bluuebunny/crossref_metadata_2025_split huggingface dataset:
2404 Hepatic Double Trouble—A Case of Combined Hepatocellular Carcinoma and Cholangiocarcinoma
Authors: Ponna Pramod , Saxena Rovin , Kulkarni Mayuri , Diaczok Benjamin , Krishnamoorthy Geetha 
Published: October 2019

INTRODUCTION:
Combined Hepatocellular carcinoma and Cholangiocarcinoma (cHCC-CC) accounts for <1% of all liver malignancies and is difficult to diagnose pre-operatively. We present a case of cHCC-CC diagnosed by imaging, tumor markers and biopsy.

CASE DESCRIPTION/METHODS:
A 61-year-old male with advanced cirrhosis due to hepatitis C and alcohol, was admitted for hepatic encephalopathy. His alpha-fetoprotein (AFP) was elevated at 17, 771 ng/mL. MRI abdomen revealed a 2 cm mass that showed early enhancement and rapid wash-out consistent with HCC in the right lobe and 1 lesion in the left lobe that showed hyperenhancement in post contrast images which was not consistent with HCC. CA 19-9 level was elevated at 54.3 U/mL. Biopsy of the left lobe lesion showed Cholangiocarcinoma. Metastatic work up (CT chest, MRI brain, bone scan) was negative. Patient and his family chose comfort care due to the poor functional status and need for hepatectomy.

DISCUSSION:
There are 3 types of cHCC-CC: In type A, HCC and CC are seen at different sites in the liver, as in ours. Type B consists of juxtaposed HCC and CC that mingle with ongoing growth and type C has both within the same tumor. Imaging shows HCC features of arterial enhancement and washout and CC features of irregular surface and late enhancement. The presence of both elevated AFP and CA 19-9 should lead to the suspicion of cHCC-CC. Hepatectomy is the only curative treatment for cHCC-CC and transplant is contraindicated. Survival after resection for cHCC-CC is worse than HCC.
2405 Even When All Hell Breaks Loose…We Have a Plan!
Authors: Wander Praneet , Ashamalla Michael , Pizzuti Jessica , Lech Diana , Satapathy Sanjaya K. 
Published: October 2019

INTRODUCTION:
Acute variceal bleeding is a severe complication of portal hypertension. Endoscopic banding successfully controls the vast majority of acute variceal bleeding. Refractory variceal bleeding refers to a small percentage of acute variceal bleeding not controlled by endoscopic therapy, requiring more aggressive modalities such as a Sengstaken–Blakemore tube. We present a case series of two patients with hematemesis secondary to varices, requiring the use of Self-expandable metal stents (SEMS) with successful hemostasis.

CASE DESCRIPTION/METHODS:
Patient 1: A 38-year-old male with decompensated cirrhosis in the setting of alcohol use complicated by esophageal varices presented with hematemesis. On presentation, he was hypotensive and tachycardic with several large bouts of hematemesis prompting endotracheal intubation for airway protection. He required a massive transfusion protocol and was started on vasopressor support. Initial upper endoscopy showed five columns of large varices (>5 mm) in the middle third and lower third of the esophagus. One varix was actively spurting at about 38 cm from the incisor, for which four bands were successfully placed with resolution of the active bleeding. The patient had a repeat episode of massive hematemesis the following day requiring upper endoscopy during which active bleeding was appreciated but a source could not be accurately identified. Due to lack of visualization, banding could not be repeated and a fully covered 23 mm × 105 mm esophageal stent was placed starting at 30 cm from the incisor to the GE junction with excellent hemostasis. The patient had no further episodes of hematemesis and was transferred for liver transplant evaluation. Patient 2: A 30-year-old male with incompletely treated hepatitis B complicated by hepatocellular carcinoma invading the portal vein and extending to the Superior Mesenteric Vein presented with hematemesis. He was intubated and required upper endoscopies on two consecutive days for management of active bleeding from esophageal varices with banding. He was considered not to be a candidate for TIPS. On day 3, he had another episode of hematemesis causing hypotension. An upper endoscopy was performed and a fully covered esophageal stent was placed to tamponade the varices. He did not have any more episodes of bleeding in the remaining hospitalization.

DISCUSSION:
SEMS should be considered as an option for management of refractory variceal bleeding.
2408 Carbamazepine-Induced Immuno-Allergic Hepatitis!
Authors: Daneshvar Danial , Haddad Fady , Abergel Jeffrey 
Published: October 2019

INTRODUCTION:
Drug induced liver injury (DILI) is an uncommon cause of abnormal liver tests. It is suspected based on clinical and chronological criteria and is usually a diagnosis of exclusion. Carbamazepine (CMZ) is a commonly prescribed medication for the treatment of epilepsy, trigeminal neuralgia and bipolar disorder. It is a well-known cause of transient liver tests elevation but is only rarely associated with severe hypersensitivity reactions that involve the liver. We present a case of a patient who developed CMZ-induced immuno-allergic hepatitis.

CASE DESCRIPTION/METHODS:
A 66 year-old Chinese man with history of trigeminal neuralgia presented with several days of fever, asthenia and generalized rash. He had been on CMZ 100 mg daily for trigeminal neuralgia for 8 weeks. Three weeks prior to admission he returned from a 2 week trip to China. He denied herbal remedies, alcohol intake or exposure to farm animals. Physical examination was notable for diffuse confluent maculopapular rash involving his palms and soles (Figure 1). Blood tests were significant for an alkaline phosphatase of 350 IU/L (30-115 IU/L), alanine aminotransferase of 165 U/L (0-41 U/L), aspartate aminotransferase of 84 U/L (0-41 U/L) (Graph 1). Blood tests for viral hepatitis and infectious organisms were negative (Table 1). CMZ was discontinued and the patient was managed conservatively. Three days afterwards, notable improvement in the patient's rash, constitutional symptoms and labs was noted. The patient was discharged uneventfully.

DISCUSSION:
DILI affects up to 22% of patients exposed to CMZ. It usually occurs within the first 6 months of medication use. The pattern of liver test elevation can be hepatocellular, cholestatic or mixed. CMZ-induced immune-allergic hepatitis affects 16 out of 10,000 individuals per year and mostly presents as part of drug reaction with eosinophilia and systemic symptoms (DRESS syndrome). Although hypersensitivity reaction has been suggested as the most common mechanism of liver injury, reactive metabolites of CMZ have been shown to induce direct cytotoxicity. A direct association between CMZ-induced hepatitis and HLA-B X1502 has been specifically found in Southeast Asian population. After stopping the medication, symptoms resolve within 5-7 days but normalization of the liver enzymes may take up to 4 weeks. CMZ reuse may cause rapid severe recurrence. Heightened awareness of drug toxicity is advised in view of its non-specific symptoms, commonly delayed diagnosis and potentially fatal outcomes.
2410 Unusual Cause of Ascites in Liver Cirrhosis: Peritoneal Tuberculosis
Authors: Mann Rupinder , Gulati Abhishek 
Published: October 2019

INTRODUCTION:
Peritoneal tuberculosis is a rare disease with increasing incidence in recent years, especially in patients with immunocompromised state. Tuberculous peritonitis (TBP) in cirrhotic patients can mimic spontaneous bacterial peritonitis (SBP) and infrequently considered in differential diagnosis, resulting in delayed diagnosis and mortality. We present a case of TBP in a patient with cirrhosis.

CASE DESCRIPTION/METHODS:
37-year-old man with history of alcoholic cirrhosis and alcohol abuse presented with gradually worsening abdominal distension for 3-6 months and abdominal pain for 2 days. Patient had pulmonary tuberculosis 20 years ago for which he received multi-drug regimen for 6 months. On presentation, vitals were stable and he had epigastric tenderness. Labs revealed AST - 61 U/L and normal CBC. CT abdomen showed moderate ascites with thin peripheral enhancement suggestive of peritonitis. He was started on empiric antibiotics for presumed SBP. Paracentesis removed 1.4 L of straw colored fluid with WBC 791 cells/L with lymphocytes (94%), SAAG-0.4 g/dl, negative gram stain, ascitic fluid culture and cytology showed benign mesothelial cells and small mature lymphocytes. Given continued low-grade fever upto 100.4 F and lymphocytic predominance in the ascitic fluid, serum Quantiferon gold was done which came back positive. A laparoscopic peritoneal biopsy revealed exudates, loculated ascites and biopsy showed granulomatous inflammation with caseous necrosis confirming Mycobacterium tuberculosis. Patient was started on Ethambutol, Isoniazid, Pyrazinamide and Rifampin for 2 months followed by isoniazid and Rifampin for 4 months.

DISCUSSION:
Tuberculous peritonitis should be considered as differential diagnosis, in addition to SBP in cirrhotic patients who presents with ascites and abdominal pain. Similar to SBP, TBP in patients with cirrhosis presents with nonspecific signs and symptoms including abdominal distension, fever and abdominal pain. However, treatment of TBP and SBP differs vastly. TBP should be considered with the following criteria: cirrhotic patients with Child Pugh B; TB identified at additional sites; lymphopenia in the peripheral blood; ascitic protein >25 g/l; lymphocytes predominance in ascites; ascitic ADA activity >27 U/l; and ascitic LDH >90 U/l. Treatment of TBP with anti-tuberculosis drugs for atleast 6 months with 4-drug regimen for initial 2 months followed by two-drug regimen. 20%–40% of patients with TBP presents with an acute abdomen and need surgical intervention.
2412 A Unique Case of Acute Liver Injury Due to Severe Epstein-Barr Virus Infection
Authors: Shah Jamil M. , Lingiah Vivek A. , Pyrsopoulos Nikolaos T. , Galan Mark A. 
Published: October 2019

INTRODUCTION:
The liver is often affected by EBV infection, but involvement is commonly subclinical and self-limited. Infrequently, severe and potentially fatal EBV hepatitis has been reported in immunocompromised patients and, more rarely, in immunocompetent individuals.

CASE DESCRIPTION/METHODS:
A 25 y/o reasonably healthy man was transferred to a tertiary care hospital for advanced liver care due to increasing liver enzymes and concern for acute liver failure. Prior to presentation, he had experienced dry mouth, fatigue, and dark urine for six days. Of note, he worked in the police academy and regularly engaged in rigorous training. He used multiple OTC supplements, including clomiphene, creatine, ligandrol, and ibutamoren. Also, he would ingest 1600-2400 mg of ibuprofen in a day, for about 12 days per month, for general soreness from his workouts. Upon admission, his physical exam was notable for scleral icterus and generalized jaundice. He was A+Ox3 with no mental status changes. His labs were significant for AST 1,611, ALT 3,529, ALP 114, and total bilirubin 15.2 (direct 12.3). He had strongly positive EBV IgM titers, and was found to have a positive EBV PCR (52,000 copies/mL). During the admission, he had two episodes of seizure-like activity, the second of which was recorded on EEG without epileptiform activity. The episodes were attributed to syncope/presyncope in the setting of symptomatic anemia. He received a total of three units of packed RBCs due to anemia, but his hemoglobin did not initially improve. However, the last transfusion was warmed and there was adequate improvement in the hemoglobin, supporting a diagnosis of cold-agglutinin disease. Liver biopsy showed severe acute hepatitis, a mixed portal and lobular inflammatory infiltrate, and marked cholestasis. The overall picture was consistent with an EBV-driven hepatitis, along with a severe hemolytic anemia due to cold-agglutinin disease induced by EBV, in conjunction with likely predisposition to liver injury from taking various supplements. Ultimately, his liver enzymes improved and he was discharged in stable condition.

DISCUSSION:
EBV is associated with a variety of clinical manifestations and can present as cholestatic hepatitis with or without features of infectious mononucleosis (IM). Conversely, although rare in the immunocompetent, there is a need to test for EBV in cryptogenic hepatitis even if it remains difficult to prove its causative role. The mainstay of treatment for IM and other primary EBV diseases is supportive care.
2414 One Time Hepatitis a Virus Vaccination Might Not Be Enough in Cirrhotic Patients
Authors: Gonzaga Ernesto Robalino , Rojas Patricia Guzman , Camargo Kathlyn , Blonski Wojciech , Ho Minh 
Published: October 2019

INTRODUCTION:
Acute HAV infection was a highly prevalent infection in the US prior to the development of the vaccine in 1995, after which a drastic decline was observed. Unfortunately, increasing outbreaks have been reported around the world in the last 5 years. In 2016 there was a 44% increase in cases compared to 2015 in the US. Immunogenicity to the HAV vaccine occurs in more than 95% of recipients. However, the increasing number of cases reported is thought to be associated with the immunocompromised population which does not experience a similar rate of seroconversion after vaccination.

CASE DESCRIPTION/METHODS:
We present a 58-year-old male with a history of liver cirrhosis who presented to the ED with generalized weakness and jaundice for one week. The patient denied recent travel or drug use, however, admitted to daily alcohol use. His vital signs were normal. Physical exam was unremarkable aside from generalized jaundice. Laboratory results were relevant for markedly elevated transaminases, INR and total bilirubin (Table 1). Ethanol and acetaminophen levels were negative, but viral hepatitis serologies were reactive for HAV IgM and IgG (Table 2), despite prior immunity to HAV two years ago. Supportive treatment was started. His hospital stay was complicated by fulminant liver failure and hepatorenal syndrome. The patient was not a candidate for liver transplant due to continued alcohol use. He pursued hospice care and later expired.

DISCUSSION:
Immunity to HAV occurs after exposure to its antigen (Ag) confirmed by a positive IgG. Vaccination should offer lifelong immunity. T-cells play a main role in Ag presentation, cytokine induction and B cell differentiation. However, patients with a compromised immune system often experience T-cell dysfunction, hindering a proper immune response. Immunocompromised states, such as HIV infection, affect seroconversion rates after vaccination. One study showed 4% of patients with HAV infection were HIV positive and 55% were previously vaccinated. Our patient was negative for HIV but had a history of liver cirrhosis. The liver is the first organ in contact with the HAV Ag, delivered from the gut via the portal vein. Liver macrophages prevent systemic spread of Ag and hepatocytes synthesize complement. Both are essential for a robust immune response. This case highlights the risk of reinfection with HAV in cirrhotic patients, even with prior immunization. We suggest consideration for booster immunization in this population similar to that suggested for HIV patients.
2422 Post-Transplant Lymphoproliferative Disorder
Authors: Cavaliere Kimberly , Ganti Anita , Satapathy Sanjaya K. 
Published: October 2019

INTRODUCTION:
Post-transplant lymphoproliferative disorder (PTLD) is a rare but severe complication in both solid organ and hematopoietic stem cell transplantation. PTLD is caused by the dysfunction of T-cells as a result of the immunosuppressive therapy commonly used in transplant patients. This dysfunction then causes abnormal lymphoid proliferation leading to malignancy. We discuss a case of PTLD presenting in the form of a small bowel obstruction in a patient with dual liver, kidney transplantation.

CASE DESCRIPTION/METHODS:
A 68-year-old man with previous NASH cirrhosis status post a deceased donor liver and kidney transplant presented to the hospital with nausea, vomiting, and abdominal distension. Prior to presentation he had been maintained at home on Cellcept and Tacrolimus for many years. He was doing well until 3 months prior to presentation when he noted the onset of night sweats. He had no other symptoms until two days prior to presentation when he had the abrupt onset of abdominal pain, distention, nausea and vomiting causing his presentation to the ED. On arrival his initial work up was significant for a mild leukocytosis, anemia, and AKI. He had a CT abdomen and pelvis done which was significant for a small bowel obstruction secondary to a small bowel mass along with mesenteric and retroperitoneal lymphadenopathy, raising the concern of PTLD on initial presentation. Interventional radiology was then consulted and performed a para-aortic lymph node biopsy. EBV and CMV PCR returned negative but the surgical pathology returned as Diffuse Large B Cell Lymphoma with double expression, suggesting a diagnosis of Post Transplant Lymphoproliferative Disorder. He was started on the R-CHOP chemotherapy regimen inpatient and was discharged for further outpatient treatment.

DISCUSSION:
This case is a rather classic presentation of a rare complication of immunosuppressive therapy, demonstrating the possible lethal side effects of these often life saving drugs. Swift diagnosis was made possible due to early clinical suspicion and rapid involvement of a multitude of different medical specialties. This case demonstrated the need for multi-disciplinary team at all transplant centers and how close communication between consultants is key to these patients success.
2424 Hepato to the Metal: The Irony of Wilson Disease
Authors: Pak Kevin , Ordway Sarah , Torres Dawn , Sjogren Maria 
Published: October 2019

INTRODUCTION:
Wilson Disease (WD) is a disorder of copper metabolism resulting in the accumulation of copper within the liver and other organs. It is caused by mutations in the ATP7B gene, which codes for a copper transport protein in the liver. The absent or compromised ATP7B protein not only causes copper accumulation in the liver but also reduces the amount of circulating ceruloplasmin. Hemochromatosis describes an iron overload syndrome that can be either primary or secondary, the latter carrying a broad differential. We describe a case of a patient with newly diagnosed WD with concomitant iron overload.

CASE DESCRIPTION/METHODS:
30-year-old otherwise healthy male presents with eight-month history of persistently elevated LAEs (liver associated enzymes). Eight months ago his ALT was 127 U/L and his AST was 67 U/L with all other elements of his liver function being normal. He uses NSAIDs once a month for neck and low back pain. He denies supplement use and does not consume alcohol. No known family history of metabolic liver disease. Review of systems was otherwise normal including no neuropsychiatric symptoms Physical exam was normal. LAEs at current presentation were ALT of 155 U/L and AST of 75 U/L, with normal total bilirubin and ALP. He had new thrombocytopenia of 143,000/μL. INR was normal. Infectious, autoimmune, and metabolic serologic testing were all unremarkable except ceruloplasmin <3.0 mg/dL and ferritin of 646 ng/mL. Iron (70 μg/dL) and iron saturation (24.1%) were normal. Concern for WD prompted a 24-hour urine copper collection. His 24 hour urine copper level was elevated (113 μg). Slit-lamp exam was normal. Liver ultrasound was unremarkable. Vibration controlled transient elastography score was elevated (11.8 kPa, IQR/med 8%). Liver biopsy revealed bridging fibrosis with negative copper staining, but iron stain showing moderate hepatocellular iron deposition.

DISCUSSION:
In addition to its copper carrying property, ceruloplasmin has ferroxidase activity. Hypoceruloplasminemia found in WD consequently leads to decreased amount of circulating iron and increased iron stores, leading to iron accumulation in the liver. Although primary hemochromatosis should be considered in the evaluation of patients with WD with evidence of iron overload, it is important to realize that iron overload can also be a second order effect of WD. Iron indices should be monitored in patients with WD, particularly during chelation therapy, as ceruloplasmin levels may further decrease and worsen iron accumulation.
2426 Cholestatic Liver Injury Caused by Kratom Ingestion
Authors: Pronesti Vincent , Sial Moaz , Talwar Aditya , Aoun Elie 
Published: October 2019

INTRODUCTION:
Kratom is an herbal product derived from Mitragyna speciosa trees and was originally used by indigenous peoples of southeast Asia. Ingestion is thought to relieve fatigue, diarrhea, and general pain. There are fewer than five reported cases in the literature from North America detailing kratom-induced liver injury and only one with specific hepatic histologic findings. This is the case of a 30-year-old male who ingested kratom and presented with dark urine and jaundice with labs showing liver injury. Liver biopsy revealed cholestatic injury. This case is significant because it temporally relates the use of kratom with liver injury and contributes unique histologic findings.

CASE DESCRIPTION/METHODS:
The patient is a 30-year old male with a history of diabetes who presented with one week of dark urine and light, chalky stools and one day of yellow eyes. He did not endorse drug or acetaminophen use. Vitals were unremarkable. Labs revealed alkaline phosphatase 556, AST 125, ALT 308, total bilirubin 5.7, and direct bilirubin 4.5. Computed tomography (CT) of the abdomen and pelvis was conducted and was unremarkable. A chronic liver disease panel including hepatitis A, B, and C, iron studies, ceruloplasmin, alpha-1 antitrypsin level, mitochondrial antibody, and liver-kidney microsomal antibody were negative with the exception of a ferritin 405 and an anti-smooth muscle antibody 1:20 titer. Liver ultrasound revealed a coarsened liver echotexture. The patient admitted to ingesting kratom powder with water to help him sleep for the past 4-6 weeks. A liver biopsy was conducted with the histology seen in Figures 1 and 2. It revealed inflammation with hepatocellular and canalicular cholestasis without fibrosis suggesting kratom-induced liver injury. With supportive care, one month labs had normalized and are shown in the accompanying Figure 3.

DISCUSSION:
Kratom is a derivative of Mitragyna speciosa trees and is used to treat fatigue, myalagias, and pain. It has been shown in rare cases to cause intrahepatic cholestasis and related liver enzyme elevation, following two weeks of ingestion. It can also be accompanied by kidney and bone marrow injury. Liver histology seen in Figures 1 and 2 from our patient is consistent with hepatocellular and canalicular cholestasis with portal areas showing focally prominent eosinophils. Similar findings were also seen in one prior reported case. This case contributes unique histologic findings to the body of evidence that kratom is associated with liver injury.