bluuebunny/crossref_metadata_2025_split huggingface dataset:
2339 Hemobilia-Associated Acute Cholecystitis Post-Percutaneous Liver Biopsy: A Unexpected Sequelae of a Known Complication
Authors: Pakala Tina , Cohen Jason , Bunim Ari , Hussain Syed 
Published: October 2019

INTRODUCTION:
Percutaneous liver biopsy is often a part of the diagnostic workup of unexplained abnormal liver enzymes. Known complications include hemobilia and unintentional perforation of an adjacent organ but rarely do these complications lead to sepsis.

CASE DESCRIPTION/METHODS:
We present a case of a 65-year old female being evaluated for abnormal liver enzymes (ALT 40 U/L, normal alkaline phosphatase) with a positive anti-mitochondrial (titer 1:1280) and anti-nuclear antibodies (titer 1:640). A percutaneous liver biopsy was performed under ultrasound guidance without any immediate complication. The biopsy revealed moderate-to-marked macrovesicula steatosis with focal centrilobular and periportal fibrosis (Stage 1 of 4). Five days later she presented to the emergency department with persistent RUQ pain, fevers and melena. Vitals notable for temperature of 39.3 °C. Physical examination revealed RUQ tenderness to palpation. The leukocyte count was 5.04 K/uL (predominantly neutrophils), AST 558 U/L, ALT 350 U/L, ALP 287 U/L, total bilirubin 1.9 mg/dL. CT abdomen demonstrated only cholelithiasis without other abnormalities. An abdominal ultrasound showed gallbladder sludge and wall thickening with a negative Murphy’s sign (Figure 1). Blood cultures were positive for Klebsiella pneumonia and IV antibiotics were started. Over the ensuing several days, the patient had worsening abdominal pain and developed melena. Imaging was remarkable for hyperdense material within the gallbladder. An endoscopic ultrasound was performed which revealed moderate amount of hyperechoic material in the gallbladder consistent with clotted blood. Given concern that an infected blood clot in gallbladder was a source of bacteremia, a laparoscopic cholecystectomy was performed. The surgical gallbladder specimen showed acute hemorrhagic acalculous cholecystitis. Postoperative course was uncomplicated and the patient was discharged home feeling back to normal.

DISCUSSION:
Hemobilia is a well-recognized complication of percutaneous liver biopsy, although this case is unusual because it appears to have led to acalculous cholecystitis and Klebsiella bacteremia. Blood, similar to sludge, can accumulate and mimic obstructive processes such as acute cholecystitis and acute pancreatitis. This case highlights the importance of early recognition of delayed complications of percutaneous liver biopsy.
2341 An Interesting Case of Drug-Induced Liver Injury Related to Khat
Authors: Waintraub Daniel J. , Zivari Kaveh , Fazio Richard M. , Weinberger Jonathan , Rahmani Rabin , Tsirlin Yuriy , Park James S. 
Published: October 2019

INTRODUCTION:
Drug-induced liver injury (DILI) is the most common cause of acute liver failure in the United States (U.S). The United States Drug-Induced Liver Injury Network (DILIN) reported that approximately 15-20% of DILI cases per year could be attributed to herbal and dietary supplements. Khat is a stimulant derived from the leaves of the shrub Catha edulis, which is native to North Yemen and other East African countries. Chewing khat, a drug of abuse, is an established social habit in areas endemic to the shrub. Khat has been associated with clinically relevant acute and chronic liver injury. We present a case of drug induced liver injury related to Khat.

CASE DESCRIPTION/METHODS:
A 47 year old Yemeni male with no medical history presented with jaundice. He denied prior liver disease, alcohol use or prescription drugs. He reported routine use of Khat. Labwork is shown in Figure 1. MRCP revealed mild hepatosplenomegaly. Viral workup revealed immunity to hepatitis A. The patient presented 3 months later with jaundice and persistently elevated liver enzymes. Abdominal ultrasound was unrevealing. Extensive workup revealed a positive antinuclear antibody 1:320, in homogeneous pattern and an elevated serum immunoglobulin G and was otherwise unrevealing. Liver biopsy revealed mild portal mononuclear infiltration associated with focal interface hepatitis and widespread lobular hepatitis with plasma cell prominence in the infiltrates (Figures 1 and 2). Subsequently the patient was started on a course of Prednisone and Ursodiol with complete resolution of liver injury.

DISCUSSION:
Liver injury related to Khat typically occurs after years of use and may present acutely with nausea, fatigue, and jaundice or chronically with evidence of portal hypertension. Biochemical injury is typically hepatocellular and liver enzymes may be significantly elevated. Autoantibodies can mimic autoimmune hepatitis. Resolution of liver injury typically occurs with cessation of khat use. Patients may require corticosteroid therapy however the response is typically partial. Liver transplantation due to Khat related liver failure has been reported. Given immigration of individuals from countries endemic to Khat, an extensive history including use of cultural drugs such as Khat and other herbal remedies is critical in making a diagnosis of unexplained liver toxicity. Our case highlights the importance of a complete drug and supplement history and maintaining a high index of suspicion for DILI in the appropriate clinical context.
2342 Periodontal Flora Isolated From Pyogenic Liver Abscess in a Retired Dentist With Hepatic Metastasis of Colon Carcinoma
Authors: Chokshi Tanuj , Botti Evan , Arroyo-Mercado Fray , Likhtshteyn Michelle , Hossain Naseem , Huynh Chi Doan , Tello Daniela , McFarlane Isabel M. 
Published: October 2019

INTRODUCTION:
The association of Streptococcus milleri group with pyogenic liver abscess is well recognized. Streptococcus gordonii, however, is a bacterium not of the milleri group and is included among the colonizers of the periodontal environment as it has a high affinity for molecules in the salivary pellicle on tooth surfaces. Here, we describe a case where Streptococcus gordonii was isolated from a pyogenic liver abscess in a retired dentist with hepatic metastasis of colon carcinoma. The clinical features, work up, management, and significance are described.

CASE DESCRIPTION/METHODS:
An 85-year-old male with colon carcinoma status post hemicolectomy complicated by metastasis to the liver status post chemotherapy and resection presented to the ED with intermittent abdominal discomfort for 2 weeks. Laboratory values were significant for WBC count of 16,000 with a predominance of granulocytes at 85%. CT of the abdomen and pelvis demonstrated a large, 7.6 cm by 5.3 cm, collection in the liver, likely an abscess. Infectious Diseases was consulted and recommended initiation of Meropenem and Daptomycin, in addition to drainage of the collection. The suspected abscess was drained by IR and Streptococcus gordonii sensitive to Linezolid was isolated on bacterial culture. The patient was transitioned to IV Linezolid and Metronidazole given susceptibilities. The patient's WBC count then began trending upwards. CT of the chest exhibited a 1.2 cm by 0.7 cm loculated pleural effusion on the right side. The pleural fluid collection was drained and a chest tube was placed. Studies of the drainage revealed an exudative process, although gram stain and culture were negative. Repeat CT imaging one week later revealed reduction in the size of the liver abscess. The WBC count normalized to less than 10,000 and the patient was discharged with a two-week course of oral Linezolid and Metronidazole with close outpatient follow-up with Infectious Diseases and Oncology.

DISCUSSION:
Pyogenic liver abscesses are generally associated with enteric gram-negative bacilli, Streptococcus milleri group, Streptococcus pyogenes, and Staphylococcus aureus. Hepatic abscesses secondary to periodontal flora have not been demonstrated in the literature without direct trauma to the GI tract involving foreign bodies contaminated with these organisms. We propose a possible hematogenous route of infection likely associated with possible risk factors related to the patient’s occupation as a dentist and history of dental manipulation.
2344 A Case of TACE: A Rare Complication of Transarterial Chemoembolization
Authors: Lorio Eric , Alameri Aws , Wathen Patricia 
Published: October 2019

INTRODUCTION:
Transarterial chemoembolization (TACE) represents a proven therapy providing survival advantage in patients with large, unresectable hepatocellular carcinoma (HCC) not amenable to transplant or ablative therapies. Here we discuss a case of post-TACE liver abscess, a rare complication of this procedure.

CASE DESCRIPTION/METHODS:
A 65-year-old male with 10-year history of alcoholic cirrhosis (MELD-Na 12) presented for follow-up after a recent TACE procedure. Despite initial HCC isolation to segment 3, the patient had refused surgical intervention at the time of initial diagnosis. The mass rapidly enlarged, with new satellite lesions in segments 5 and 6. TACE of the left gastric artery supplying the HCC was performed 7 months after initial diagnosis, with subsequent ultrasound-guided HCC microwave ablation of a 7 cm segment 3 mass. One month after TACE, the patient presented to the emergency department with 2 weeks of weakness, fevers, and an episode of dizziness leading to a fall. Admission studies were notable for marked leukocytosis and blood cultures yielding Streptococcus lutetiensis. The patient was started on broad-spectrum antibiotics and scheduled for further imaging for evaluation of bacteremia source. CT abdomen revealed multifocal hepatic abscesses and a large 7 cm abscess communicating with distal stomach/proximal duodenum. On day 6 of hospitalization, IR placed a CT-guided hepatic abscess drain. Abscess culture was positive for E.coli and Enterococcus, and blood cultures from day after the procedure grew out extended spectrum beta-lactamase E.coli. He was started on a 3-week course of Ertapenem and discharged home with JP drain in place for follow-up in 3 weeks. JP drain was removed 10 days after discharge, and follow-up CT showed a significant decrease in the left hepatic lobe abscess with a small residual collection several centimeters above the drain. Ertapenem was discontinued after total of 5 weeks of antibiotic therapy.

DISCUSSION:
Liver abscess is an uncommon complication of TACE, occurring in about 2% of cases. Here our patient received the recommended therapy of percutaneous abscess drainage and parenteral antibiotics, resulting in a resolution of symptoms. Recognition of this complication is critical, as post-TACE liver abscess mortality has been estimated to be as high as 13.3%. Recent studies have even suggested prophylactic antibiotics when performing chemoembolization, with results showing promise, though this is not currently a routine or recommended practice.
2346 Primary Neuroendocrine Tumor of the Porta Hepatis in a Patient With Crohn’s Disease
Authors: Blau Lance N. , Parikh Rohan B. , Khalid Muhammad U. , Shina James F. 
Published: October 2019

INTRODUCTION:
Well-differentiated neuroendocrine tumors (NETs) are rare entities usually of the GI tract and lung. A small subset of NETs have been identified in the biliary tree and liver, and large majorities of these are identified due to high concentrations of somatostatin receptors. We describe the rare case of a patient with Crohn’s disease and a primary porta hepatis NET.

CASE DESCRIPTION/METHODS:
An 80 year-old female with PMH of Crohn’s disease status post small bowel resection x3 and 30-pack year smoking history presented to clinic with a 5-year history of intermittent RUQ/mid-epigastric pain with known 2 cm liver mass. She denied any weight loss or changes in appetite or bowel habits. Abdominal US revealed a porta hepatis mass with a patent portal vein. Abdominal CT revealed mild diffuse infiltration of the liver and a 4.1 × 3.5 × 3.2 cm porta hepatis mass. The common bile duct measured 10 mm with thickening and irregularity of the antrum, pylorus, and proximal duodenum. There was moderate mesenteric lymphadenopathy. Biopsy of the porta hepatis mass revealed a low/intermediate grade NET of possible GI or pancreatic origin. Urine 5-HIAA was normal, and octreotide scan revealed abnormal activity in the area of the porta hepatis only. EGD revealed H. pylori (+) gastritis, and colonoscopy was normal. The patient underwent exploratory laparotomy revealing biliary invasion and positive metastatic lymph nodes. Open cholecystectomy was performed, and the patient underwent ERCP with common bile duct stent placement.

DISCUSSION:
Well-differentiated NETs are particularly rare. In a National Cancer Institute series, age-adjusted incidence for non-pancreatic primaries was 4.7 per 100,000. Most primary NETs are located in the GI tract (55%) and bronchopulmonary system (30%) and tend to metastasize to the liver. Patients may experience pain, jaundice, early satiety, flushing, or diarrhea. Our patient’s only complaint was pain. Despite an extensive workup to stage the cancer and identify a potential primary, no additional culprit lesion was identified. Immunohistochemical staining and/or molecular classifier assays of the specimen can be helpful to identify the primary site but are not definitive. We believe this is a primary hepatic lesion which is very rare. Metastasis to the biliary tree and hilar lymph nodes portends a poorer prognosis. Our patient was started on Somatuline. Somatostatin analogs are highly effective in controlling symptoms associated with advanced GI NETs.
2347 Acute Liver Failure: Drug-Induced Liver Injury and a Perfect Thyroid Storm
Authors: Harris Patrick , Shoreibah Mohamed 
Published: October 2019

INTRODUCTION:
Acute liver failure (ALF) is a rare but serious condition defined by severe acute liver injury with coagulopathy (INR ≥ 1.5) and encephalopathy without preexisting cirrhosis. ALF carries a high morbidity and mortality. Liver transplantation (LT) is the only definitive treatment for patients that fail other supportive therapies.

CASE DESCRIPTION/METHODS:
A 28 year-old female with hyperthyroidism due to Grave disease was transferred to our institution for acute liver failure (ALF) and transplant evaluation. One month prior, she developed jaundice and pruritus. She had been treated with propylthiouracil (PTU) for 1 year but that was stopped 1 week prior to transfer due to elevated liver enzymes. On evaluation she was found to have elevated AST/ALT (2800/1900), hyperbilirubinemia (28.6) and an elevated INR (2.85). The patient progressively worsened and developed encephalopathy thus fulfilling the criteria for ALF. On admission, her MELD-Na was 33 and she had grade III hepatic encephalopathy. Her thyroid studies were found to be TSH <0.010, free T3 17.9 and free T4 >5.6. Her Burch-Wartofsky Point Scale was >45, which is highly suggestive of thyroid storm. She was subsequently started on plasmapheresis, methimazole, hydrocortisone and cholestyramine for thyroid dysfunction. Patient continued to clinically decompensate requiring an emergent thyroidectomy followed by LT. Post-operatively patient had an acute change in her neurological status with loss of reflexes. CT head showed diffuse global cerebral edema with brainstem compression and herniation. Medical care was withdrawn and patient expired.

DISCUSSION:
This is a case of ALF from PTU drug induced liver injury complicated by thyroid storm. PTU is the second most common non-acetaminophen related cause of DILI that requires liver transplantation. PTU-related ALF can occur at any point of treatment and the onset is usually sudden with rapid progression. While extremely rare, thyroid storm is also a reported cause of ALF. Excess thyroid hormone may cause hepatocyte dysfunction. This case poses a diagnostic dilemma given the coexistence of thyroid storm and PTU therapy. It is possible that the initial hepatic injury due to PTU-related DILI made the liver more susceptible to fulminant hepatic failure from thyroid storm. Despite the rapid listing and transplantation within 48 hours of arrival, the patient did not survive. This case extends the spectrum of the presentation of ALF in the setting of thyroid dysfunction.
2348 A Rare Case of Biktarvy-Induced HBV Flare
Authors: Gujjula Srilaxmi , Barakat Mohamed , Misra Jaideep , Aloreidi Khalil , Berkowitz Leonard , Reddy Madhavi 
Published: October 2019

INTRODUCTION:
Exacerbation of chronic hepatitis B virus (HBV) is defined as an acute rise in alanine aminotransferase (ALT) more than five times the upper limit of normal. Flare-ups of chronic HBV and human immunodeficiency virus (HIV) coinfection receiving antiretroviral therapy is seldom due to discontinuation or initiation of emtricitabine treatment. Here, we present a rare case of reinitiation of Biktarvy causing HBV flare.

CASE DESCRIPTION/METHODS:
A 53-year-old male presented to the emergency department from infectious disease clinic for worsening transaminitis, nausea and right upper quadrant (RUQ) pain for two days. Patient did not report any alcohol, supplement or acetaminophen use. Past medical history is significant for HIV and chronic HBV. He had been non-adherent to Biktarvy (bictegravir, emtricitabine, tenofovir alafenamide) for months and was restarted on the medication three weeks prior to presentation. His vitals were within normal limits. Physical examination revealed RUQ tenderness. Complete blood count showed platelet count of 137K. Coagulation study, basic metabolic panel, lipase were within normal limits. HBV Viral load: 7,126,237, HIV Viral load: undetectable, aspartate aminotransferase (AST): 599, ALT: >680. Hepatitis panel showed immunity to Hepatitis A, Hepatitis C: negative, HBV surface antigen: positive, HBV core IgM: positive and no seroconversion of Hep Be antigen to antibody. All viral serologies, HIV, HBV status and transaminases listed in Tables 1 and 2 from former and current admission. Autoimmune and hereditary conditions work up done during current admission were negative (Table 3). RUQ ultrasound was unremarkable. Patient was seen in clinic two weeks later and reported adherence with Biktarvy. Liver enzymes continued to trend down and his symptoms of nausea and RUQ pain subsided.

DISCUSSION:
Emtricitabine is one of the components of HIV regimen of Biktarvy. Treatment flares due to emtricitabine arise only in 5-10% of patients and are usually asymptomatic. Our patient had symptomatic hepatotoxicity after restarting Biktarvy over the span of three weeks. Hepatotoxicity could be due to the variations of viral replication activating immune responses. Even though the flare ups of chronic HBV can be due to initiation of emtricitabine, it is recommended to continue the agent and monitor for down trending pattern of aminotransferases which was depicted in our case.
2350 An Unlikely Presentation of Diffuse Large B-Cell Lymphoma Manifesting as Hepatic Failure
Authors: Pandey Nishi , Truscello David , Parikh Sharan , El Genaidi Hisham 
Published: October 2019

INTRODUCTION:
Primary Hepatic Lymphoma (PHL) is a very rare subtype of Diffuse Large B-Cell Lymphoma (DLBCL), accounting for less than 1% of all cases. In rare instances, a patient can present with fulminant hepatic failure. The prognosis is grim with an average survival of 10.7 days from admission. The mainstay of diagnosis is liver biopsy, which must be performed as early as possible to prevent progression to acute liver failure.

CASE DESCRIPTION/METHODS:
A 55-year-old male with no pertinent medical history presented with a two week history of abdominal pain, fever, lethargy and mild jaundice. He was a former smoker and drinker who denied any alcohol use for the past 15 years. Upon presentation, the patient’s labs showed acute liver injury, anemia, thrombocytopenia and acute kidney injury. The patient’s model for end-stage liver disease (MELD) was 29. He was subsequently admitted to the medical intensive care unit (ICU) where emergent liver transplant evaluation was initiated. A full work up for the etiology of his liver failure was initially unrevealing so a liver biopsy was performed, which came back positive for DLBCL. The patient was then started on a chemotherapeutic regimen consisting of cyclophosphamide, vincristine, etoposide and high dose steroids. The patient’s condition further deteriorated during his ICU stay, leading to the need for mechanical ventilation, vasopressor therapy for circulatory shock, continuous renal replacement therapy for worsening renal failure and transfusion of blood products for worsening coagulopathy. Despite all of these aggressive measures, the patient’s clinical status only continued to worsen. The family decided to institute comfort measures and the patient died on ICU day 12.

DISCUSSION:
DLBCL predominantly affects Caucasian men over the age of 50. Some viruses, specifically EBV, HBV and HCV, have shown correlation with Non-Hodgkin Lymphoma (NHL); our patient had serologies indicative of past exposure to EBV and HBV. The only way to definitively diagnose DLBCL is via liver biopsy with immunohistochemical staining that reveals CD20, CD45 and BCL-6. The prevailing treatment modality is the use of Dose Adjusted Etoposide, Prednisone, Oncovin, Cyclophosphamide, Hydorxydauorubicin and Rituximab (DA-EPOCH R) Therapy. Due to its poor prognosis, early diagnosis and initiation of treatment for PHL is crucial. For this reason, it must be considered early in the differential when evaluating a patient with acute liver failure.
2351 NAC of All Trades: Use of N-acetylcysteine in Cocaine-Induced Acute Liver Failure
Authors: Bill Katherine , Chaar Abdelkader , Barawi Mohammed 
Published: October 2019

INTRODUCTION:
Among patients with acute liver failure (ALF), drug-induced liver injury (DILI) presents a challenging clinical syndrome with limited therapeutic options. N-acetylcysteine (NAC) is a mainstay of treatment in acetaminophen-induced ALF, acting as an antioxidant, a vasodilator and a glutathione precursor. However, it has been used with success in other toxic ingestions causing ALF, and its beneficial effects do not seem to be unique to acetaminophen-induced hepatotoxicity. We present a case of ALF after acute cocaine ingestion with rapid recovery after administration of IV NAC.

CASE DESCRIPTION/METHODS:
A 58 year-old-male with a past medical history of chronic hepatitis C without cirrhosis and polysubstance abuse presented with acute psychosis. On arrival he was tachycardic but hemodynamically stable, with psychomotor agitation and fear delusions. He endorsed recent heavy cocaine ingestion. Initial labs demonstrated acute kidney injury, rhabdomyolysis and mild transaminitis; AST 59, ALT 56. Toxicology workup was positive for cocaine with undetectable acetaminophen, ethanol and salicylate levels. The following day however, he developed fulminant hepatic failure, AST >7000, ALT 2,568 (Figure 1) with progressive coagulopathy, INR 2.14, albumin 2.9, platelets 120. Of note, despite chronic hepatitis C, there was no evidence of cirrhosis and preserved liver synthetic function at presentation, INR 1.10, albumin 4.7, platelets 254. Our patient was not a candidate for liver transplant (LT), and decision was made to initiate IV NAC therapy, 140 mg/kg bolus followed by 70 mg/kg daily. Transaminases rapidly normalized after only 3 days of therapy, and he was discharged in stable condition.

DISCUSSION:
ALF is a rare but challenging syndrome, for which LT is the only curative treatment available. NAC is well established as an antidote in acetaminophen ALF, yet its mechanisms are applicable to other forms of DILI as well. Cocaine hepatotoxicity has been reported in humans, and is well studied in animal models. Studies in mice suggest toxic metabolites play a critical role, much like acetaminophen ALF. These species deplete glutathione, decrease hepatic blood flow, generate reactive oxygen species and cause lipid peroxidation of membranes. We present a case of ALF secondary to cocaine ingestion in the setting of underlying chronic hepatitis C, with rapid recovery after fluid resuscitation and IV NAC. NAC therapy has minimal adverse effects, and may be lifesaving in patients with ALF who are not candidates for LT.