RESUMEN
Anorexia nervosa (AN) presents with a variety of physical complications such as hypoglycemia, electrolyte abnormalities, and dehydration associated with starvation, requiring rapid weight gain through nutritional therapy. However, despite nutritional therapy, patients are at risk of many serious medical complications, including hypoglycemia, hypophosphatemia, edema, and liver damage. Starvation has been found to cause hepatocyte injury with mild-to-severe increases in liver enzyme levels, and distinguishing between autophagy and refeeding syndrome is important for treatment strategies. Herein, we report a rare case of sudden liver injury after the initiation of nutritional therapy in a patient with AN. A 35-year-old woman was admitted to our hospital for the treatment of weight loss due to AN. Nutritional therapy was initiated at 600 kcal/day and increased to 1500 kcal/day on the 21st day of admission. On the 22nd day after admission, rapid liver injury was observed, with an aspartate aminotransferase level of 141 U/L and an alanine aminotransferase level of 221 U/L. After the exclusion of refeeding syndrome, since there was no evidence of hypokalemia, hypophosphatemia, or fatty liver disease based on blood tests and abdominal echography, we diagnosed starvation-induced hepatocyte autophagy, and she was treated with the same calories. Her liver dysfunction gradually improved thereafter. This case report highlights the clinical utility of identifying the etiology of hepatic dysfunction in patients with AN. Clinicians must make appropriate decisions regarding continuing or reducing nutritional therapy based on relevant tests when patients with AN develop liver dysfunction after the initiation of nutritional therapy.
RESUMEN
BACKGROUND: Valproic acid (VPA) is a relatively safe drug widely used for the treatment of epileptic seizures and mania in bipolar disorder, as well as the prevention of migraine headaches. Here, we present a case of VPA-induced pancreatitis in a patient with vascular dementia, epileptic seizures, and psychiatric symptoms. He had no distinctive abdominal symptoms. CASE PRESENTATION: A 66-year-old Japanese man was treated with VPA for agitation and violent behavior due to vascular dementia, epileptic seizures, and psychiatric symptoms. During admission, he experienced a sudden decrease in consciousness and blood pressure. Abdominal findings were unremarkable; however, blood tests showed an inflammatory response and elevated amylase levels. Contrast-enhanced abdominal computed tomography showed diffuse pancreatic enlargement and inflammation extending to the subrenal pole. VPA-induced acute pancreatitis was diagnosed, VPA was discontinued, and high-dose infusions were administered. Acute pancreatitis resolved after treatment initiation. CONCLUSIONS: Clinicians should be aware of this relatively rare side effect of VPA. Diagnosis may be challenging in elderly people and patients with dementia as they may present with non-specific symptoms. Clinicians should consider the risk of acute pancreatitis when using VPA in patients who cannot report spontaneous symptoms. Blood amylase and other parameters should be measured accordingly.