitochondria and endoplasmic reticulum together with an increase in autophagosomes , similar to the findings of a recent study . these alterations illustrate the consequences of autophagy , which is a physiological mechanism that the cell activates during episodes of stress including severe starvation . during this process , cytoplasmic components are degradated and appear as autophagosomes at electron microscopy studies , as in the present case . therefore , it is tempting to speculate that the elevated transaminases originate from the altered mitochondria . in conclusion , . it can be associated with acute liver injury that is slowly reversible with careful enteral nutrition . in this clinical situation , profound hepatic glycogen depletion in association with autophagy appears as the leading cause of liver injury .
introduction . mild elevation of transaminase may be observed in anorexia nervosa , but acute liver injury is uncommon . 
 a complex programmed cell death in response to starvation , called autophagy , has been described in experimental and human studies . 
 case presentation . 
 a 24-year - old woman suffering from anorexia nervosa was hospitalized for severe malnutrition . at admission 
 , there were biological signs of acute liver injury but no electrolytic imbalance . 
 after having ruled out the most common causes of liver injury , the patient was carefully refed . 
 as liver tests remained abnormal , liver biopsy was performed . at histology and electron microscopy , 
 numerous signs suggestive of starvation - induced hepatocyte autophagy were found . 
 discussion . 
 severe starvation can be associated with acute liver injury that is slowly reversible with careful enteral nutrition . in this clinical situation , 
 profound hepatic glycogen depletion in association with autophagy appears as the leading cause of liver injury .