Androgens have long been recognized as oncogenic agents. They can induce both benign and malignant hepatocellular neoplasms, including hepatocellular adenoma (HCA) and hepatocellular carcinoma, though the underlying mechanisms remain unclear. Androgen-induced liver tumors are most often solitary and clinically silent. Herein, we reported an androgen-induced HCA complicated by spontaneous rupture. The patient was a 24-year-old male presenting with fatigue, diminished libido, radiology-diagnosed hepatocellular adenomatosis for 3 years, and sudden-onset, severe, sharp, constant abdominal pain for one day. He used Aveed (testosterone undecanoate injection) from age 17 and completely stopped one year before his presentation. A physical exam showed touch pain and voluntary guarding in the right upper quadrant of the abdomen. An abdominal CT angiogram demonstrated multiple probable HCAs, with active hemorrhage of the largest one (6.6 × 6.2 × 5.1 cm) accompanied by large-volume hemoperitoneum. After being stabilized by a massive transfusion protocol and interventional embolization, he underwent a percutaneous liver core biopsy. The biopsy specimen displayed atypical hepatocytes forming dense cords and pseudoglands. The lesional cells diffusely stained β-catenin in nuclei and glutamine synthetase in cytoplasm. Compared to normal hepatocytes from control tissue, the tumor cells were positive for nuclear AR (androgen receptor) expression but had no increased EZH2 (Enhancer of Zeste 2 Polycomb Repressive Complex 2 Subunit) protein expression. The case indicated that androgen-induced hepatocellular neoplasms should be included in the differential diagnosis of acute abdomen.

Nucleoside or nucleotide analogues (NAs) have the potential to cause lactic acidosis by inhibiting DNA polymerase-γ of human mitochondria and impairing aerobic metabolism. Patients may be asymptomatic, have mild non-specific symptoms, or present in multisystem organ failure. There is a paucity of data to guide management of life-threatening lactic acidosis due to NA therapy. Here we describe a case of a 60-year old critically ill male with decompensated cirrhosis secondary to hepatitis B virus (HBV) infection who developed severe lactic acidosis (13.8 mmol/L) 2 days after initiation of tenofovir alafenamide (TAF). All other possible etiologies for the elevated lactate were ruled out. Lactic acidosis resolved rapidly with TAF discontinuation and supplementation with cofactors supporting mitochondrial oxidative phosphorylation, including coenzyme Q10, levocarnitine, riboflavin, and thiamine. This case highlights the ability of TAF to cause lactic acidosis early after therapy initiation, especially in susceptible hosts, and reviews the potential role for cofactor supplementation for drug-induced mitochondrial injury.

Introduction: Pregnant patients with antiphospholipid syndrome (APLS) are at risk for thromboembolic complications. They are more likely to present with hemolysis, elevated liver enzymes, low platelets (HELLP) syndrome. Hepatic infarction is a rare complication which can lead to hepatic rupture, fulminant liver failure and death. We present a case of a pregnant patient with known history of APS who presented with HELLP and a large liver infarction despite treatment with anticoagulation. Case Description/Methods: A 36-year-old pregnant female with history of pulmonary embolism, prothrombin gene mutation and APLS, presented to an outside hospital with right upper quadrant pain. Labs showed AST 255, ALT 274 and platelets 116. Labs also showed evidence of hemolytic anemia. Her medications included enoxaparin and aspirin. Due to concern for HELLP syndrome she underwent an emergent cesarean section. Post-delivery her labs worsened with AST 2712, ALT 2783, and platelets 43. Abdominal CT showed a large ill-defined hypodensity within segment 3 of the liver concerning for hepatic infarcts. She was treated with plasmapheresis and methylprednisolone. Given concern for impending acute liver failure she was transferred to a liver transplant center. After transfer, MRI abdomen confirmed a large infarction of the liver which involved the entirety of segments 6 and 7, as well as adjacent portions of segments 5 and 8 (Figure 1). The hepatic and portal veins appeared normal. She was observed in the ICU and over several days her abdominal pain and labs improved, with repeat showing AST 577, ALT 975 and platelets 51. Additional workup including viral hepatitis panels were normal. She was continued on enoxaparin and transitioned to warfarin for long term anticoagulation. Her hepatic panel 1 month later showed AST 39, ALT 29. Discussion: Hepatic infarction is a rare complication of APS due to the dual blood supply of the liver. 93% of reported cases of hepatic infarction in pregnant women with APS were associated with HELLP syndrome. Even when patients are on anticoagulation it is important to consider hepatic infarction as a complication in patients with APS and HELLP who presents with abdominal pain, worsening lab values and hepatic failure. Multidisciplinary care with maternal-fetal medicine, hematology, and hepatology, and transfer to a transplant center should be considered given the high morbidity associated with this condition.Figure 1.: Venous phase MRI with contrast showing large infarct in the liver.

Introduction: After clot formation, the fibrinolytic system is essential to restore normal blood flow through vessels. Hyperfibrinolysis can result in abnormal fibrin breakdown and lead to bleeding complications. We present a case of a patient with cirrhosis who developed hemorrhagic shock secondary to a large spontaneous retroperitoneal (RP) bleed, which was due to a hyperfibrinolytic state. This is a known complication of end stage liver disease, difficult to diagnose by standard coagulation testing. Here, the diagnosis was made using thromboelastogram (TEG) testing. Case Description/Methods: A 76-year-old male with history of decompensated cirrhosis was admitted for weakness and altered mental status. Initial labs were notable for hemoglobin 7.9, platelet count 129, international normalized ratio (INR) 2.1, and creatinine 1.76. One week later he had an acute drop in his hemoglobin from 8.0 to 5.3 without overt bleeding. He was lethargic and hypotensive, necessitating transfer to the intensive care unit and intubation for airway protection. Upper endoscopy showed portal hypertensive gastropathy but no active bleeding. Computed tomography (CT) of the abdomen and pelvis revealed a large retroperitoneal hematoma which measured 10.1 by 12.4 by 17.3 cm with foci of active bleeding (Figure 1). He had no history of recent trauma. Additional labs revealed platelets of 126, INR of 1.7, and fibrinogen level of 112. A TEG showed decreased alpha angle and increased fibrinolytic index percentage which indicated decreased clot formation and hyperfibrinolysis. He was treated with tranexamic acid as part of his resuscitation. No active extravasation was noted in the hematoma during angiogram. His blood count and blood pressure stabilized, and no further transfusions were required. Discussion: Patients with cirrhosis are at risk of hypocoagulation or hypercoagulation but traditional coagulation tests, such as INR, do not predict bleeding risk in these patients. One mechanism of increased bleeding is hyperfibrinolysis, a complication of the cirrhotic coagulopathy which cannot be diagnosed with standard labs. Alternative testing such as TEG is being studied in the context of patients with cirrhosis, which has the potential to help guide diagnosis and clinical decision making and prevent unnecessary transfusion. Here, TEG assisted in the diagnosis and correct management of hyperfibrinolysis because it allowed for real time measure of clot dissolution.Figure 1.: CT Abdomen and Pelvis image depicting retroperitoneal hematoma circled in white.

In cirrhotic patients, hepatic encephalopathy after transjugular intrahepatic portosystemic shunt (post‐TIPS HE) is common. Measures that reduce the severity of post‐TIPS HE are limited. Though recent data suggest an association between PPI use and HE, the risk in post‐TIPS HE is not well understood.

INTRODUCTION: Coronavirus disease 2019 (COVID-19), caused by severe acute respiratory syndrome coronavirus 2 virus, is a predominantly respiratory tract infection with the capacity to affect multiple organ systems. Abnormal liver tests, mainly transaminase elevations, have been reported in hospitalized patients. We describe a syndrome of cholangiopathy in patients recovering from severe COVID-19 characterized by marked elevation in serum alkaline phosphatase (ALP) accompanied by evidence of bile duct injury on imaging. METHODS: We conducted a retrospective study of COVID-19 patients admitted to our institution from March 1, 2020, to August 15, 2020, on whom the hepatology service was consulted for abnormal liver tests. Bile duct injury was identified by abnormal liver tests with serum ALP > 3x upper limit of normal and abnormal findings on magnetic resonance cholangiopacreatography. Clinical, laboratory, radiological, and histological findings were recorded in a Research Electronic Data Capture database. RESULTS: Twelve patients were identified, 11 men and 1 woman, with a mean age of 58 years. Mean time from COVID-19 diagnosis to diagnosis of cholangiopathy was 118 days. Peak median serum alanine aminotransferase was 661 U/L and peak median serum ALP was 1855 U/L. Marked elevations of erythrocyte sedimentation rate, C-reactive protein, and D-dimers were common. Magnetic resonance cholangiopacreatography findings included beading of intrahepatic ducts (11/12, 92%), bile duct wall thickening with enhancement (7/12, 58%), and peribiliary diffusion high signal (10/12, 83%). Liver biopsy in 4 patients showed acute and/or chronic large duct obstruction without clear bile duct loss. Progressive biliary tract damage has been demonstrated radiographically. Five patients were referred for consideration of liver transplantation after experiencing persistent jaundice, hepatic insufficiency, and/or recurrent bacterial cholangitis. One patient underwent successful living donor liver transplantation. DISCUSSION: Cholangiopathy is a late complication of severe COVID-19 with the potential for progressive biliary injury and liver failure. Further studies are required to understand pathogenesis, natural history, and therapeutic interventions.

INTRODUCTION: Variceal hemorrhage represents a major life threatening event in patients with decompensated cirrhosis. In comparison to esophageal varices, gastric variceal hemorrhage has a worse prognosis with higher rates of morbidity, mortality, and rebleeding. Gastric varices (GV) are currently classified based on anatomical location, but this approach fails to distinguish between different vascular compensatory mechanisms that develop in portal hypertension. Unlike esophageal variceal bleeds where endoscopic management is largely successful, endovascular approaches including transjugular intrahepatic portosystemic shunt (TIPS) and balloon-occluded retrograde transvenous obliteration (BRTO) play a more crucial role. We performed a retrospective review of patients with GV hemorrhage with and without splenorenal shunt (SRS) who underwent TIPS or BRTO to document outcomes that would help further our understanding of this disease process. METHODS: A retrospective chart review of patients at NYU Langone Health with ICD-9/10 codes for GV was performed. We extracted data for the presence of GV on endoscopy (i.e. Sarin Classification) and radiographic findings from contrast-enhanced imaging to determine the presence or absence of vascular shunt. Analysis was performed on patients with GV hemorrhage who underwent either TIPS or BRTO. RESULTS: Thirteen patients with GV bleeds were included in our analysis; 5 with SRS and 8 without SRS shunt. We found that hepatic encephalopathy, as well as 30-day and 1-year readmissions were higher in the TIPS group, compared with patients who underwent BRTO (Table 1). Average MELD-Na score and platelets after a GV bleed trended toward improvement in patients with SRS who underwent either BRTO or TIPS (Table 2, P > 0.05) after an average of 47 days. This trend was not seen in patients without SRS. CONCLUSION: Our data suggest that patients who presented with GV hemorrhage with underlying SRS trended toward improved hepatic function (based on MELD-Na and platelets) 2 weeks after intervention compared to patients without SRS. We propose that mapping of gastrointestinal vasculature early in the course of GV hemorrhage has a role in determining prognosis and treatment. In the presence of a splenorenal shunt, BRTO should be highly considered if technically feasible irrespective of Sarin classification. Further understanding of the vascular anatomy and pathogenesis of shunt formation may assist in future management of GV hemorrhage.Table 1Table 2

Hepatitis E virus (HEV), of the family Herpesviridae, is a virus that infects nearly 20 million people per year throughout the world. HEV is most commonly transmitted via the fecal-oral route and has long been described as a virus that afflicts only those in resource-poor countries. However, HEV has been detected in numerous animal carriers, various food sources, and even in human blood products in resource-rich regions of the world. HEV is of importance in the transplant patient population because of its ability to cause chronic viral infection in these patients can lead to graft loss and cirrhosis. In this review, we discuss the current knowledge of HEV as it pertains to the liver transplant patient population and discuss diagnosis and treatment of this infection.

Although hepatitis B virus (HBV) reactivation has been reported in hepatitis C patients who received interferon therapy, rare cases of HBV reactivation occur in the context of direct-acting antiviral (DAA) agent therapy for treatment of hepatitis C virus (HCV) infection. Recent studies observed that the reactivations were predominantly in hepatitis B surface antigen (HBsAg) positive patients, but reactivation can rarely occur in patients who are HBsAg negative and hepatitis B core antibody (HBcAb) positive. The severity of an HBV flare varies. In some cases, severe liver injury or fulminant hepatic failure may occur. HBV reactivation may occur regardless of HCV genotype and type of DAA regimens. The onset of HBV reactivation can range from 4 to 48 weeks after initiating DAA therapy. These patients may have undetectable levels of HBV deoxyribonucleic acid (DNA) prior to DAA treatment. Pre-emptive antiviral therapy for HBV should be considered in HBsAg-positive patients with high levels of viremia who are not receiving HBV treatment. If HBV DNA viral load is less than the guideline criteria for HBV treatment, one should consider pre-emptive HBV antiviral versus HBV DNA monitoring during DAA therapy. For patients who are HBsAg negative but HBcAb positive, close monitoring of serum alanine aminotransferase (ALT) levels during/post-treatment is highly recommended. The current review summarizes the recommendations of different society guidelines and discusses the appropriate management strategies in various patient profiles.

Linked Content This article is linked to Robles‐Diaz et al paper. To view this article, visit https://doi.org/10.1111/apt.15211 .

Spontaneous Intrahepatic Portosystemic shunts are rare in their own. Formation of a thrombus within the shunt is even rarer. To our knowledge this is the first case reported of a spontaneous intrahepatic portosystemic shunt thrombosis causing pulmonary embolism after partial dislodgement. A 65 year old cirrhotic female due to non alcoholic steatohepatitis with a large porto-systemic varix (shunt) from the posterior branch of the right portal vein to the right hepatic vein with non-occlusive thrombus within the varix presented to the emergency department with shortness of breath for 1 day. Exam remarkable for tachypnea and tachycardia with normal oxygen saturation. Labs were unremarkable. Chest x-ray showed stable moderate size hepatic hydrothorax. CT angiography showed filling defect within the left lower lobe sub-segmental branch consistent with pulmonary embolism. MRI abdomen showed prior non occlusive thrombus had embolized. She was started on anticoagulation with resolution of her symptoms. The plan was to close the veno -venous shunt by embolization at the time of her initial diagnosis since she suffered from hepatic encephalopathy. However her symptoms were controlled with vegan diet along with Lactulose and Rifaxamin. She is listed for liver transplant with plan to embolize the shunt given the risk of pulmonary embolism and create a trans jugular intrahepatic portosystemic shunt (TIPS) to reduce portal hypertension.2352_A Figure 1. A large intrahepatic veno-veno varix (shunt) connecting the right main portal vein to the hypertrophied right hepatic vein. There is filling defect which represents a non-occlusive thrombus within the varix (arrow). Cross sectional viewCirrhosis creates a prothrombotic state. The incidence of deep vein thrombosis in patients with cirrhosis supports this evidence. Pulmonary emboli usually arise from thrombi that originate in the deep venous system of the lower extremities, however, they rarely also originate in the pelvic, upper extremities etc. Spontaneous portosystemic shunts are rare malformations of the vessels supplying the liver usually found in cirrhotic patients with portal hypertension. It seems clear that in this case the thrombus developed in situ in the veno-venous shunt most likely due to low flow within the shunt and hypercoaguable state from cirrhosis. Many vascular shunts that occur in cirrhosis with portal hypertension that shunt blood away from the liver causing hepatic encephalopathy. This case raises the question of whether even patients with well controlled hepatic encephalopathy with spontaneous intrahepatic portosystemic shunts should undergo a closure procedure due to the risk of thromboembolism, which can potentially be life threatening.2352_B Figure 2. A large intrahepatic veno-veno varix (shunt) connecting the right main portal vein to the hypertrophied right hepatic vein. There is filling defect which represents a non-occlusive thrombus within the varix (arrow). Coronal View

Direct intrahepatic portocaval shunt (DIPS) is a procedure involving intravascular stent placement through the caudate lobe of the liver for management of portal hypertension. It is employed less frequently than TIPS, and extrinsic biliary compression due to DIPS has never been described in the literature. A 65 year old female with history of non-cirrhotic fibropolycystic liver disease and PVT with cavernoma and sinistral portal hypertension underwent DIPS and ileal variceal embolization for massive ileal variceal bleeding. TIPS was attempted but unsuccessful, so DIPS was subsequently performed. Pre-procedural alkaline phosphatase (AP) was 56U/L, total bilirubin (TB) 1.1mg/dL, and direct bilirubin (DB) was 0.4mg/dL. Post-procedurally she was noted to have AP 326U/L, TB 9.8mg/dL, and DB 6.9mg/dL. There was report of dark stools, with initial concern of hemobilia versus bilhemia. Imaging revealed stable mild intrahepatic and common bile duct (CBD) dilatation. Given new fevers and possible enhancement of CBD, she was treated with piperacillin-tazobactam for presumed cholangitis with subsequent improvement and was discharged home. She returned ten days later with alkaline phosphatase of 2,925U/L with total bilirubin of 41.9mg/dL and direct bilirubin of 29.8mg/dL. MRI revealed intra- and extra-hepatic biliary dilatation to the mid-CBD felt to be due to extrinsic compression by the crossing DIPS. ERCP revealed CBD stenosis which did not appear to be related to crossing DIPS but was stented. Afterwards, her AP peaked at 3,062U/L with TB 56.9mg/dL and DB 38.1mg/dL. Liver biopsy revealed bland cholestasis. Her liver chemistries started to improve. Due to persistent fevers, ERCP was repeated for stent exchange and revealed sigmoid-shaped stenosis in the upper CBD due to extrinsic compression from the crossing DIPS, thus revealing the ultimate diagnosis. Stent was replaced and AP subsequently improved to 104U/L with TB 1.4mg/dL.The differential of hyperbilirubinemia after DIPS procedure includes hemolysis (typically presents with indirect hyperbilirubinemia), as well as hepatic decompensation (increase in all liver chemistries), bilhemia from biliary-venous fistula (isolated hyperbilirubinemia), infection (often a mixed picture), and biliary compression (cholestatic picture). This complicated case illustrates the difficulty in diagnosis of extrinsic biliary compression in a patient with known mild biliary dilation, requiring a second ERCP to make the final diagnosis.2187_A Figure 1. MRCP image of the 1.9 cm segmental narrowing of the mid common bile duct, thought to be related to the crossing DIPS.2187_B Figure 2. MRCP image of 1.9cm segmental narrowing of CBD secondary to extrinsic compression by the crossing TIPS

Spontaneous bacterial peritonitis (SBP) is a potentially life-threatening complication of ascites diagnosed by paracentesis. We determined predictors of SBP to facilitate patient selection. The 301 paracenteses performed in 119 patients (51 women, 68 men) from July to November 2015 were retrospectively reviewed. Presentation, lab data, depth of the deepest ascites pocket on ultrasound, total volume of ascites removed, absolute neutrophil count, and complications were studied. Of 301 paracenteses, 16 (5%) diagnosed SBP. On univariate analysis, SBP was associated negatively with history of cirrhosis and positively with history of cancer, abdominal pain, greater depth of the fluid pocket, prior SBP, and leukocytosis. Multivariate analysis using these variables to predict SBP was significant (P < 0.0001); only depth of the largest fluid pocket (P = 0.008) and complaint of abdominal pain (P = 0.006) were independent predictors. Receiver-operator curve analysis showed that a 5-cm cutoff of pocket depth yielded 100% sensitivity and 32% specificity. Two (0.1%) hemorrhagic complications occurred, one causing death and one necessitating laparotomy. In conclusion, deeper ascites pockets and abdominal pain are independent predictors of SBP. When the largest ascites pocket is <5 cm, the probability of SBP is nearly negligible. Given the potential for hemorrhagic complications, findings may help triage patients for paracentesis.

Hereditary hemochromatosis (HH) is an autosomal recessive disease caused by mutations of HFE gene that increases iron absorption in the intestine. It is commonly found in Caucasians. Men have 24 times higher rate of iron overload compared to women. 85-90% of patients with homozygous HFE gene mutation C282Y will be affected. 10% of them will develop clinical symptoms or end organ damage like cirrhosis of liver. Role of heterozygous C282Y or H63D mutations in the development of cirrhosis is still questionable. Alpha 1-Antitrypsin (AAT) deficiency is usually characterized by impaired secretion of α-1 AT from liver cells.This disorder is usually inherited as autosomal co-dominant. AAT deficiency usually is associated with Pi ZZ, Pi SZ, or Pi Null haplotypes and can progress to liver cirrhosis. On the contrary, Pi MZ which is considered the most common heterozygous type often does not lead to liver disease. We are reporting a rare case of both heterozygous HH and AAT deficiency that developed cirrhosis requiring liver transplant. 57 yr old white male who received a liver transplant for end stage liver disease with complications of cirrhosis. Both his father and grandmother had liver disease. Patient was found to have elevated liver enzymes at age 17 during routine physical exam. Lab exam showed elevated iron saturation (83%) and elevated Ferritin (1061) with low α-1 AT. Genetic testing showed HFE heterozygous for C282Y wild type and heterozygous for alpha 1 antitrypsin deficiency MZ phenotype. MRI showed cirrhosis with evidence of portal hypertension. Liver biopsy showed cirrhotic liver with grade 2/4 intra hepatocyte iron deposition. Immunohistochemical stain and PAS- D stains were positive with presence of α-1 AT globule. As Ferritin level continued to rise, patient underwent multiple sessions of phlebotomy. In matter of few years he developed intractable ascites, hepatic encephalopathy, and hepatic hydrothorax. Transjugular intrahepatic portosystemic shunt was not performed due to high MELD score. After thorough workup patient underwent a successful orthotopic liver transplant. Conflicting evidence on the association of the two disorders and on the severity of the condition in patients in whom these disorders coexist have rised from reviewing small numbers of patients. Our case is the first reported case of cirrhosis developed from heterozygous HH C282Y wild type and heterozygous AAT deficiency Pi MZ type which required liver transplant.Figure: Hepatocellular siderosis (Iron stain).Figure: Alpha-1-antitrypsin globules within hepatocytes (Immunostain).Figure: Alpha-1-antitrypsin globules within hepatocytes (PASD stain).

Thrombocytopenia is the most common hematological abnormality encountered in patients with chronic liver disease (CLD). In addition to being an indicator of advanced disease and poor prognosis, it frequently prevents crucial interventions. Historically, thrombocytopenia has been attributed to hypersplenism, which is the increased pooling of platelets in a spleen enlarged by congestive splenomegaly secondary to portal hypertension. Over the past decade, however, there have been significant advances in the understanding of thrombopoiesis, which, in turn, has led to an improved understanding of thrombocytopenia in cirrhosis. Multiple factors contribute to the development of thrombocytopenia and these can broadly be divided into those that cause decreased production, splenic sequestration, and increased destruction. Depressed thrombopoietin levels in CLD, together with direct bone marrow suppression, result in a reduced rate of platelet production. Thrombopoietin regulates both platelet production and maturation and is impaired in CLD. Bone marrow suppression can be caused by viruses, alcohol, iron overload, and medications. Splenic sequestration results from hypersplenism. The increased rate of platelet destruction in cirrhosis also occurs through a number of pathways: increased shear stress, increased fibrinolysis, bacterial translocation, and infection result in an increased rate of platelet aggregation, while autoimmune disease and raised titers of antiplatelet immunoglobulin result in the immunologic destruction of platelets. An in-depth understanding of the complex pathophysiology of the thrombocytopenia of CLD is crucial when considering treatment strategies. This review outlines the recent advances in our understanding of thrombocytopenia in cirrhosis and CLD.

Disseminated varicella infection in immunocompetent patients is extremely rare. Here, we present a previously healthy man, who developed varicella hepatitis after a short course of steroid therapy. A 44-year-old man with no medical history presented with four days of malaise, rhinorrhea, and diarrhea followed by epigastric and RUQ pain, anorexia, chills, fever, nausea, and vomiting. These symptoms developed shortly after finishing a 10-day dose pack of methylprednisolone for musculoskeletal pain. His two year old son and wife had a viral upper respiratory infection during the preceding week, neither with abdominal symptoms, and both recovered fully. On presentation, patient was afebrile and with normal vital signs. His exam was notable for RUQ tenderness, abdominal guarding, and positive Murphy's sign. Skin exam revealed a new non pruritic papular vesicular rash on the forehead, neck, trunk, and soft palate in a non-dermatomal pattern, which he reported started on the face and neck, then spread in centripetal fashion. These appeared as “dew drops” on an erythematous base. Patient denied history of VZV infection or vaccination, but his son had received the vaccine three weeks prior. Initial studies showed normal leukocyte count, elevated AST and ALT at 363/542, and lactate of 1.9. RUQ ultrasound and CT of the abdomen were unremarkable. Patient's transaminases trended up to a peak of AST/ALT 1836/2044 and bilirubin 4.2. Laboratory studies for viral hepatitides were negative. Due to high suspicion for primary VZV, he was started on intravenous acyclovir empirically. Cell culture and PCR from vesicular fluid and skin biopsy confirmed the diagnosis of varicella. The patient was switched from IV acyclovir to valacyclovir oral tablets and discharged home after all lesions crusted over on hospital day 10. In summary, we presented a case of a previously immunocompetent healthy man, who suffered severe varicella hepatitis after completing a short course of high dose steroids in the setting of a household member's recent vaccination for varicella. Despite being a live vaccine, the varicella vaccine is not typically thought to be virulent enough to cause an active infection, let alone hepatitis. Our case is the first case of primary VZV infection complicated by hepatitis, in an otherwise healthy patient without direct exposure to the virus. These two relative common occurrences can create a synergistic effect to lead to a unique presentation of a rare disease.

Drug or Toxin induced liver injury can present as hepatocellular and/or cholestatic hepatitis and the course of the disease can be from acute liver injury to fulminant liver failure resulting in death or required orthotopic liver transplantation. We present a case of acute subfulminant liver injury from ingestion of Ackee fruit which is a member of the Sapindaceae and it is a native fruit to Jamaica and some parts of West Africa. 42-year-old Jamaican woman with postpartum hypertension had undergone an unremarkable pregnancy and delivery 5 months prior. She presented with dark urine, jaundice, malaise for 2 weeks and one episode vomiting on the day of admission. She was afebrile. She was taking Enalapril 2.5mg daily and labetatol 100mg TID. No history of alcohol, Tylenol or liver disease. Labs revealed AST/ALT 1239/1551 U/L and bilirubin 11.3 mg/dl. Extensive serologic workup was negative for viral, metabolic and autoimmune with exception for positive antibody to mitochondria. Imagings ruled out common bile duct obstruction and ascites. Liver biopsy showed subfulminant hepatitis with lobular, interface and piecemeal necrosis. Amlodipine 5mg was started for hypertension on discharge. At 2 week follow up, her bilirubin increased to 20.1 and AST/ALT 1148/869. Vitals remained stable with no confusion. Obtaining detailed history, it was found that she had eaten Ackee fruit which had been brought by her relatives from Jamaica two weeks before her initial admission. She continued to have Ackee dish even after the first hospital discharge. Repeat liver biopsy showed mild steatosis, bridging and centrilobular necrosis with rare eosinophils(Fig 1). She was instructed to avoid Ackee on discharge and her results became normal after 3 months.Figure 1The toxicity of Ackee is hypoglycin A and B. Hypoglycin A is translocated from aril to the seeds of the fruit during maturity(Fig 2) resulting in impaired gluconeogenesis and beta oxidation of fatty acid in mitochondria. Studies mentioned toxicity due to Enalapirl appeared at daily dose of 20mg or more. Thorough history taking is crucial in patients presenting with liver injury. To the best of our knowledge, this is the first case of acute subfulminant liver injury related to ingestion of Ackee fruit in a healthy middle age woman who subsequently had complete recovery with no liver transplantation after withdrawal of the offending agent. The importation of ackee is prohibited in the United States and only canned fruit is available.Figure 2

TIPS is recommended to control portal hypertension related complications in cirrhotic patients with diuretic resistant or refractory. We present a case of biliary stricture in a patient with left to left TIPS that required placement of a biliary stent. 63-year-old woman with cirrhosis due to non-alcoholic steatohepatitis (NASH), complicated by symptomatic ascites and hepatic hydrothoraces on diuretics, presented for liver transplant evaluation(OLT). She required paracenteses every 3 to 4 weeks and thoracocenteses twice in the last 4 months with no history of infection. MRI of abdomen showed cirrhosis, and a bland partially occlusive thrombus in the distal main portal vein, the right portal vein and branches. TIPS was created from the left hepatic to left portal vein (left to left TIPS) (Fig 1) with final portosystemic pressure gradient of 5mmHg from 12mmHg. She developed melena next day and it was controlled in 24 hours after optimization of coagulopathy without further invasive intervention. She presented for jaundice and fever 2 weeks later. Labs showed bilirubin 20.4mg/dl with direct 13.8, AST/ALT 59/63U/l, Alk phos 114U/l. MRCP showed new left biliary obstruction proximal to the point of crossing of the TIPS (Fig 2). ERCP revealed moderately dilated left intrahepatic branches with obstruction at the level of the TIPS. A 7mm x 15cm biliary stent, with a full external and internal pigtail loops, was placed into the left intrahepatic bile duct (Fig 3). Subsequently, she underwent OLT 2 months ago with current excellent liver graft function.Figure 1Figure 2Figure 3Most TIPS are done between the right hepatic vein to the right or left portal system, with the reason right portal vein is larger in size, more favorable direction and longer branches of right hepatic vein compared to left in literature. Our case had left to left TIPS due to the thrombus in right portal system which only happened in rare circumstances (eg, Budd Chiari syndrome). Biliary stricture caused by TIPS is an unusual event and in some reported cases, percutaneous biliary drainage is required because of tight strictures endoscopically. Successful placement of a biliary stent via ERCP was observed in this case. Attention should be paid to the possibility of biliary obstruction during follow-up after the TIPS procedure. Our case leads us to perform a study at our institution, currently ongoing, on symptoms management and complications of left to left TIPS compared to conventional method using right sided veins.

Russell bodies are pink eosinophilic accumulations within plasma cells. To date, two hypotheses have attempted to elucidate the biological events behind the formation of these bodies. One theory sustains that such bodies constitute cytoplasmic accumulation of immunoglobulin derivatives contained in the perinuclear cistern of the smooth endoplasmic reticulum because of an increased synthesis or altered secretion. On the other hand, since its initial description in the medical literature, several authors have attributed the formation of such bodies to the presence of microorganisms such as in the case of Russell body gastritis and its association to Helicobacter pylori infection. In an attempt to possibly characterize the presence of an infectious organism, we performed a thorough biomolecular analysis on a case of a 69-year-old female presenting with Russell body duodenitis which, to the best of our knowledge, constitutes the second report of this clinical entity in the English literature. In light that the events behind formation of such bodies in H. pylori-negative individuals remain unclear, we hypothesize on the possible pathways that could have led to their reactive mechanical and immune derivation.