bluuebunny/crossref_metadata_2025 huggingface dataset:
2274 Splenic Infarction in Alcoholic Hepatitis
Authors: Aijazi Muaz , Gill Brendan , Kalaria Arjun , Ahuja Ashish
Published: October 2019

INTRODUCTION:

Case reports can be found in the literature describing elderly cirrhotic patients developing splenic infarctions (1,2). Herein, we describe a relatively young female who developed splenic infarction likely secondary to alcoholic hepatitis (AH).

CASE DESCRIPTION/METHODS:

A 40-year-old Caucasian female with past medical history of alcohol abuse and irritable bowel syndrome presented with jaundice, nausea, and vomiting. Laboratory showed ALT 54, AST 246, alkaline phosphatase 589, total bilirubin 14.0, INR 1.9, and ethanol level 240. WBC count was elevated to 20,900 with a 92% neutrophilic predominance. Leukocytosis was initially thought to be secondary to UTI as she also presented with urinary symptoms and urinalysis concerning for UTI. After a 5 day course of IV ceftriaxone, her WBC count decreased only to 18,400. Her abdominal exam began to worsen. RUQ ultrasound showed hepatic steatosis. CT scan with contrast showed moderate hepatomegaly and borderline splenomegaly with mild ascites. Abdominal pain, leukocytosis, and total bilirubin continued to worsen. Because of her severe abdominal pain and WBC count >50,000 despite a 7-day course of meropenem, contrast CT scan was repeated. At this time, lesions in the spleen concerning for infarction were seen. From here on, she was managed conservatively and her condition improved until discharge.

DISCUSSION:

Splenic function has been shown to decrease in patients with AH, but the exact pathophysiology is unclear (3). Splenic infarctions have been described in the literature in cirrhotic patients with co-morbidities (e.g. primary biliary cirrhosis), but to the authors’ knowledge there is not much mention in the literature of spontaneous splenic infarction in AH. In the right clinical context, physicians should consider splenic infarction in AH patients, especially in those with persistent leukocytosis which could be classified as a leukemoid reaction. Our report shows splenic vasculature infarction may be worth investigating in the future as an explanation for hyposplenia in AH.
2280 Propafenone-Induced Hepatocellular and Cholestatic Injury
Authors: Rivas Cynthia , Castano Juan J. , Pozo Leonardo , Huang Rex , Rapoport Grigoriy , Zamir Asif
Published: October 2019

INTRODUCTION:

Propafenone, an antiarrhythmic medication, decreases cardiac automaticity and increases refractory periods slowing cardiac conduction. Propafenone-induced hepatic injury is rare with only eight reported cases in the literature. We report a case of propafenone-induced hepatic injury in a patient presenting with painless jaundice.

CASE DESCRIPTION/METHODS:

A 60-year-old woman presented with sudden onset jaundice and a one week history of 10-pound weight loss, right upper quadrant abdominal pain, nausea and vomiting. Two months prior to presentation, she was diagnosed with atrial fibrillation and was begun on Propafenone 325 mg oral twice daily. She had no history of alcohol, drugs, or herbal medication use. Physical exam was significant only for generalized jaundice. On admission, laboratory studies were significant for AST 304 IU/L, ALT 601 IU/L, ALP 334 IU/L, total bilirubin 7.9 mg/dL, and direct bilirubin 5.4 mg/dL.Abdominal ultrasound revealed fatty liver without biliary obstruction. CT abdomen was unremarkable for hepatic or biliary pathology. Viral serologic markers and acetaminophen levels were negative as well as workup for Autoimmune hepatitis, and Primary biliary cholangitis. Liver biopsy revealed steatohepatitis with superimposed ductular and centrilobular cholestasis suggestive of drug-induced injury.The patient was begun on N-Acetylcysteine and Propafenone was discontinued. Several days after withdrawal of Propafenone, liver function tests began to improve slowly. The patient was discharged home and one month later, transaminases returned to normal and jaundice had resolved.

DISCUSSION:

Propafenone is a Class 1C antiarrhythmic indicated for symptomatic atrial fibrillation without structural abnormalities. The mechanism for hepatic injury is unknown. Like in our patient, the injury is self-limited and has not been linked to acute liver failure, chronic liver injury, or vanishing bile duct syndrome. Once identified as the cause, the medication should be immediately stopped and never prescribed because re-exposure is associated with recurrence of symptoms. As in other reports, our patient’s liver injury occurred within a 2-6-week period after exposure and, resolved 3-5 weeks after cessation of the offending medication. Propafenone-induced hepatic injury should be suspected in a patient presenting with hepatocellular and cholestatic injury, especially in a patient recently begun on that medication after exclusion of other causes of abnormal liver function.
2283 Herpes Simplex Virus Hepatitis in Immunocompetent Hosts - A Case Series Demonstrating the Importance of Early Recognition and Empiric Antiviral Therapy
Authors: Douglas Scott R. , Miller Jennifer , Henry Zachary
Published: October 2019

INTRODUCTION:

Herpes simplex virus (HSV) is a highly prevalent virus but only rarely results in fulminant hepatitis. The prevalence of HSV1 and HSV2 are reportedly 53.9% and 15.7% in the general United States population. However, despite the high prevalence it is only responsible for 1% of all acute liver failure. Immunocompetent individuals represent only 24% of these cases. We present three cases of HSV hepatitis in the presumed immunocompetent host.

CASE DESCRIPTION/METHODS:

Case 1: A 70 y.o male with type II diabetes presented with high fevers. His transaminases peaked at AST 973 and ALT 1183. His INR and T Bili both peaked at 1.4. Due to the anicteric nature of his hepatitis, he was started on empiric acyclovir. He developed nonspecific encephalopathy, later attributed to hospital acquired delirium. Cerebrospinal fluid was negative for HSV. His HSV serum PCR was positive for HSV1 on day 8. He later developed painful oropharyngeal ulcers. His liver enzymes and mental status would normalize. Case 2: A 19 y.o female with osteogenesis imperfecta and lupus (treatment naive) presented after a sexual assault with fevers. She developed right upper quadrant pain and a pustular rash on upper extremities. Her liver enzymes peaked at AST 2,480 and ALT 824 on day five of admission. Her INR and total bilirubin peaked at 2.8 and 1.5, respectively. Due to the anicteric nature of her hepatitis, she was empirically treated with acyclovir. Her serum HSV PCR returned positive for HSV2 on day twenty. Liver enzymes improved and she was discharged on PO valganciclovir. Case 3: A 21 y.o female with history of chlamydial infection presented with a diffuse urticarial rash, fever and right upper quadrant pain. Her AST was 2389 and ALT 1896. Total bilirubin peaked at 1.3. Due to the anicteric nature of her hepatitis, she was empirically treated with acyclovir. PCR of an oral lesion was positive for HSV2 and her serum PCR was positive for HSV2. She recovered completely.

DISCUSSION:

Despite low occurrence rates, our cases demonstrate HSV hepatitis must be kept in the differential diagnosis of hepatitis in the immunocompetent host. Progression to acute liver failure (ALF) occurs in 74% of HSV hepatitis cases. ALF from HSV has a mortality rate of 90%. Therefore, high clinical suspicion must be maintained for favorable outcomes. Fortunately, our patients had resolution of their HSV hepatitis due to early recognition of anicteric hepatitis and treatment with empiric acyclovir.
2284 Coagulopathy and Jaundice in Alagille Syndrome, Not All That Glitters Is Gold
Authors: Altamimi Barakat Aburajab , Vancura James , Sanchez Antonio J.
Published: October 2019

INTRODUCTION:

Alagille-Watson syndrome is an autosomal dominant disease associated with cardiac, hepatic and kidney abnormalities. Estimated prevalence of disease is 1 in 100,000 live births. Symptoms and severity of Alagille syndrome range from mild to cases requiring organ transplantation.

CASE DESCRIPTION/METHODS:

32-year-old male patient with history of Alagille Syndrome s/p biliary diversion and right hemicolectomy at age 5 who was lost to follow up after he turned 18. Patient known to have Allele 1: 551 G >A (R184H), Allele 2 with no mutation. Patient was admitted to the hospital with one month of worsening jaundice, fever and two episodes of non-bloody vomiting. Pertinent history included alcohol use 6-8 beers over the weekend for several years. Patient had baseline bilirubin of 2.4 and had elevated bilirubin for most of his life. On admission his AST/ALT were 209/143 U/L, bilirubin 18.6 mg/dl, direct 13.6 mg/dl; total bilirubin peaked at 24.4 mg/dl , INR was 10 and PTT was 51s. CBC and chemistries were normal. After vitamin K administration, INR corrected to 1.5. Patient received antibiotics and had negative blood and urine cultures. US done showed splenomegaly. MRCP showed a cirrhotic liver and nondilated bile ducts. Liver biopsy showed biliary cirrhosis, absent interlobular bile ducts, bile stasis and prominent Mallory Hyaline. Patient bilirubin levels improved and patient is currently undergoing liver transplant workup.

DISCUSSION:

90% of patients with Alagille syndrome have bile duct paucity. This usually presents as cholestasis in the first four months of life, in our patient this issue improved with the biliary diversion. However this was complicated by low absorption of fat soluble vitamins. It is likely that infection and alcohol use contributed to his worsening liver disease. Pulmonic stenosis is the most common cardiac anomaly and most patients have classical syndromic facial features and butterfly vertebrae as did our patient. Posterior embryotoxon is also common. Conclusion: While 15% of nontransplanted patients with Alagille disease progress to cirrhosis, this case highlights that common liver diseases are still common in unique patient populations and should always be considered. Our patient alcohol intake contributed to his liver disease, his elevated INR was related to vitamin K deficiency rather than synthetic liver dysfunction, and marked improvement in his liver enzymes followed with alcohol cessation.
2285 HSV Hepatitis in an Immune-Competent Patient
Authors: Francis Pilin D. , Tosounian Shannon L. , Kalman Richard
Published: October 2019

INTRODUCTION:

A rare complication of herpes simplex virus (HSV) infection is hepatitis, especially in an immunocompetent host. It is important to recognize this diagnosis, as HSV hepatitis is potentially fatal if untreated due to the risk of acute liver failure. We present a case of HSV hepatitis in an immunocompetent patient with a benign clinical course.

CASE DESCRIPTION/METHODS:

A 58-year-old female with history of diabetes mellitus, breast cancer with distant history of chemotherapy, presented to the emergency department for one week history of right upper quadrant pain and fevers at home. On presentation she was febrile with a temperature of 39.3 degrees Celcius, blood pressure 118/72 mmHg, heart rate 100 bpm. Physical exam findings included tenderness to palpation of upper quadrants, flanks, and suprapubic area. Laboratory findings revealed alanine aminotransferase (ALT) 139 IU/L, aspartate aminotransferase (AST) 172 IU/L, and alkaline phosphatase 73 IU/L. She was negative for Hepatitis A, B, C, HIV, and influenza. A liver ultrasound showed an enlarged liver (19.5cm) with homogeneous parenchyma and increased echogenicity consistent with hepatic steatosis. The liver contour was smooth and there was no duct dilation. Her liver tests worsened with ALT and AST peaking at 822 and 1558, respectively. Due to persistent fevers, the patient was evaluated for HSV, and was found to be HSV-2 IgM positive (titer >1:320) and HSV-2 DNA was detected. The patient was started on intravenous acyclovir. A liver biopsy showed findings of periportal and pericentral necrosis, favoring infection. An immunohistochemical stain for HSV was positive. She completed 2 weeks of acyclovir, achieving improvement in liver tests to normal range.

DISCUSSION:

HSV is a common infection, but a rare cause of hepatitis, comprising < 2% of cases and < 1% of all causes of acute liver failure. HSV hepatitis is usually described in immunocompromised hosts, pregnant women, and neonates. Presentation is vague, but most commonly with fever, abdominal pain, and only 30% with typical oral or genital lesions. Diagnostic tools are serological testing for HSV and liver biopsy. Treatment with acyclovir is effective in preventing transplant or can be life saving in 51% if initiated promptly, and thus, a high index of suspicion is warranted in patients with appropriate risk factors or with an unclear etiology of severe transaminitis. Given our immunocompetent patient’s relatively benign course, this is a unique presentation of a potentially fatal disease.
2286 Cholestatic Hepatitis as a Paraneoplastic Syndrome of Endometrial Carcinoma
Authors: Wade Francis , Odufalu Florence-Damilola , Prather Charlene , Marsicano Elizabeth
Published: October 2019

INTRODUCTION:

Cholestatic hepatitis is a rare manifestation of both solid organ and hematologic malignancies. It has been reported to occur with ovarian cancer, but not other female genitourinary tract malignancies to our knowledge. We report a case of simultaneous cholestatic hepatitis and acute sensorimotor polyneuropathy as paraneoplastic syndromes of endometrial adenocarcinoma.

CASE DESCRIPTION/METHODS:

A 66-year-old woman with past medical history of newly diagnosed stage IIIC endometrial adenocarcinoma and cholecystectomy presented with ascending bilateral lower extremity weakness and numbness for 14 days. Physical exam revealed bilateral foot drop and distal lower extremity numbness. Patient did not have jaundice or scleral icterus. Laboratory assessment showed ALT 172 U/L (normal < 61 U/L), AST 149 U/L (normal < 40U/L), ALP 243 U/L (normal < 126 U/L), and GGT 461 U/L (normal < 85 U/L). Lumbar puncture showed CSF albuminocytologic disassociation. Further neurologic workup was consistent with an acute sensorimotor polyneuropathy, which was attributed to a paraneoplastic process of her cancer. During investigation of her polyneuropathy, transaminases and ALP continued to rise to peak values of ALT 245 U/L, AST 202 U/L, and ALP 659 U/L so workup of cholestatic hepatitis was pursued. Total bilirubin and INR remained normal. Fractionated ALP showed a majority liver fraction. Infectious, autoimmune, pharmacologic, malignant, metabolic, and drug-induced causes of cholestatic hepatitis were screened for and ruled out. Liver ultrasound with doppler was negative for acute biliary or liver pathology. CT of the chest, abdomen, and pelvis with IV contrast showed a normal liver. Additional workup for cholestatic hepatitis, including liver biopsy, was not pursued as ascending paralysis progressed to paraplegia and patient opted for hospice care. Patient was diagnosed with paraneoplastic, acute cholestatic hepatitis from endometrial adenocarcinoma.

DISCUSSION:

To our knowledge, this is the first case report of cholestatic hepatitis as a paraneoplastic syndrome of endometrial adenocarcinoma. Our patient’s liver injury may have occurred due to paraneoplastic proinflammatory state or tumor antigen-antibody cross reactivity with liver cell antigens, or a combination of both. Gastroenterologists should include paraneoplastic processes of cancer in the differential diagnosis for liver injury, especially when workup of alternative causes is unrevealing.
2288 Diabetic Hepatosclerosis Presenting as Severe Pruritis
Authors: Long Amanda , Yalamanchili Silpa , Heightchew Kimberly , Wong Patricia
Published: October 2019

INTRODUCTION:

Diabetic hepatosclerosis (DH) is an uncommon type of hepatic injury associated with poorly controlled diabetes mellitus (DM). Unlike steatohepatitis or glycogenic hepatopathy, DH is a form of end-organ damage due to microvascular injury. This case illustrates a patient with advanced DM who presented with cholestatic liver injury and histologic findings of DH.

CASE DESCRIPTION/METHODS:

A 34 yo woman with poorly controlled type 1 DM (HgA1C 17%) complicated by diabetic nephropathy presented with one month of generalized pruritis. Symptoms were most severe after hot showers and at night. She denied rash, fevers, unusual exposures, ingestions, or new medications. On exam, she appeared well, had no visible skin lesions, no scleral icterus, and a soft abdomen without organomegaly. Labs were notable for ALP 612 U/L, ALT 205 IU/L, AST 109 IU/L, TB 0.9 mg/dL, WBC 8.3 K/uL, PLT 306 K/uL. Abdominal ultrasound revealed a normal appearing liver and biliary ducts. Ultrasound-guided liver biopsy showed perivenular and perisinusoidal fibrosis without inflammation, steatosis, or bile duct injury. These findings were consistent with DH. After one year of aggressive glycemic control, her pruritus resolved. Her HgA1C was 7.6%, ALP 313 IU/L, ALT 32 IU/L, AST 29 IU/L.

DISCUSSION:

While non-alcoholic fatty liver disease (NAFLD) and glycogenic hepatopathy are more commonly seen in patients with advanced DM, DH is a distinct form of microangiopathic liver injury characterized by dense perisinusoidal fibrosis (Figure 1), lack of steatosis (Figure 2), and basement membrane deposition of laminin and type IV collagen1,2. DH can be seen in both type 1 and type 2 DM, and rarely occurs in the absence of other microvascular complications. DH is characterized by a predominantly elevated ALP, suggesting a primary bile duct or canalicular injury. Diabetics with hypertension seem to be at increased risk for DH3. The long term consequences of DH remain unclear. In our patient, a decrease in HgA1c level resulted in normalization of AST and ALT levels, a marked reduction in ALP, and resolution of pruritus.
2290 A Unique Presentation of Severe Cholestatic Autoimmune Hepatitis With an Associated Biliary Stricture
Authors: Reinhart Evan , Garner Jessica , Jeffries Mark A. , Sing James
Published: October 2019

INTRODUCTION:

Autoimmune hepatitis, usually associated with hepatocellular injury patterns, has rarely been described in current literature presenting with severe cholestasis. Even fewer cases have associated autoimmune hepatitis in patients with Mixed Connective Tissue Disease (MCTD). We describe a rare case report of a young male with suspected MCTD who presented with severe cholestatic autoimmune hepatitis with an associated biliary stricture.

CASE DESCRIPTION/METHODS:

A 33 yo AA male veteran with no significant PMHx presented with a 3 months of RUQ abdominal pain with associated jaundice, fatigue, and subjective fevers. On further review, he endorsed dry mouth, joint pain, and pain in his fingers in cold temperatures. He denied alcohol use, taking herbals or prescription medications. He endorsed travel to Korea. Physical examination was notable for RUQ abdominal tenderness and jaundice. Initial labs were significant for: Bilirubin: 11.6, Alk Phos: 338, AST/ALT: 1086, 116, Tylenol level: below assay, INR 1.2, platelets 213, Ferritin: 6,767, and Ceruloplasmin: 32. Acute viral hepatitis testing for A, B, C, and E were negative. HFE gene mutation was negative. Autoimmune markers included: positive ANA 1:320, positive RNP Ab, positive Smooth Muscle Ab 1:80; elevated IgG subclass 1 (2,010) and IgG subclass 2 (589). RUQ ultrasound and CT Abdomen/Pelvis showed evidence of cirrhosis. MRCP and ERCP revealed: gallbladder distension, cirrhosis of the right hepatic lobe, biliary strictures of the common hepatic and right intrahepatic bile ducts. The biliary stricture brushings were negative for malignancy. Ileocolonoscopy was unremarkable without inflammatory bowel disease. He underwent laparoscopic cholecystectomy with intraoperative liver biopsies. Interestingly, his liver biopsies revealed marked cholestasis with lymphoplasmacytic portal inflammation and minimal fibrosis (stage 1-2) despite imaging suggestive of cirrhosis. Ultimately , these findings were consistent with severe cholestatic autoimmune hepatitis with an associated biliary stricture in a patient with suspected underlying MCTD.

DISCUSSION:

Our patients demographics, travel and pattern of liver injury posed a diagnostic dilemma for diagnosing autoimmune hepatitis. After a thorough evaluation for the etiology, his liver histopathology, positive autoimmune markers, and favorable response to steroids were all compatible with the diagnosis of cholestatic autoimmune hepatitis with a biliary stricture in a patient with suspected MCTD.
2294 The Unusual Wolf in Sheep's Clothing
Authors: Khan Zarak H. , Korpole Pranay R. , Zavoyskikh Anton , Paul Jonathan R. , Misirliyan Roy , Salah Zahra'a , Wolok Ryan
Published: October 2019

INTRODUCTION:

Dronedarone is frequently employed for rhythm control in patients with atrial fibrillation (AF). Chronic therapy with Dronedarone has been associated with mild liver enzymes elevations in up to 12% of patients. There are also several reports of dronedarone induced Acute Renal Failure (ARF) on Adverse Drug Reaction reporting databases worldwide.

CASE DESCRIPTION/METHODS:

An 86-year-old male with past history of AF, COPD, CKD and HTN presented with 1 day duration of dyspnea and palpitations. He was found to be in AF with rapid ventricular response with a heart rate of 127. Vitals were otherwise stable. He was also suspected to have acute on chronic diastolic CHF likely precipitated by atrial fibrillation. Initial labs were pertinent for creatinine of 2.02 (baseline-1.60). Patient was initially started on Diltiazem drip in the ED which was later discontinued due to an IV site reaction. Upon transfer to the medical floor, Cardiology was consulted who recommended Dronedarone for rhythm control. Patient received a total of 3 doses of Dronedarone but did not cardiovert, therefore electrical cardioversion was performed. He developed fatigue few hours after the cardioversion. Liver function tests (LFTs) one day after the last dose of dronedarone and post cardioversion showed elevated ALT (3155), AST (3930), Alkaline Phosphatase (144), total (2.4) and direct (1.0) bilirubin levels. INR was also high (6.1). Viral hepatitis testing was negative. The patient's course was further complicated by acute renal failure (ARF) with creatinine rising to 5.38. Dronedarone mediated hepatic and renal injury was suspected. Dronedarone was discontinued and supportive measures were initiated. Patient's LFTs and creatinine trended down with improvement of symptoms four days following discontinuation of Dronedarone. Patient was discharged home with complete resolution of hepatic and renal failure noted during outpatient follow up.

DISCUSSION:

Dronedarone mediated acute liver toxicity is rare. Almost none of the cases involved rapid onset of liver injury after drug initiation, which resolved quickly after cessation of the agent. The onset of injury in reported cases ranged from 2 to 11 months. Besides reports on pharmacovigilance databases, two cases of dronedarone-associated ARF have also been published, one of which required hemodialysis. Only one of these cases reported a combined hepatic and renal failure. Our case is unique due to its early onset and severe features with concurrent involvement of both organ systems.
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.