scholarly journals Acute liver injury and anorexia nervosa: a case report

2019 ◽  
Vol 13 (2) ◽  
pp. 128-131
Author(s):  
Simona Pascolini ◽  
Michele Cevolani ◽  
Federico Lari ◽  
Luigi Muratori ◽  
Marco Lenzi
Keyword(s):  
Body Weight ◽  
Anorexia Nervosa ◽  
Liver Injury ◽  
Parenteral Nutrition ◽  
Nutritional Assessment ◽  
Acute Liver Injury ◽  
Transaminase Level ◽  
Progressive Increase ◽  
Psychiatric Institute ◽  
History Of

Anorexia nervosa is an eating disorder characterized by restriction of energy intake leading to a significant decrease in body weight. While it is primarily a psychiatric disorder, numerous medical complications can occur. In this article we describe a case of a 25-year-old woman with a 12-year history of severe restrictive anorexia nervosa that was referred to the Emergency Service of our Hospital, transferred from a psychiatric institute, for severe weight loss, dehydration, and progressive increase in transaminases. During the hospital stay she developed an acute liver injury with an increase in transaminase level up to 40× the ULN. Infective and immunological causes of acute hepatitis were excluded. In the suspect of severe starvation acute liver injury, we performed a nutritional assessment and started parenteral nutrition. After 15 days of parenteral nutrition, she gained 2.5 kg of body weight and liver tests were drastically reduced and nearly normal.

scholarly journals Liver Autophagy in Anorexia Nervosa and Acute Liver Injury

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Marouane Kheloufi ◽  
Chantal M. Boulanger ◽  
François Durand ◽  
Pierre-Emmanuel Rautou
Keyword(s):  
Cell Death ◽  
Anorexia Nervosa ◽  
Liver Injury ◽  
Acute Liver Injury ◽  
Protective Mechanism ◽  
Liver Insufficiency ◽  
Electron Microscopy Analysis ◽  
Microscopy Analysis ◽  
Rescue Mechanism ◽  
Liver Cell Death

Autophagy, a lysosomal catabolic pathway for long-lived proteins and damaged organelles, is crucial for cell homeostasis, and survival under stressful conditions. During starvation, autophagy is induced in numerous organisms ranging from yeast to mammals, and promotes survival by supplying nutrients and energy. In the early neonatal period, when transplacental nutrients supply is interrupted, starvation-induced autophagy is crucial for neonates’ survival. In adult animals, autophagy provides amino acids and participates in glucose metabolism following starvation. In patients with anorexia nervosa, autophagy appears initially protective, allowing cells to copes with nutrient deprivation. However, when starvation is critically prolonged and when body mass index reaches 13 kg/m2or lower, acute liver insufficiency occurs with features of autophagic cell death, which can be observed by electron microscopy analysis of liver biopsy samples. In acetaminophen overdose, a classic cause of severe liver injury, autophagy is induced as a protective mechanism. Pharmacological enhancement of autophagy protects against acetaminophen-induced necrosis. Autophagy is also activated as a rescue mechanism in response to Efavirenz-induced mitochondrial dysfunction. However, Efavirenz overdose blocks autophagy leading to liver cell death. In conclusion, in acute liver injury, autophagy appears as a protective mechanism that can be however blocked or overwhelmed.

scholarly journals Bicalutamide-Associated Acute Liver Injury and Migratory Arthralgia: A Rare but Clinically Important Adverse Effect

2018 ◽  
Vol 12 (2) ◽  
pp. 266-270 ◽  
Author(s):  
Helga M. Gretarsdottir ◽  
Elin Bjornsdottir ◽  
Einar S. Bjornsson
Keyword(s):  
Prostate Cancer ◽  
Liver Injury ◽  
Causality Assessment ◽  
Acute Liver Injury ◽  
Assessment Method ◽  
Hepatitis Viruses ◽  
Drug Induced ◽  
History Of ◽  
Upper Abdomen ◽  
Liver Tests

We describe a case of acute liver injury and migratory arthralgia in a patient receiving bicalutamide treatment for prostate cancer. A 67-year-old male with metastatic prostate cancer presented with a 6-day history of migratory arthralgia. He had been undergoing treatment with bicalutamide for 4 months; 3 weeks prior to symptom appearance the bicalutamide dose had been increased. He had no other symptoms. Liver tests and inflammatory markers were markedly elevated. Serology for hepatitis viruses A, B, and C, CMV, and EBV and autoimmune causes were all negative, and an ultrasound of the upper abdomen was normal. There was no history of blood transfusion, intravenous drug abuse, or alcohol abuse. Due to the suspicion of a drug-induced symptomatology, bicalutamide was discontinued and the patient started on 30 mg prednisolone daily. Three weeks later he was symptom free and after 6 weeks his liver tests were almost normal. The Roussel Uclaf Causality Assessment Method (RUCAM) suggested a high probability of liver injury. Bicalutamide has very rarely been reported as a causative agent for liver injury and to our knowledge never for migratory polyarthralgia. The migratory polyarthralgia was attributed to bicalutamide due to the absence of other etiological factors and the disappearance of symptoms after discontinuation of the drug. To our knowledge, this is the first published case report of migratory arthralgia and concomitant liver injury attributed to bicalutamide.

scholarly journals Severe Starvation-Induced Hepatocyte Autophagy as a Cause of Acute Liver Injury in Anorexia Nervosa: A Case Report

2013 ◽  
Vol 2013 ◽  
pp. 1-4 ◽  
Author(s):  
S. Restellini ◽  
L. Spahr ◽  
L. Rubbia Brandt
Keyword(s):  
Anorexia Nervosa ◽  
Liver Injury ◽  
Acute Liver Injury ◽  
Clinical Situation ◽  
Severe Malnutrition ◽  
Hepatic Glycogen ◽  
Glycogen Depletion ◽  
Case Presentation ◽  
Common Causes ◽  
Liver Tests

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.

scholarly journals Diphenhydramine as a Cause of Drug-Induced Liver Injury

2017 ◽  
Vol 2017 ◽  
pp. 1-4 ◽  
Author(s):  
Yunseok Namn ◽  
Yecheskel Schneider ◽  
Isabelle H. Cui ◽  
Arun Jesudian
Keyword(s):  
Liver Injury ◽  
Acute Liver Injury ◽  
Chromosomal Translocation ◽  
Altered Mental Status ◽  
Drug Induced ◽  
Drug Induced Liver Injury ◽  
Patient Reported ◽  
History Of ◽  
Concomitant Medications ◽  
Unites States

Drug-induced liver injury (DILI) is the most common cause of acute liver failure in the Unites States and accounts for 10% of acute hepatitis cases. We report the only known case of diphenhydramine-induced acute liver injury in the absence of concomitant medications. A 28-year-old man with history of 13/14-chromosomal translocation presented with fevers, vomiting, and jaundice. Aspartate-aminotransferase and alanine-aminotransferase levels peaked above 20,000 IU/L and 5,000 IU/L, respectively. He developed coagulopathy but without altered mental status. Patient reported taking up to 400 mg diphenhydramine nightly, without concomitant acetaminophen, for insomnia. He denied taking other medications, supplements, antibiotics, and herbals. A thorough workup of liver injury ruled out viral hepatitis (including A, B, C, and E), autoimmune, toxic, ischemic, and metabolic etiologies including Wilson’s disease. A liver biopsy was consistent with DILI without evidence of iron or copper deposition. Diphenhydramine was determined to be the likely culprit. This is the first reported case of diphenhydramine-induced liver injury without concomitant use of acetaminophen.

scholarly journals Rifampicin for Treatment of Cholestatic Pruritus Caused by Drug-Induced Acute Liver Injury as Assessed by the RUCAM Classification

2020 ◽  
Vol 2020 ◽  
pp. 1-5
Author(s):  
Ali R. Ahmadi ◽  
Maria Chicco ◽  
Marcel van den Berge
Keyword(s):  
Risk Factors ◽  
Liver Injury ◽  
Laboratory Testing ◽  
Acute Liver Injury ◽  
Anabolic Steroids ◽  
Black Market ◽  
Radiographic Imaging ◽  
Drug Induced ◽  
Liver And Kidney ◽  
History Of

A male bodybuilder of 39 years of age developed severe pruritus, nausea, and jaundice after injecting anabolic steroids purchased on the black market. The patient had no history of liver disease and no risk factors for viral hepatitis. Extensive laboratory testing, radiographic imaging, and liver biopsy excluded a majority of potential pathologies. The patient was diagnosed with drug-induced acute liver injury and secondary acute renal failure most likely caused by testosterone purchased on the black market. The pruritus caused insomnia and significant psychological distress. Treatment was initiated with cholestyramine and naltrexone for one week with no effect on the pruritus. Subsequently, all medications were stopped, and rifampicin was started. Pruritus resolved after starting rifampicin, and liver and kidney function improved rapidly and normalized within 5 months.

scholarly journals The Natural History of Severe Acute Liver Injury

2017 ◽  
Vol 112 (9) ◽  
pp. 1389-1396 ◽  
Author(s):  
David G Koch ◽  
J L Speiser ◽  
V Durkalski ◽  
R J Fontana ◽  
T Davern ◽  
...  
Keyword(s):  
Liver Injury ◽  
Natural History ◽  
Acute Liver Injury ◽  
History Of

Preventive Effect of Dai-saiko-to (Da-Chai-Hu-Tang) Extract on Disrupted Hepatic Active Oxygen Metabolism in Rats with Carbon Tetrachloride-induced Liver Injury

1995 ◽  
Vol 23 (01) ◽  
pp. 53-64 ◽  
Author(s):  
Yoshiji Ohta ◽  
Emi Sasaki ◽  
Keiji Nishida ◽  
Takashi Kobayashi ◽  
Minoru Nagata ◽  
...  
Keyword(s):  
Body Weight ◽  
Carbon Tetrachloride ◽  
Liver Injury ◽  
Acute Liver Injury ◽  
Cell Damage ◽  
Liver Lipid ◽  
Lipid Peroxide ◽  
Oxygen Metabolism ◽  
Active Oxygen ◽  
Active Oxygen Metabolism

In order to clarify the preventive action of Dai-Saiko-to (Da-Chai-Hu-Tang) extract (TJ-8) on the progression of acute liver injury in rats intoxicated with carbon tetrachloride ( CCl 4), we examined the effect of post-oral TJ-8 administration on hepatic active oxygen metabolism following the progression of this liver damage. When TJ-8 (1.0 g/kg body weight) was administered orally to male Wistar rats aged five weeks 2 hrs after i.p. injection of CCl 4 (1.0 ml/kg body weight), an apparent liver injury occurred. Significant prevention against the progression of liver injury was found at 24 hrs after injection, judging from the activities of serum transaminases, indexes of liver cell damage. Liver cytosolic superoxide dismutase (SOD) activity decreased 2 and 24 hrs after CCl 4 injection, while liver cytosolic catalase and glutathione reductase (GSSG-R) activities decreased 24 hrs after the injection. At 2 and 24 hrs after CCl 4 treatment, liver cytosolic Se-containing glutathione peroxidase (GSH-px) activity did not change and liver cytosolic glucose-6-phosphate dehydrogenase (G-6-PDH) activity increased. Post-oral TJ-8 administration significantly ameliorated decreases in liver SOD, catalase, and GSSG-R activities at 24 hrs after CCl 4 injection, but did not affect liver Se-GSH-px and increased liver G-6-PDH activities at 24 hrs after the injection. Although increased liver lipid peroxide level and decreased liver reduced glutathione and ascorbic acid levels were observed 2 and 24 hrs after CCl 4 injection, post-oral TJ-8 administration significantly prevented these changes found at 24 hrs after injection. These results indicate that post-oral TJ-8 administration can prevent the progression of acute liver injury in CCl 4-injected rats by inhibiting enhanced lipid peroxidation and by improving disrupted active oxygen metabolism in the injured liver.

scholarly journals Adderall Induced Acute Liver Injury: A Rare Case and Review of the Literature

2013 ◽  
Vol 2013 ◽  
pp. 1-3 ◽  
Author(s):  
Rohini R. Vanga ◽  
Bikram Bal ◽  
Kevin W. Olden
Keyword(s):  
Liver Injury ◽  
Rare Case ◽  
Acute Liver Injury ◽  
Past History ◽  
English Literature ◽  
Review Of The Literature ◽  
Intensive Monitoring ◽  
Hyperactivity Disorder ◽  
History Of ◽  
Time Of Presentation

Adderall (dextroamphetamine/amphetamine) is a widely prescribed medicine for the treatment of attention-deficit/hyperactivity disorder (ADHD) and is considered safe with due precautions. Use of prescribed Adderall without intention to overdose as a cause of acute liver injury is extremely rare, and to our knowledge no cases have been reported in the English literature. Amphetamine is an ingredient of recreational drugs such as Ecstacy and is known to cause hepatotoxicity. We describe here the case of a 55-year-old woman who developed acute liver failure during the treatment of ADHD with Adderall. She presented to the emergency room with worsening abdominal pain, malaise, and jaundice requiring hospitalization. She had a past history of partial hepatic resection secondary to metastasis from colon cancer which was under remission at the time of presentation. She recovered after intensive monitoring and conservative management. Adderall should be used carefully in individuals with underlying liver conditions.

Anamnestic similarities in bulimic inpatients with and without a history of anorexia nervosa

1989 ◽  
Vol 4 (2) ◽  
pp. 107-110
Author(s):  
S. Bossert ◽  
R. Laessle ◽  
M. Junker
Keyword(s):  
Body Weight ◽  
Anorexia Nervosa ◽  
Treatment Outcome ◽  
Family History ◽  
Retrospective Analysis ◽  
Medical Records ◽  
Diagnosis And Treatment ◽  
Lower Body ◽  
Lower Body Weight ◽  
History Of

SummaryThe significance of a history of anorexia nervosa as regards the diagnosis and treatment outcome for bulimia is unclear. In a retrospective analysis of medical records of 59 inpatients with bulimia (DSM-III), variables related to personal and psychiatric family history did not reveal any differences in bulimics subtyped according to previous anorexia nervosa as defined in the criteria of Russell (1979). These anamnestic data support the results of studies indicating that no specific clinical and outcome variables are correlated with a history of anorexia nervosa in bulimia. The lower body weight and longer duration of bulimia found in bulimic inpatients with a history of anorexia nervosa, however, should be further examined.

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