bluuebunny/crossref_metadata_2025_split huggingface dataset:
2295 Shunt Hunting: A Case of Long-Standing Encephalopathy Secondary to Anatomic Porto-Systemic Shunt
Authors: Lin Brian , Patel Dhruvan , Munoz Santiago 
Published: October 2019

INTRODUCTION:
Abernethy malformation is a very rare congenital vascular malformation defined by diversion of portal blood away from liver [1]. Morgen and Superina classified extrahepatic portosystemic shunt into 2 types, as seen in Table 1 [3]. We describe in this case a type II extrahepatic portosystemic shunt.

CASE DESCRIPTION/METHODS:
A 67-year-old female with history of untreated hepatitis C, major depression disorder, hypertension, peripheral vascular disease, GERD, rheumatoid arthritis and HFrEF was admitted for altered mental status and elevated ammonia level on outpatient labs. This patient has a longstanding history of unexplained encephalopathy and elevated ammonia, treated with lactulose. She has no known history of cirrhosis and denied fevers, chills, nausea, vomiting or GI bleed. Patient was hypertensive on admission at 173/89, tachycardic to 109 and afebrile. She was saturating 98% on 2L O2. Exam was significant for bilateral coarse crackles, RUQ and epigastric tenderness and JVD. Ammonia was 106 on admission. Alkaline phosphatase 112, ALT 39, AST 84. Abdominal ultrasound revealed mildly heterogenous echogenicity of the liver with no evidence of cirrhosis. CT Abdomen was significant for congenital abnormalities including intestinal malrotation, hypoplastic IVC and abnormal pelvic variceal communication with the internal iliac vein, splenic vein and portal venous system (image). Patient underwent transjugular biopsy of liver with hepatic wedge pressures measured at 29 mmHg (gradient 14 mmHg). Pathology showed bridging fibrosis consistent with chronic viral hepatitis infection. Her encephalopathy improved to baseline after treatment with lactulose.

DISCUSSION:
We present a case of long-standing encephalopathy without cirrhosis, treated with lactulose. The patient also had markedly elevated hepatic portal pressures in the setting of HFrEF, without findings of cirrhosis on pathology. On this admission, CT abdomen/pelvis revealed an anatomic porto-systemic shunt, revealing the etiology of the patient’s unexplained “hepatic” encephalopathy. Multiple intra-abdominal congenital abnormalities were found on CT abdomen/pelvis, including a hypoplastic IVC, intestinal malrotation, and most significantly abnormal variceal communication with the internal iliac vein, splenic vein and portal venous system. The patient's collateral portosystemic shunts describes a type II extrahepatic portosystemic shunt.
2302 A Case of Hepatitis B Reactivation Resulting in Fulminant Hepatic Failure
Authors: Campos Marilia , Henn Andrew , Malli Ahmad 
Published: October 2019

INTRODUCTION:
Patients with chronic HBV/HIV coinfection are at high risk of HBV chronicity and reactivation. Here we present a case of a patient who presented with acute liver failure secondary to hep B reactivation after adjustment of his HIV medication regimen.

CASE DESCRIPTION/METHODS:
A 56 year old male with HIV/HBV coinfection with undetectable viral loads was evaluated in the ED for new onset nausea and jaundice. Examination was significant for jaundice in the absence of any encephalopathy or other stigmata of chronic liver disease. Blood tests revealed INR 3, ALK-P 210, ALT 2186, AST 2934 and Bili T/D 25.6/17, platelet count 197K, Cr 1.98, and CD4 count 394. Liver US showed normal hepatic echotexture with patent vasculature. Serologic evaluation showed undetectable HIV viral load, negative Hep C PCR, positive HepBsAg, and highly positive hepatitis B DNA (>1 billion copies). About 5 months prior to this acute presentation, he was switched from (Cobicistat, Elvitegravir, Emtricitabine, and Tenofovir) to another regimen that doesn’t include hepatitis B coverage (Atazanavir, Cobicistat , Rilpivirine, and Abacavir) due to concerns about Tenofovir contributing to his unexplained CKD. He was started on dual therapy with tenofovir and entecavir and was transferred to a nearby liver transplant center. His passed away after a short complicated hospital stay with acute liver failure and colonic pneumatosis.

DISCUSSION:
Our patient presented with acute fulminant liver failure after a brief period of inadvertent Hep B treatment interruption. Medical treatment was not helpful despite attempts at combination therapy with Tenfovovir and Entecavir (in contrast to Tenofovir monotherapy) despite the scarcity of data in this specific situation. There are case reports that demonstrated clinical improvement especially early treatment in the course; however progression to hepatic failure, liver transplantation, and death has also been widely reported despite therapy. This case serves as a reminder to all medical providers about the complexity of concomitant chronic HBV and HIV coinfection. Any medication regimen change in this patient population needs a multidisciplinary team based approach between HIV specialists and Hepatologists.
2308 A Rare Cause of Pyogenic Liver Abscess
Authors: Vohra Ishaan , Attar Bashar M. , Katiyar Vatsala , Randhawa Tejinder , Palacios Pedro , Salazar Miguel , Haque Zohaib , Nwaichi Chineme , Mathew Madhu , Majeed Muhammad , Desai Parth M. , Elkhouly Mohamed A. , Flores Estefania , Lingamaneni Prasanth , Mishra Satya 
Published: October 2019

INTRODUCTION:
Pyogenic liver abscess (PLA) is a rare clinical entity with an annual incidence of 0.5 to 0.8 percent. While these infections are typically polymicrobial, Staphylococcus aureus has also rarely been implicated. Here, we report a case of a community acquired Methicillin resistant Staphylococcus aureus (MRSA) hepatic abscess, which responded to clindamycin.

CASE DESCRIPTION/METHODS:
A 67-year-old man with history of untreated chronic hepatitis C and intranasal heroin abuse presented with shortness of breath, right sided pleuritic chest pain and generalized abdominal discomfort. Physical examination was notable for skin pallor, cachexia and right upper quadrant tenderness. Laboratory tests revealed albumin 2.6 g/dl (ref: 3.8-5.2), total bilirubin 2.8 mg/dl (ref: 0.2-1.2), direct bilirubin 1.3 mg/dl (ref: 0.0-0.2), hemoglobin 6 g/dl (ref: 12.9-16.8) and no leukocytosis. Computed tomography (CT) scan of abdomen demonstrated an ill-defined right hepatic lobe mass concerning for hepatocellular carcinoma (HCC). A triple phase CT scan revealed liver cirrhosis and a complex cystic solid mass 10 × 5 × 6 cm in size, raising suspicion for HCC versus a hepatic abscess (Figure 1). Biopsy yielded pus and a pig tail catheter was placed. He was started on ampicillin-sulbactam for possible polymicrobial hepatic abscess, but it was later switched to IV Vancomycin when the cultures grew MRSA (Figure 2). On further testing, no source of infection was identified. He left against medical advice and was discharged with four weeks of clindamycin. A repeat CT scan five months later showed resolution of the hepatic abscess and the drain was removed (Figure 3).

DISCUSSION:
Community acquired MRSA is an uncommon cause of PLA with only a few cases reported in literature. The source of infection if identified is usually cutaneous or intraabdominal. We could not identify any infectious foci in our patient. Radiographic appearance of multi-loculated hepatic abscess can masquerade HCC, as in our patient, warranting further diagnostic workup. The mainstay of treatment is drainage and prolonged antibiotic therapy. Intravenous vancomycin is the drug of choice. Linezolid has been used as an oral alternative previously, but our patient responded well to clindamycin, suggesting that it could be a less expensive but equally efficacious choice. Surgical intervention maybe necessary if there is no improvement after 4 to 7 days of percutaneous drainage or if there is viscous pus in thick-walled or multilobulated abscesses.
2320 A Case Report of Herpes Simplex Virus Hepatitis Presenting as Fever of Unknown Origin
Authors: Dimaria Christina , Putthapiban Prapaipan , Marte William Jimenez , Sandhu Karanjit 
Published: October 2019

INTRODUCTION:
Herpes simplex virus (HSV) hepatitis accounts for only 2% of all viral hepatitis. It often presents in patients who are immunocompromised and pregnant women. Besides cutaneous findings which present in less than half of these patients, HSV hepatitis often lacks specific clinical findings leading to missed diagnosis and rapid progression to fulminant liver failure and multiorgan collapse. We report a case of a 58-year-old immunocompetent female who presented with fever of unknown (FUO) origin who developed transaminitis with pancytopenia and was diagnosed with HSV hepatitis by liver biopsy.

CASE DESCRIPTION/METHODS:
A 58-year-old female with past medical history of hypertension, hyperlipidemia, and cholelithiasis status post cholecystectomy presented with high grade fever and worsening abdominal pain for over a week. Physical examination revealed marked right upper quadrant tenderness, but no mucocutaneous lesions including genitalia. Initial laboratory findings showed transaminitis with ALT 139 (0-55 IU/L) and AST 172 (5-34 IU/L). Ultrasound of liver and MRCP showed mild hepatomegaly with hepatic steatosis without cirrhosis and biliary ductal dilatation. She developed pancytopenia and abrupt elevation in both ALT and AST to 822 IU/L and 1558 IU/L, respectively. She never developed coagulopathy or hepatic encephalopathy. Hepatitis A, B, C serologies were negative, ANA 1:320, anti-SMA 1:80, HSV2 IgM positive > 1:320 and HSV2 qualitative PCR was positive in serum. Acyclovir was initiated on day 6 of hospitalization with gradual improvement of fever and transaminitis (Figure 1). A liver biopsy was performed which showed hepatic necrosis with rare nuclei positive for HSV immunostaining (Figure 2).

DISCUSSION:
HSV hepatitis often presents as fulminant liver disease, with a mortality rate greater than 80%. Clinical features often include fever, anorexia with nausea and vomiting, abdominal pain, leukopenia, and coagulopathy. Our patient was originally diagnosed with FUO, defined as temperature higher than 38.3ºC on several occasions, duration of fever for at least three weeks, or uncertain diagnosis after one week of study in the hospital. In this case, we were able to diagnose and treat the patient early into her HSV hepatitis course, preventing acute liver failure and other complications. For this reason, we believe it is important test early for HSV in immunocompetent patients with FUO, mild to moderate transaminitis and pancytopenia to decrease morbidity and mortality.
2322 Liraglutide-Induced Liver Injury With Superimposed Acute Pancreatitis
Authors: Then Eric O. , Maddika Srikanth , Gayam Vijay , Ofosu Andrew , Culliford Andrea , Gaduputi Vinaya 
Published: October 2019

INTRODUCTION:
Liraglutide, commercially known as Victoza is a glucagon-like peptide 1 (GLP-1) receptor agonist that was recently approved for the treatment of diabetes mellitus type 2. Due to its recent arrival in the realm of anti-diabetic medications, the side effects of GLP-1 receptor agonists are not fully established. It is thought that the release of GLP-1 is mediated by sensory neurons located in the intestine and in the liver. This is clinically significant as many of the reported side-effects occur in these sites, namely the liver as was the case with our patient.

CASE DESCRIPTION/METHODS:
A 64-year-old woman with a medical history of hypertension, diabetes mellitus, hyperlipidemia, and cholecystectomy presented to our emergency department complaining of diffuse abdominal pain for 4 days. The patient denied alcohol consumption, illicit drug use, recent travel or any recent changes in her diet. Laboratory workup included alanine aminotransferase (ALT) of 1359 IU/L, aspartate aminotransferase (AST) of 565 IU/L, alkaline phosphatase (ALP) of 405 IU/L, and lipase of 287 U/L. Physical examination was notable for epigastric tenderness. Of note the patient was seen at our outpatient clinic 6 months at which point she was started on Liraglutide. Liver function tests at that time were within normal limits. Upon hospital admission Liraglutide was held and the patient was promptly started on intravenous fluids and N-acetylcysteine protocol. During her admission markers for viral hepatitis and autoimmune hepatitis were negative. On her third hospital day after discontinuation of Liraglutide the patients symptoms completely resolved and her liver function tests trended down (ALT: 335, AST: 58, ALP: 386). The patient was then discharged home with outpatient follow up scheduled.

DISCUSSION:
Acute pancreatitis is an established possible complication of liraglutide therapy. The mechanism behind its development is likely attributable to a hypersensitivity or metabolic idiosyncratic reaction. Drug induced liver injury however, is an exceedingly rare complication of liraglutide therapy. Current theories suggest the development of anti-liraglutide antibodies as the main culprit. Liraglutide is a peptide that is 97% homologous with human GLP-1. This is problematic as the development of antibodies against liraglutide may also cross-react with the GLP-1 receptor found on human hepatocytes thus resulting in liver injury. We highlight a rare case of liraglutide induced liver injury with concurrent acute pancreatitis.
2325 Severe Cholestatic Hepatitis: An Atypical Presentation of Epstein-Barr Virus Infection
Authors: Sanchez Antonio J. , Brown Kyle , He Xiaoping 
Published: October 2019

INTRODUCTION:
Infectious mononucleosis (IM) is a benign lymphoproliferative disease caused by Epstein-Barr Virus (EBV). In adults, EBV infection can cause an acute hepatitis with elevation of transaminases, usually resolving spontaneously. We report a rare case of a severe cholestatic hepatitis following an acute EBV infection.

CASE DESCRIPTION/METHODS:
A 24-year-old previously healthy Caucasian woman presented with fever, body aches, headache, odynophagia and dry cough for 5 days. Initially CBC was normal but she had significant liver test abnormalities: aspartate transaminase (AST) 723 IU/L, alanine transaminase (ALT) 647 IU/L, alkaline phosphatase (ALP) 708 IU/L, and normal total bilirubin (TB) 1.2 mg/dl (Figure 1). Patient took acetaminophen (<2 g/day) at home for fever for 5 days. She had no prior history of hepatitis, blood transfusions, intravenous drug use, high-risk sexual activity, or significant alcohol use. Monospot test was positive. Chest x-ray showed left lower lobe pneumonia, azithromycin was prescribed for 5 days. The fever subsided, but she became jaundiced (TB 9.2 mg/dl) on day 11 and the patient was admitted. RUQ ultrasound showed no evidence of biliary obstruction, masses or gallstones. CBC showed profound lymphocytosis. Hepatitis A, B, C and E serologies were negative. EBV VCA IgM Ab was positive, CMV and EBV PCR were negative. Autoimmune markers revealed mildly elevated ANA (1:160). Liver biopsy was done revealing sinusoidal lymphocytic infiltration typical of EBV hepatitis (Figure 2). Cholestasis worsened after admission with peak TB of 9.6 mg/dl and ALP 2080 IU/L. Follow-up lab work a month later showed a normal TB with mild elevation of ALP, GGT, AST and ALT. At 4-month follow up, all liver tests normalized with positive EBV serology (VCA IgG and EBNA), which confirmed the patient’s recent EBV infection.

DISCUSSION:
Acute cholestatic hepatitis is an extremely rare presentation of EBV infection, with few cases reported in the medical literature. To the best of our knowledge, our patient had the highest ALP elevation reported in association with EBV infection. It is essential for physicians to recognize this unusual EBV infection presentation in patients with fever and progressive cholestasis in the absence of biliary obstruction, to avoid prolonged hospitalization and invasive procedures.
2328 Ectopic Liver: A Silent Killer
Authors: Jakkidi Manisha , Edirisuriya Cynthia , Elfant Adam , Holdbrook Thomas , Chaaya Adib 
Published: October 2019

INTRODUCTION:
We present a rare case of Ectopic Liver (EL) tissue along the pancreatic tail, that developed into HCC. Based on our research, there are only 4 reported cases of primary HCC in EL tissue around the pancreas. Our case originates in the retroperitoneum near the pancreas.

CASE DESCRIPTION/METHODS:
70 y.o Female with Tuberous Sclerosis was referred for an incidental finding of an abdominal mass. She was seen by her PCP for back pain and difficulty ambulating. Physical exam showed chronic facial rash. Abdominal exam was negative for a palpable mass, tenderness, guarding or rebound. Labs revealed normal LFTs and normocytic anemia. Viral hepatitis panel was negative. MRI abdomen showed a 6.8 × 7 cm mass in the LUQ with a central cystic cavity and a surrounding solid component.The mass abuted the pancreatic tail and loops of bowel and was of unclear origin. EUS showed a normal appearing pancreas. A hypoechoic mass with cystic and solid components was noted next to the pancreas. FNA was performed. Immunohistochemical staining was positive for Hepatocyte specific antigen (HSA), supporting hepatic origin and CK7 highlighting the presence of a bile ductules. This supported the diagnosis of hepatic tissue. Surgical resection was recommended. A 8 cm mass involving the splenic vein and pancreatic tail was noted and distal pancreatectomy and splenectomy was performed. Surgical pathology showed carcinoma with hepatic differentiation, most consistent with primary HCC, adherent to the pancreas, but not involving the pancreatic parenchyma. No benign liver tissue was identified. A diagnosis of HCC arising within and replacing a rest of ectopic liver was made. AFP post-op was normal. Post-op course was uneventful.

DISCUSSION:
EL is defined as liver tissue found outside and not in communication with the normal liver. It is susceptible to same diseases as normal liver and especially prone to malignancy, despite the lack of risk factors. Given the difference in arteriovenous and bile system, EL tissue may have longer exposure to carcinogens. MRI shows "post contrast peripheral solid enhancement" - suggestive of HCC with ectopic tissue enhancement in arterial phase, however is less highlighted compared to HCC in normal liver. AFP is > 20ng/mL in 60% cases. Surgical resection is the primary treatment with no reported tumor recurrence. Our case highlights the importance that any EL is at high risk for HCC development, despite the lack of risk factors and negative FNA biopsies and surgical therapy needs to be offered.
2333 Acute Iron Toxicity in an Adult: Intentional or Accidental?
Authors: Desai Aakash , Twohig Patrick , Sandhu Dalbir S. 
Published: October 2019

INTRODUCTION:
In adults, iron overdose is usually associated with suicide attempts. Unfortunately, a majority of acute iron toxicity cases are fatal given the rapid progression to multi-organ failure. Literature on management of acute iron toxicity is scant with most of current available information reported in pediatric population. Here in, we report a case of acute iron toxicity in an adult.

CASE DESCRIPTION/METHODS:
A 58-year-old African American woman with a history of depression, prior suicide attempt and post-traumatic stress disorder presented to the emergency room with a 3-day history of coffee-ground emesis and abdominal pain. She was found to be hypotensive (74/45 mm Hg), and tachycardic (124 beats per minute). Laboratory investigation revealed a markedly elevated AST/ALT at 10518/5430 IU/L, alkaline phosphatase 260 IU/L, direct bilirubin 2.9 mg/dL, total bilirubin 4.9 mg/dL, INR 1.47, PT 16.8 sec, sodium 127 mmol/L, bicarbonate 14 mmol/L, BUN 45 mg/dL, Cr 5.92 mg/dL, anion gap 29 and lactate of 3.1 mmol/L. Additional comprehensive workup for acute liver injury was negative. She was fluid resuscitated with 5 liters of 0.9% normal saline. CT abdomen and pelvis with contrast revealed multiple radiopaque objects in the proximal ileum. Serum iron level was >500, iron saturation >273, TIBC 183, Transferrin 131 and Ferritin level of 867. She was started on a deferoxamine infusion at 5 mg/kg/hour and whole bowel irrigation with Colyte at 200 cc/hour. She was also started on continuous venovenous hemofiltration (CVVH) for anuric acute kidney injury. Deferoxamine was discontinued 24 hours after initiation, as her urine was clear and iron level was less than 350. Colyte was discontinued once stool output was clear. Her hospital course was complicated by small bowel obstruction, which resolved with bowel rest and non-operative supportive care. Psychiatry was consulted for a suicide risk assessment however, patient consistently denied any suicide attempt and collateral information from family was reassuring. The idea of accidental ingestion was entertained, however, the patient denied being on iron supplementation. Her iron levels, LFTs, and urine output were back to baseline 1-week post-discharge.

DISCUSSION:
Acute iron toxicity in adults can rapidly progressive to multiorgan failure and death. Deferoxamine should be initiated early in severe cases. Clinicians should be aware of other adjunctive measures like WBI and CVVH; they should be employed early in the treatment course to improve survival outcomes.
2336 Multiple Uncommon Complications After TACE
Authors: Bofill Aliana , Mirza Zeyn , Santiago Loscar 
Published: October 2019

INTRODUCTION:
TransarteriaL chemoembolization (TACE) is a widely-used treatment for unresectable hepatocellular cancer (HCC). Although TACE is minimally invasive, major complications occur in 5% of cases. These include acute cholecystitis, which is self-limiting and rarely requires surgical intervention. Liver abscess is a rare complication but can increase length-of-stay and morbidity. Our case focuses on multiple uncommon complications of TACE occurring in conjunction; gangrenous cholecystitis requiring emergent cholecystectomy, liver abscess and portal vein thrombosis.

CASE DESCRIPTION/METHODS:
A 67-year-old male with history of hepatitis C, cirrhosis and HCC status-post recent successful TACE who presented to the ER with right upper quadrant pain associated with fever. Physical examination with right upper quadrant tenderness and positive murphy’s sign. Laboratories showed leukocytosis and elevated alkaline phosphatase. Normal bilirubin, liver and pancreatic enzymes. Abdominopelvic CT with hydropic gallbladder with enhancing walls and pericholecystic inflammatory changes, new ill-defined hypodensities suggestive of abscess and extensive thrombus in the right portal vein. The patient received antibiotics and underwent an uneventful cholecystectomy. Post-operation findings consistent with a gangrenous gallbladder with severe adherent hepatic flexure and omentum to the gallbladder fundus. The patient was discharged on antibiotics and anticoagulation. Follow up MRI showed resolution of fluid filled lesions with almost complete resolution of the portal vein thrombosis.

DISCUSSION:
Cholecystitis is a complication of TACE due to reflux of the embolic material into the cystic artery. In most cases, management can be conservative. Our case is rare given that the patient developed gangrenous cholecystitis which is a serious complication that requires immediate surgical intervention. Liver abscess occurs infrequently unless there is a history of prior biliary reconstruction unlike our patient. Management includes antibiotics and percutaneous drainage for larger abscesses. In our case, our patient responded well to antibiotics. Because symptoms are non-specific, these complications may be mistaken for post embolization syndrome, which is usually self-limiting and abates by one week. Normal post-TACE CT findings can also confound the diagnosis of hepatic abscess formation. This case highlights the importance of being aware of complications of TACE as failure to recognize these may confer a higher mortality risk.