Infection with hepatitis A virus (HAV) can cause severe illness in adult patients with chronic liver disease (CLD) caused by hepatitis C. In endemic areas such as South Asia, however, most adult patients already have been exposed to HAV but could still be susceptible to hepatitis E virus (HEV) infection. We document that HEV superinfection in 4 of our CLD patients caused severe liver decompensation. We then determined the seroprevalence of HAV and HEV in 233 patients with stable CLD, with the goal of defining the need for protection against these viruses in these patients. Overall, 41 ( T he hepatitis A virus (HAV) and the hepatitis E virus (HEV) are endemic in South Asia and are the most common causes of acute hepatitis in this region. 1,2 Both viruses have a number of common characteristics: they are transmitted by the fecal-oral route and generally cause an acute self-limiting illness followed by complete recovery. However, a number of clinical and epidemiologic differences exist between HAV and HEV. For example, HEV can cause a severe fulminant hepatitis in pregnant women if the infection occurs during late pregnancy, 3 whereas exposure to HAV infection during pregnancy does not impose a higher risk. 4,5 Exposure to HAV infection occurs at a very early age in endemic areas, so that by the age of 10 years almost 100% of children show evidence of exposure to HAV, as determined by a positive HAV immunoglobulin G (IgG) antibody test result. 6 This early exposure to HAV is followed by longterm, possibly lifelong, immunity to the virus. 7 On the other hand, in the same community, exposure to HEV commonly takes place during adult life. The duration of HEV immunity is unclear, but it is possibly shorter term than is HAV immunity. 8 This could theoretically lead to recurrent episodes of HEV infection in the same patient. 9 Large-scale epidemics have been described in South Asia attributable to both HAV and HEV. Epidemics caused by HEV have occurred in Kashmir and Kanpur, as well as recently in Islamabad. [10][11][12] The common features of these epidemics were an incubation period of 2 to 9 weeks, highest clinical attack rates in adults between 15 and 40 years old, and low overall mortality of between 0.5% and 4% but high mortality (15%-25%) in pregnant women.Infection with HAV has been shown to cause a severe illness in adult patients with chronic liver disease (CLD), in particular in patients with hepatitis C, in areas where HAV is not endemic. 13 Because of the increased risk of an adverse outcome and low background exposure to HAV in these areas, vaccination against HAV is now routinely

Metastatic lesions to the pancreas present as incidental, solitary mass lesions on staging or surveillance imaging. Endoscopic ultrasonography-guided fine-needle aspiration is an important tool in the characterization and further differentiation of metastatic lesions to the pancreas from primary pancreatic cancer.

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EUS-FNA is a reliable modality for further characterization of suspected lesions and for establishing a tissue diagnosis. The occurrence of complications of EUS-FNA in this setting is low. Non-functional PNET are more frequently encountered than functional PNET.

Glycogenic hepatopathy (GH) remains underrecognized in adults as most clinicians mistake it for the more common hepatic abnormality associated with uncontrolled diabetes mellitus in this age group, non-alcoholic fatty liver disease. This is also complicated by the fact that both entities are indistinguishable on liver ultrasound. We herein describe a similar predicament in which a young adult female presented with bilateral upper quadrant abdominal pain, tender hepatomegaly, lactic acidosis and a >10-fold increase in liver enzymes, which worsened after the administration of high-dose steroids. Despite intravenous normal saline resuscitation, serum transaminitis persisted in a fluctuating manner. Ultimately, a liver biopsy confirmed GH. Biochemically, GH is driven by high amounts of both circulating glucose and insulin or by the administration of high-dose steroids. Improving glycemic control is the mainstay of treatment for GH. However, in our case, improvement in glycated hemoglobin of just 0.6% was enough to achieve symptomatic relief, supporting recent claims of the involvement of other identified factors in disease development.

In the United States, the seroprevalence rate for hepatitis E virus (HEV) is ≈20%. This study examined HEV seroprevalence in persons with and without chronic liver disease. Our data indicate that HEV seropositivity is high in patients with chronic liver disease and that HEV seroprevalence increases signifi cantly with age.

Biliary tract complications are an important source of morbidity after liver transplantation, and present a challenge to all involved in their care. With increasing options for transplantation, including living donor and split liver transplants, the complexity of these problems is increasing. However, diagnosis is greatly facilitated by modern noninvasive imaging techniques. A team approach, including transplant hepatology and surgery, interventional endoscopy and interventional radiology, results in effective solutions in most cases, such that operative reintervention or retransplantation is rarely required.

Deficiency of any of the 5 enzymes in the urea cycle results in the accumulation of ammonia, leading to encephalopathy; which if untreated, can be lethal and produce devastating neurologic sequelae in long-term survivors. We hereby present an interesting case that presented with hyperammonemia and encephalopathy; later found to have an urea cycle defect.