More Than a Rash: Recurrent Hepatocellular Carcinoma After Liver Transplantation.

Recurrent hepatocellular carcinoma (HCC) after liver transplant is uncommon in patients who have favorable pretransplant characteristics. We present a 56-year-old man with a history of liver transplant 8 weeks prior for hepatitis C cirrhosis and HCC who presented for shortness of breath. He was found to have a microangiopathic hemolytic anemia and an erythematous, nodular skin rash on his left lower abdomen. Biopsy of the skin rash would demonstrate metastatic HCC, determined to be the cause of hemolysis as well. Recurrent malignancy should be considered in patients with a history of HCC who present with new, unexplained skin nodules.

Drug-induced liver injury.

PURPOSE OF REVIEW: Drug-induced liver injury (DILI) remains an important disease in clinical practice. It is difficult to predict, diagnose and manage. Studies in the peer-reviewed literature in the last 2 years, focusing on the diagnosis, prediction and management of DILI will be reviewed. RECENT FINDINGS: Antibiotics remain the most common drug causing DILI in the United States and Europe. Expert opinion may still be the better method of diagnosing DILI compared with an objective tool such as the Roussel-Uclaf Causality Assessment Method. Hepatitis E represents an alternative diagnosis to some cases of presumed drug hepatotoxicity. There is ongoing research into the genetics of the pathophysiology and susceptibility of DILI. A genome-wide association study confirmed the association between human leukocyte antigen (HLA) class II and susceptibility to coamoxiclav (amoxicillin-clavulanic acid) induced DILI. There is new information on the protective effect of HLA-DRB1*07 family of alleles. MicroRNAs are a potential marker of DILI. Keratin variants may predict outcome of acute liver failure. N-acetylcysteine may be protective against DILI while taking antituberculosis medication. SUMMARY: Recent findings in the genetics of pathophysiology and susceptibility of DILI can help with predicting and avoiding DILI in clinical practice and provide the foundation for ongoing research.

Nonalcoholic fatty liver disease.

Nonalcoholic fatty liver disease is a clinicopathologic syndrome that encompasses several clinical entities. The spectrum of conditions ranges from simple steatosis to steatohepatitis, fibrosis and end stage liver disease. The condition was originally described in obese, diabetic, middle-aged females without a history of significant alcohol use with liver histology consistent with alcoholic hepatitis. It is known that this entity occurs without any particular sex predilection, in lean individuals, as well as an increasing number of obese children. Other terms have been used to describe this clinical entity such as alcohol-like hepatitis, pseudo-alcoholic hepatitis, diabetic hepatitis and steatonecrosis. Ludwig and colleagues introduced the term nonalcoholic steatohepatitis (NASH) to describe patients fitting the picture of alcoholic hepatitis but without a history of significant alcohol abuse. The term nonalcoholic fatty liver disease (NAFLD) is used more frequently to include the spectrum of conditions that range from steatosis through steatohepatitis, fibrosis and cirrhosis. NASH is reserved for patients with steatohepatitis and fibrosis. NAFLD is now being recognized as the most common cause of elevated liver enzymes in the United States. Although the exact etiology of NAFLD is not known, it may be caused by insulin resistance coupled with increased oxidative stress to the hepatocytes. No specific therapy has been approved for this condition and the mainstay of management is weight loss.