Hepatitis E virus (HEV) is among the most common causes of acute viral hepatitis. It typically causes acute infection, but some cases of chronic infection have also been recorded. These cases were particularly seen in developed countries, in patients who were immunocompromised, organ transplant recipients, or those with underlying hematological malignancy. However, we encountered a case of hepatitis E presenting as a chronic liver disease in an immunocompetent patient from a developing country. Therefore, more underlying risk factors need to be studied, which may lead to such a rare presentation of hepatitis E.

Lipid metabolism disorders are recognized to be one of the most frequent complications of renal transplantation, while dyslipidemia and chronic kidney disease (CKD) are strong risk factors for arteriosclerotic cardiovascular disease (ASCVD). Proprotein convertase subtilisin/kexin type 9 inhibitors (PCSK9i) are novel lipid-lowering drugs, the safety and efficacy of which are yet to be confirmed in transplanted patients. There have been several small-sample studies using PCSK9i in patients after heart transplantation, while fewer cases use PCSK9i after kidney transplantation. We report a case of a renal transplant recipient complicated with hepatitis B treated with PCSK9i, which achieved a remarkable lipid-lowering efficacy, and no significant adverse effects were found during the follow-up.

Acute acalculous cholecystitis is inflammation of the gallbladder without any evidence of gallstones. Although acalculous cholecystitis is less common than its calculous counterpart, it can be fatal if not treated. It is essential to rule out the cause of acalculous cholecystitis to aid in the treatment and management of the patient. We present a case of acalculous cholecystitis wherein a comprehensive workup found the etiology to be viral. Albeit rare, hepatitis A and cytomegalovirus can be causes of acute cholecystitis. Both viruses were observed simultaneously in this patient, proving it to be a unique case. This early diagnosis allowed conservative management of the patient, sparing him from unnecessary surgical intervention.

Hepatitis A virus can cause liver damage ranging from mild illness to fulminant hepatic failure, constituting 0.35% of all cases of fulminant liver failure. While rates of spontaneous remission are higher for hepatitis A, recent outbreaks attributable to vaccine shortages in highly populated urban cities plagued by insufficient affordable housing and inaccessible sanitation, and changes in the epidemiology of viral strains have resulted in increased hospitalizations and deaths. While the prognosis for patients with FHF has improved since the introduction of transplantation, the decision to transplant is often difficult to reach. We present five patients with HAV and subsequent FHF, one of whom successfully received a liver transplant. We have reviewed all published cases of HAV FHF in the literature and report ten patients, seven of whom received liver transplantation. There are few predictive models that attempt to distinguish between fulminant hepatitis A and spontaneous recovery. Patients found to have positive hepatitis A IgM, encephalopathy, worsening LFT\'s and coagulation should be monitored closely and referred to transplant centers urgently for management.

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The following fictional case is intended as a learning tool within the Pathology Competencies for Medical Education (PCME), a set of national standards for teaching pathology. These are divided into three basic competencies: Disease Mechanisms and Processes, Organ System Pathology, and Diagnostic Medicine and Therapeutic Pathology. For additional information, and a full list of learning objectives for all three competencies, see http://journals.sagepub.com/doi/10.1177/2374289517715040.

Hepatitis E virus (HEV) typically causes an acute, self-limiting hepatitis and is among the commonest cause of such presentations. Hepatitis E viral infection is also increasingly recognized as a cause of chronic hepatitis amongst the immunocompromised, particularly amongst solid organ transplant recipients. Chronic HEV infection remains an underdiagnosed disease and chronic infection can lead to rapidly progressive liver fibrosis and cirrhosis. This review examines current understanding of the HEV. We illustrate typical clinical presentations, management strategies [(based upon guidelines from both the British Transplant Society (BTS) and European Association for the study of liver (EASL)] and outcomes of HEV infection in different cohorts of patients by highlighting select transplant and non-transplant patient cases, from one of the largest tertiary Hepatology centres in Europe.

When the evaluation of newly elevated liver enzymes is unrevealing, a common diagnosis of exclusion is drug-induced liver injury. A 39-year-old active duty service member who presented with jaundice after returning from a mission in Thailand was found to have an acute hepatitis and developing acute liver failure. He was ultimately diagnosed with acute hepatitis E, but his diagnosis was initially confounded by multiple exposures to supplements known to cause drug-induced liver injury. This case illustrates the importance of broadened serologic testing in patients with acute liver injury returning from countries endemic with hepatitis E and also highlights the challenges in diagnosis of acute hepatitis E with currently available testing.

The objective of our study was to recognize hepatitis B reactivation as a complication of rituximab chemotherapy and to realize the importance of screening for prior Hepatitis B virus (HBV) exposure in all patients with hematologic malignancies who will receive rituximab as part of their therapy. Rituximab is a monoclonal antibody targeting CD 20 receptors on the membrane of B cells. In this case report, we described a 79-year-old man who presented to our department with nausea, fatigue, and jaundice. Two months ago, he had received the last dose of the chemotherapy regimen containing rituximab for follicular B cell lymphoma. Ultrasound and computed tomography (CT) scan of abdomen did not show any focal lesions. Liver function tests showed worsening hepatic failure and viral serology demonstrated active HBV infection. Antiviral therapy with entecavir and tenofovir disoproxil fumarate failed to improve his symptoms, and he died of fulminant hepatic failure. Rituximab targets CD 20 receptors positive B cells. It can destroy both cancerous and normal B cells. A decline in immune function can activate occult HBV infection. Prior to initiation of rituximab therapy, screening should be conducted in all cases for HBV associated serological markers. Patients with active or occult HBV infection must be started on appropriate antiviral therapy to prevent any severe outcomes with rituximab-containing regimens.

Hepatitis E infection is a global disorder that causes substantial morbidity. Numerous neurologic illnesses, including Guillain-Barre syndrome (GBS), have occurred in patients with hepatitis E virus (HEV) infection.
We report a 58 year-old non-immunocompromised man who presented with progressive muscle weakness in all extremities during an episode of acute HEV infection, which was confirmed by measuring the anti-HEV IgM antibodies in the serum. Both cerebrospinal fluid examination and electrophysiological study were in agreement with the diagnosis of HEV-associated GBS. Following the treatment with intravenous immunoglobulin, the patient\'s neurological condition improved rapidly.
HEV infection should be strongly considered in patients with neurological symptoms, especially those with elevated levels of liver enzymes.