bluuebunny/crossref_metadata_2025 huggingface dataset:
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.
2428 Direct Intrahepatic Portocaval Shunt (DIPS) as a Therapeutic Option in Acute Variceal Hemorrhage
Authors: Tripathi Alok , Tavri Sidhartha , Cohen Stanley Martin
Published: October 2019

INTRODUCTION:

Direct Intrahepatic Portocaval Shunt (DIPS) is a modified transjugular intrahepatic portosystemic shunt (TIPS) procedure, in which a stent is placed across the inferior vena cava directly into the portal vein under intravascular ultrasound guidance. DIPS is a recognized salvage therapy for acute variceal hemorrhage, but not commonly utilized. Indications for DIPS include patients with hepatic venous anomalies not amenable to TIPS, distorted post-surgical vascular anatomy of the liver, intrahepatic portal venous thrombus, or a prior failed TIPS.

CASE DESCRIPTION/METHODS:

A 73-year-old male with a history of cirrhosis from alcohol and hepatitis C virus and right lobe hepatocellular carcinoma status-post laparoscopic microwave ablation presented with hematemesis. An EGD revealed a gastric varix (Figure 1), which was deemed too large for treatment with cyanoacrylate glue deposition. A TIPS was attempted but failed due to hepatic venous anomalies. Subsequently, the varix was treated with a balloon-occluded antegrade transvenous obliteration (BATO) and a balloon occluded retrograde transvenous obliteration (BRTO). Figure 2 demonstrates the BATO, which coiled the afferent vessels to the varix (red arrow), and the BRTO, which coiled the efferent gastro-renal shunt of the varix (blue arrow). Two days after the BATO/BRTO, the patient had recurrent melena and anemia. An EGD doppler-guided glue deposition into the gastric varix was attempted but failed. A TIPS was not a viable option as an ultrasonography revealed a new portal vein thrombus extending into the anterior and posterior branches of the right portal vein. Thus, a DIPS was performed. Under intravascular ultrasound guidance, a catheter (red arrows) was advanced from the IVC directly to the left portal vein creating a shunt with stent placement as seen in Figure 3. The pre-procedure portosystemic gradient was 18 mm Hg, and post-procedure portosystemic gradient was 5 mm Hg with a reduction in the gastric varix. The patient is well three-months post-procedure without recurrent melena or anemia.

DISCUSSION:

This case demonstrates the successful utilization of DIPS in a patient where TIPS was not feasible due to hepatic venous anomalies and a portal vein thrombus. Furthermore, DIPS was successful in the treatment of a variceal hemorrhage when other therapies such as cyanoacrylate glue deposition, BATO, and BRTO failed. Therefore, DIPS should be utilized in challenging cases of variceal hemorrhage when performed by an experienced interventional radiologist.
2430 Placental Site Trophoblastic Tumor—Unusual Cause of Nodular Regenerative Hyperplasia and Portal Hypertension: Case Report
Authors: Gebreselassie Agazi , Laurine Jacqueline
Published: October 2019

INTRODUCTION:

There are various causes of non-cirrhotic portal hypertension which can be classified as pre hepatic, intra hepatic and post hepatic. One of the causes of idiopathic non cirrhotic portal hypertension is nodular regenerative hyperplasia (NRH). There are various disorders which are associated with NRH. We report a case of placental site trophoblastic tumor as a cause of NRH and portal hypertension.

CASE DESCRIPTION/METHODS:

A 36 years old Caucasian female with no known medical illness presented with progressive abdominal swelling of 5 months duration. She had a normal vaginal delivery to a healthy baby one year back. She gained almost 40 pounds since she started to notice abdominal distention. She has no history of alcohol intake or medication use. On physical examination she had markedly distended abdomen, with fluid wave and small umbilical hernia. She had Pitting edema of 3+ in the extremities. Investigations revealed that the platelet count was 114, Sodium 124, ALT 41, AST 46 and albumin 2.6. Otherwise white cell count, hemoglobin, bilirubin, PT and INR values were within normal limit. Viral hepatitis panel and work up for other causes of chronic liver disease were unrevealing. Abdominal ultrasound showed ascites and mild splenomegaly. It also showed a normal liver echotexture, no ductal dilatation and a patent portal vein. Ascitic fluid analysis was suggestive of portal hypertension with SAAG of 2. Transjugular liver biopsy was suggestive of nodular regenerative hyperplasia. Portal pressure was elevated at 11 mmHg. On abdominal CT scan an incidental enlarged heterogeneous uterus with prominent sub endometrial and parametrial vessels was noted. Serum HCG was high (762). Subsequent hysteroscopy and endometrial biopsy revealed trophoblastic maturation suggestive of trophoblastic tumor. PET scan showed that the disease was limited to the uterus. The patient underwent total hysterectomy with bilateral salpingectomy. She was also treated with three cycles of chemotherapy. The patient experienced total resolution of here symptoms. Four months after her surgery the patient continues to be symptom free with resolution of ascites and leg swelling without any medications.

DISCUSSION:

Idiopathic non cirrhotic portal hypertension can be associated with a variety of conditions including hematologic, neoplastic, immunogenic and medication related. To our knowledge, this is the first report of nodular regenerative hyperplasia associated with trophoblastic tumor.
2431 Legionella Pneumonia Masquerading as Acute Hepatitis and Rhabdomyolysis
Authors: Gudipally Sindusha , Bhatt Harsh , Salas Noain Jesus M. , Modi Simple
Published: October 2019

INTRODUCTION:

Legionella pneumonia commonly presents with myalgia, fatigue, and dyspnea and accounts to about 10-15% of all pneumonia cases. With less than 100 unusual cases of Legionella reported, this is a unique presentation with fulminant hepatic failure, acute kidney failure, and rhabdomyolysis.

CASE DESCRIPTION/METHODS:

52-year-old African-American male with no medical history presented to the emergency room with nausea, diarrhea, and fatigue. He was febrile and tachycardic on presentation. On further evaluation, he reported exposure to a new air-conditioner at work. Chest x-ray (CXR) revealed a right lower lobe pneumonia. Blood work was remarkable for elevated liver enzymes, hyponatremia, acute kidney injury, and elevated creatinine phosphokinase (CPK). His urine drug screen and alcohol level was normal. Liver ultrasound (US) showed fatty infiltration, but no cirrhosis, confirming his social history of being non-alcoholic. Hepatitis (A, B and C), Cytomegalovirus (CMV) IgM and HIV serologies were all negative. Patient was started on fluid resuscitation and antibiotics. Despite a lobar consolidation, Legionella urine antigen returned positive. This confirmed Legionella induced fulminant liver failure and rhabdomyolysis. Patient later developed respiratory symptoms and his repeat Chest x-ray revealed patchy infiltrates in multiple regions, consistent with Legionella. His liver enzymes and CPK trended down, and he was discharged home. He was followed as outpatient with resolution of the fatty infiltration on the Liver US.

DISCUSSION:

Legionella is transmitted through inhalation of aerosols derived from water or soil. It mimics alcoholic hepatitis and is distinguished from other types of hepatitis by having no evidence of cirrhosis. Presentation with gastro-intestinal symptoms, consolidation on imaging, rhabdomyolysis, and acute kidney injury makes Legionella hepatitis most likely etiology. Exact mechanism is still unclear; however, release of endotoxins and bacterial invasion have been reported in many studies. Diagnosis is made with rapid PCR or urine antigen. Levofloxacin or Azithromycin are the preferred antibiotics as these agents are bactericidal, achieve high intracellular concentrations, penetrate lung tissue, and are active against all sub-type species. Treatment usually is for 7-10 days but for immunocompromised patients is 14 days due to risk of re-infection and relapse. Legionella should be high in the differential with the other hepatitis causing diseases like HIV, Hepatitis A, B or C and CMV.
2437 Solitary Fibrous Liver Tumor Diagnosed With EUS-Guided Fine-Needle Biopsy: Case Review
Authors: Nieto Jose , Marriott Denisse , Arévalo Martha
Published: October 2019

INTRODUCTION:

Attaining SFLT's diagnosis is challenging as there are no specific clinical nor radiological characteristics to follow. Therefore, diagnosis is mainly sought based on histologic features (vascularity, mitosis, necrosis, etc.). We report a case of SFLT in a 73-year-old female diagnosed serendipitously by Endoscopic Ultrasound (EUS) - Fine Needle Biopsy (FNB), histologic, and immunophenotypic findings combined.

CASE DESCRIPTION/METHODS:

A 73-year-old female patient presented with moderate RUQ abdominal pain for 1 month and pristine lab work. Patient denied relevant past medical history. MRI with and without contrast, showed a 12.8 cm × 11.2 cm mass in the anterior segment of the right hepatic lobe and no signs of hepatic steatosis. The diagnosis was made by an EUS-FNB ambulatory procedure performed with a 19-g needle. EUS disclosed a hypoechoic and heterogenous mass and non-alcoholic steatohepatitis (NASH). FNB preliminarily showed a spindle cell lesion. The combined histologic and immunophenotypic findings were: Vimectin and CD34 positive; Smooth Muscle Actin – rare faint positive staining. Prognostication was deferred for the resection of the specimen. Metastasis were to be excluded clinically.

DISCUSSION:

Less than 100 cases of SFLT have been reported worldwide. Classically, it presents itself as benign, predominantly in females around the 5th decade, and with a 2:1 female:male ratio. Clinically, it is mainly asymptomatic, or it can depict constitutional symptoms when malignant. Radiologically, suggestive findings are non-diagnostic; making histopathological features (i.e., spindle shaped cells) critical markers to reach a diagnosis. EUS - FNB yields an advantage over Fine Needle Aspiration (FNA) in diagnosing tissues which require immunohistochemical staining - such as this one - in two ways: FNB renders a core biopsy sample (preserved tissue architecture) and is more affordable; whereas FNA requires bedside rapid onsite evaluation, increasing the overall cost. Surgical resection, adjuvant chemotherapy, and radiotherapy may be required for an effective treatment. In our case study, the patient was a 73-year-old female, which is an uncommonly reported age population. Therefore, despite SFLT's infrequent presentation, this entity should be considered in the differential diagnosis of liver tumors. Lastly, EUS-FNB is a safer and affordable procedure to reach SFLT's definitive diagnosis in comparison to other more invasive/expensive methods (i.e., Percutaneus Liver Biopsy, EUS-FNA respectively).
2440 Acute Hepatitis C in an Elderly Woman With No Risk Factors: A Rare Presentation
Authors: Bhardwaj Gaurav , Boroda Konstantin , Hertan Hilary
Published: October 2019

INTRODUCTION:

An estimated 4.1 million people of US have been exposed to hepatitis C (HCV), 70% of which were born between 1945 and 1964, known as the “baby boomer” cohort. While a majority of patients with acute HCV go undetected, 15% present as acute hepatitis.

CASE DESCRIPTION/METHODS:

A 77 year old woman presented with right upper quadrant pain, jaundice, loss of appetite and malaise for 2 weeks. She denied recent travel, alcohol or drug use, prior blood transfusions, acetaminophen ingestion and use of herbal supplements. Her exam was remarkable for scleral icterus and RUQ tenderness. Initial laboratory data showed normal chemistry and blood counts. Her liver tests disclosed ALP 128 U/L, AST 1,348 U/L, ALT 1003 U/L, total bilirubin 8.2 mg/dL, direct bilirubin 6.4 mg/dL and INR 1.4 consistent with acute hepatitis. Infectious workup was positive for HCV genotype 1b with a viral load of 27.2 M IU/mL. Ultrasound of the abdomen showed normal liver and biliary tree. Immunological workup was positive for anti-smooth muscle antibody 1:40 titer and elevated IgG at 2,070 mg/dL raising a concern for a concomitant autoimmune hepatitis (AIH). Patient's liver tests continued to climb and she had prolonged abdominal pain, so liver biopsy was performed. It showed moderate lobular lymphoplasmacytic and neutrophilic inflammation with marked hepatocellular injury and areas of hepatocyte loss consistent with active HCV hepatitis (Figures 1 and 2). She was then discharged and immediately started on sofosbuvir-ledipasvir and eventually achieved sustained virologic response.

DISCUSSION:

Acute HCV infection is usually transmitted via needle-stick injury or injection drug use. It is uncommon in elderly patients, however in nursing home residents, it is attributed to parenteral medications, hemodialysis and poor adherence to infection control measures. Our patient was from the community and it is not clear how she was exposed to HCV. Acute HCV hepatitis in elderly patients can be severe, occurring 2 to 26 weeks after exposure. Aminotransferases are often greater than 10 to 20 times normal; bilirubin may be elevated as well. Although HCV is known to induce AIH, the features of acute hepatitis can be mistaken for AIH. A biopsy aids in discerning these two entities with very different treatment strategies. Generally, a waiting period of 12 weeks is instituted to allow for spontaneous viral clearance, but immediate treatment can be initiated in cases of elderly patients with severe presentations.
2441 Hepatotoxicity by Methoxsalen: The Innocuous Culprit
Authors: Aujla Amreet K. , Gill Guneetinder S. , Shah Nihar , Pratt Perry , Hoffman Martin
Published: October 2019

INTRODUCTION:

Drug-induced liver injury (DILI) is the second most common cause of acute liver failure; 15-20% cases of DILI can be attributed to damage caused by herbal or dietary supplements. Methoxsalen, commonly known as psoralen, is the active ingredient in Bakuchi seeds and is used for treatment of vitiligo and psoriasis. DILI caused by Psoralen is rare, with only three cases reported in literature. This case demonstrates the importance of eliciting a history of herbal supplement use in patients with acute liver failure and the need for regulation of herbal supplements.

CASE DESCRIPTION/METHODS:

A 60-year-old female presented with two-week history of jaundice and right upper quadrant pain (RUQ). She started taking Bakuchi seeds four weeks prior to presentation and would apply it topically and consume it daily. Patient denied history of alcohol use, blood transfusions, or illicit drug use. Physical exam was notable for scleral icterus and jaundice. Labs revealed abnormal liver function tests (LFTs) (Figure 1) with a peak total bilirubin of 19 mg/dL and a MELD-Na on admission of 19. Work up revealed positive anti-smooth muscle antibodies and AFP elevation to 15.9 ng/mL. Pertinent negatives included viral hepatitis serologies, HSV, EBV, factor V activity, and hemochromatosis. A RUQ ultrasound showed no abnormalities. An MRI abdomen was done which revealed mild periportal edema and mildly dilated common bile duct without choledocholithiasis or obvious mass. Given concerns for DILI, patient was started on acetylcysteine. Hospital course was complicated by episodes of confusion; an ammonia level was elevated at 75 umol/l. Patient was started on lactulose. Because patient's LFTs improved with a stabe PT/INR of 12/1.2, she did not meet criteria for a liver transplant. A liver biopsy was performed which revealed submassive necrosis and collapse; hepatitis with plasma cells and eosinophils with significant cholestasis. Given biopsy results consistent with DILI, patient was discharged on oral prednisone and lactulose to follow up with hepatology in one week.

DISCUSSION:

LFT abnormalities were seen in 2% to 12% of subjects taking psoralen; the elevations were mild-moderate in severity, asymptomatic and self-limited in course with recovery of LFT seen in 6 to 8 weeks. However, severe jaundice and death from hepatic failure has been described in patients with preexisting cirrhosis. This case emphasizes the need for increased surveillance to formulate guidelines regarding regulation and use of herbal supplements.
2444 Beyond Weight Loss: Bariatric Surgery as Treatment for NAFLD in the Post-Transplant Patient
Authors: Hashmi Irma , Anjelly David , Zacharias Isabel
Published: October 2019

INTRODUCTION:

Bariatric surgery, including Roux-en-Y gastric bypass (RYGB) and laparoscopic sleeve gastrectomy (LSG), has previously demonstrated reversal of abnormal liver histology in non-alcoholic fatty liver disease (NAFLD). However, bariatric surgery following orthotopic liver transplant (OLT) performed for non-alcoholic steatohepatitis (NASH) cirrhosis is less well studied, with only a few retrospective studies cited in the literature. We present the case of bariatric surgery performed in a patient status post OLT with successful reversal of NAFLD.

CASE DESCRIPTION/METHODS:

The patient is a 69-year-old female with past medical history of metabolic syndrome (diabetes, hypertension, dyslipidemia, obesity) and cirrhosis secondary to NASH and alcohol who underwent deceased donor OLT. Eighteen months postoperatively, the patient had gained 20 pounds and required multiple medications to control her blood pressure and diabetes. Subsequent abdominal ultrasound with doppler demonstrated hepatic steatosis, patent transplant vasculature and no ascites. Despite dietary and lifestyle modifications, the patient could not lose weight. She continued to have elevated transaminases (up to aspartate aminotransferase 58, alanine aminotransferase 82) prompting suspicion for recurrent NASH. The patient was ultimately referred for LSG. Her BMI prior to LSG was 37; seven weeks postoperatively it decreased to 32. Her liver function test normalized, and she no longer required Metformin.

DISCUSSION:

NAFLD is the most common chronic liver disorder in developed countries, and NASH cirrhosis is the second most common cause for liver transplant in the United States. Approximately 3-5% of the population in the United States lives with NASH, and this number is expected to rise with the obesity epidemic. Further troubling is NASH and cryptogenic cirrhosis seen in post-OLT patients, with one study citing 39% of those transplanted for NAFLD-related cirrhosis show steatosis on biopsy six months after transplant. Bariatric surgery, both RYGB and LSG, can reverse NAFLD histology, and only recently have retrospective reviews examined bariatric surgery as a successful means of halting and reversing NAFLD in the post-transplant patient. As with the case of our patient, bariatric surgery can provide an effective means of treating NAFLD in the post-OLT patient with metabolic syndrome. More research is currently needed to establish optimal patient selection criteria and long term efficacy in this regard.
2447 A Case of Daptomycin Causing Drug-Induced Liver Injury
Authors: Gurm Hashroop , Bekele Ezana , Arefiev Yevgeniy , Mohanty Smruti R.
Published: October 2019

INTRODUCTION:

Drug-induced liver injury (DILI) is the most common cause of acute liver failure. DILI is rare and characterized by elevated creatinine kinase (CK) and liver enzymes without associated end-organ damage. We present a rare case of daptomycin associated hepatotoxicity without corresponding elevation in CK.

CASE DESCRIPTION/METHODS:

A 87-year-old man with a history of hypertension, hyperlipidemia, benign prostate hyperplasia, closed fracture of distal lateral malleolus of left ankle, and atrial fibrillation on apixaban presented to the ED from rehab facility with complaints of one day of shortness of breath, cough, diarrhea, and nausea. Patient was a poor historian. He also has had poor oral intake. He was unable to state if he had any prior gastrointestinal problems. No tobacco, alcohol, illicit drug use. On physical examination, patient was noted to have mild purulent drainage on plantar surface of right fifth metatarsal phalangeal joint. A CT scan of foot ruled out osteomyelitis. On admission, labs revealed elevated transaminases with AST 113, likely due to congestive hepatopathy, as per echocardiogram with elevated right ventricular systolic pressure. All other liver enzymes were within normal limits. Blood cultures resulted in Methicillin-sensitive Staphylococcus aureus (MSSA) bacteremia and he was subsequently started on vancomycin (due to penicillin allergy). After 7 days of vancomycin therapy, he was switched to daptomycin due to the rising creatinine levels. Next 5 days, LFTs trended up dramatically with the initiation of daptomycin. All non-essential medications were discontinued at this time. LFTs peaked at total bilirubin 1.4, AST 432, ALT 535 and alkaline phosphatase (AP) 161. CK was normal. At this time, daptomycin was discontinued. LFTs started a steep downtrend one day after cessation of daptomycin (Figure 1). The rise in creatinine, total bilirubin, and initial CK levels were temporally related to the initiation of vancomycin infusions (Figure 2). Autoimmune work up and hepatitis panel were all negative. An abdominal ultrasound showed hepatomegaly (16.5 cm) with diffuse hypoechoic texture. Liver doppler showed normal flow.

DISCUSSION:

Daptomycin induced hepatotoxicity without evidence of elevated CK levels is rare. The pathophysiology is unclear. There is limited literature on DILI without renal failure or rhabdomyolysis in setting of daptomycin use. We only found one case in literature. The long-term sequela has not been fully studied, thus liver enzymes should be monitored closely.
2448 Late Hepatic Artery Thrombosis Causing Bowel Ischemia
Authors: Garrido Daniel , Halegoua-DeMarzio Dina
Published: October 2019

INTRODUCTION:

Hepatic artery thrombosis (HAT) is a potentially life-threatening complication following orthotopic liver transplantation (OLT). HAT can be further classified as early-onset HAT (EHAT), occurring <30 days after OLT or late-onset HAT (LHAT), occurring >30 days after OLT. Symptoms include elevated transaminases, fever, abdominal pain, nausea and vomiting. We report a rare case of LHAT in a liver transplant recipient 8 years status post from OLT presenting with atypical symptoms.

CASE DESCRIPTION/METHODS:

A 58-year-old male with a history of hepatitis C virus (HCV) cirrhosis with OLT in 2011, with sustained virologic response (SVR) s/p HCV treatment, presented with severe left-sided abdominal pain and fever. Laboratory data was remarkable for leukocytosis and a mild elevation in transaminases. Due to concern of possible sepsis, he was initially treated on broad-spectrum antibiotics. Subsequent abdominal ultrasound was unable to visualize the hepatic artery, which was confirmed with CT angiogram showing cut off of the transplant hepatic artery 8 mm from its origin as well as a small right lobe infarct. He was started on anticoagulation but three days later he had worsening fever, increasing oxygen requirement, and markedly elevated transaminases. Interventional radiology attempted catheter directed thrombolysis, however this failed. Over the course of the following weeks, his transaminases started to decline, but he continued to have several days of low-grade fevers, secondary to hepatic necrosis.

DISCUSSION:

This case provides an atypical presentation of HAT in a distant status post OLT patient. The etiology of late HAT remains unclear despite multiple reviews of literature. The overall incidence of late HAT is as low as 2.1%, and the likelihood of occurring years later is even lower. In our patient, despite his distant OLT, he presented with a unique presentation of LHAT, masquerading as a sepsis-like picture. This case demonstrates the importance of considering HAT in patients with a distant OLT presenting with abdominal pain. Identifying this could help us stratify these patients for consideration of re-transplantation and appropriate treatment. A recent study demonstrated that conservative management of late HAT patients with only minor complications was deemed safe. In the case of our patient, due the improving nature of his condition, he was ultimately treated conservatively and monitored on an outpatient basis.
2449 The Great Mimicker Syphilis and a Case of Hepatitis
Authors: Raman Daya
Published: October 2019

INTRODUCTION:

Early syphilitic hepatitis during the stage of secondary syphilis is often an overlooked presentation of syphilis. Liver involvement occurs in 0.2–3% of patients with syphilis.
1

CASE DESCRIPTION/METHODS:

Here, we present the case of a 31 yr old male with type 1 diabetes and hyperlipidemia who presented with epigastric abdominal pain that began on morning of admission. Patient denied any change in bowel movements and, on initial exam, was found to be tachycardic and hypotensive. On physical exam, patient had tenderness in the epigastrium without any skin changes noted. On evaluation of lab work, patient was found to be in DKA with moderately elevated LFTs, ALP 273, AST 400 and ALT 200, Bilirubin 0.2. Hepatitis panel and Acetaminophen level were negative. A right upper quadrant ultrasound was performed that did not show any evidence of cholelithiasis or passed stone. Patients DKA resolved one day into admission, however AST/ALT more than doubled from admission to 4000/1000 respectively, with rising ALP of 320. Bilirubin remained normal. Given elevated liver enzymes, there was concern for possible passed stone and therefore MRCP was pursued. MRCP showed incidental finding of hepatomegaly without any evidence of cholelithiasis. Acute hepatitis panel was also found to be negative. On further history, patient reported that he did engage in unprotected sexual intercourse approximately 1 month prior, with another male. Patient's abdominal pain resolved and he was discharged with HIV, HSV, RPR, GC Chlamydia studies pending. Lab workup revealed RPR to be reactive, 1:16 TU with reactive Treponema pallidum particle agglutination assay (TPPA), and negative HIV testing. Patient was diagnosed with secondary syphilis with hepatitis and treated with Benzathine Penicillin 2.4 MU IM in 2 divided doses. AST/ALT trended down to 116/43 and ALP 242.

DISCUSSION:

This case highlights the critical importance of a broad differential in workup of hepatitis.