bluuebunny/crossref_metadata_2025_split huggingface dataset:
2374 Rare Microbiologic Etiologies of Spontaneous Bacterial Peritonitis
Authors: Tripathi Nishant , Koirala Niki , Kudaravalli Praneeth , Akanbi Olalekan , Ali Saad Emhmed , Yarra Pradeep , Kato Hirotaka , Thakur Kshitij , Karri Kishore , Singh Tushi 
Published: October 2019

Introduction:
Often regarded as a poor prognostic factor in ascites, spontaneous bacterial peritonitis (SBP) is usually caused by Gram negative rods (E. coli, K. pneumoniae) and Gram positive cocci (S. pneumoniae).This case report identifies 2 rare cases of SBP.

CASE DESCRIPTION/METHODS:
Case 1 A 59 yo M with h/o decompensated cirrhosis (ascites without SBP history, encephalopathy, and variceal bleed) due to HCV presented with an episode of fall requiring orthopedic procedures. Flapping tremor, mild icterus, anemia, thrombocytopenia, AKI, coagulopathy, hyperbilirubinemia, hypoalbuminemia, and MELD score of 18 were significant findings. Abdominal/pelvic CT revealed hydronephrosis, which was corrected with ureteral stent placement upon admission. While awaiting rehab placement, patient developed paralytic ileus, septic shock due to ceftriaxone susceptible E. coli bacteremia, upper GI bleed, hypernatremia, pancytopenia, worsening hepatic encephalopathy, and worsening ascites with PMN of 3062. Abdominal/pelvic CT revealed no bowel perforation or alternate peritonitis source. Initially covered with piperacillin/tazobactam (P/T) and vancomycin for 4 days, therapy was narrowed to ceftriaxone for the following 4 days. Unfortunately, ascitic culture revealed Eggerthella lenta on culture day 8 (susceptible to clindamycin, meropenem, amoxicillin/clavulanate); patient ultimately demised with multiorgan failure. Case 2 A 66 yo M with h/o HCV and alcoholic cirrhosis on ciprofloxacin SBP prophylaxis, HFrEF, PVD with non-healing ulcer, CKD, and COPD presented with abdominal distension for routine paracentesis. Patient requires 5 to 6 L of ascitic fluid drainage with albumin replacement every other week. Ascitic fluid revealed PMN of 384; ceftriaxone was administered for 5 days and patient was discharged on ciprofloxacin prophylaxis. Ascitic fluid drawn prior to discharge ultimately grew Paenibacillus barengoltzii. Patient was requested to return for repeat ascitic culture, which resulted negative.

DISCUSSION:
1. E lenta and P. barengoltzii SBPs have not been previously described in literature; thus, both represent the first cases of each. A rare anaerobic intra-abdominal pathogen, E. lenta is associated with high mortality with P/T monotherapy. Paenibacillus species have not been studied in depth but are likely susceptible to third-generation cephalosporins. Gastroenterologists and internists managing similar cases may fail to identify these etiologies and appropriate treatment resulting in unfavorable outcomes.
2378 Hepatic Actinomycosis Masquerading as Gastrointestinal Malignancy
Authors: Kang Jennifer , Tian Frances , Joseph Augustin , Russell Sarah , Jarrett Olamide , Chan Christine 
Published: October 2019

INTRODUCTION:
Abdominal actinomycosis is a rare cause of liver cysts and rectal masses. It remains a diagnostic challenge.

CASE DESCRIPTION/METHODS:
A 60 year-old male (patient L) presented with a rectal mass found on colonoscopy. Biopsies were inconclusive; however, staging CT demonstrated liver lesions presumed to be metastases from rectal carcinoma. The patient began to have recurrent fevers, night sweats, and unintended weight loss, prompting an extensive infectious work-up notable only for a positive quantiferon. In the interim, patient L underwent laparoscopy and liver biopsy to further evaluate his presumed malignancy. Frozen sections revealed caseating granulomas with negative AFB and stains. The patient was diagnosed with GI tuberculosis (TB) based on constitutional symptoms, positive quantiferon, and frozen section findings, and was started on standard four-drug therapy. Final pathology resulted in visualization of sulfur granules, diagnostic of actinomycosis. TB treatment was discontinued and augmentin was started for a 6 month course.

DISCUSSION:
Actinomyces colonizes the oropharynx and digestive and genital tracts. It infrequently causes disease. Abdominal infection accounts for 20% of actinomycoses; of these, only 15% report liver involvement. Infection is associated with compromise of the mucosal barrier, either due to instrumentation or appendicitis. Our patient had recently undergone colonoscopies to diagnose his rectal mass. As in Patient L, actinomycotic liver abscesses usually present with an indolent course; symptoms include insidious abdominal pain, fever, and weight loss. Although these symptoms may be associated with malignancy, fever even in cancer patients should be presumed infectious until proven otherwise. Imaging commonly shows loculated cysts in contrast to patient L’s simple cysts with no loculations. The signs, symptoms, and radiographic findings of abdominal actinomycosis are non-specific and indistinguishable from colorectal cancer, inflammatory bowel disease, and gastrointestinal TB, making diagnosis difficult. In one review, laparotomy was considered essential for diagnosis in 69% of cases; pre-operative diagnosis rate was less than 10%. Treatment generally involves 6-12 months of beta-lactams. In summary, GI actinomycosis poses a diagnostic challenge as it is a rare clinical entity with nonspecific symptoms and endoscopic and radiographic findings. Successful diagnosis often requires a collaborative, multi-disciplinary approach. Treatment is with prolonged antibiotics.
2383 Amiodarone-Induced Acute Liver Injury
Authors: Essrani Rajesh , Mehershahi Shehriyar , Essrani Rajesh , Bhura Sajeer , Mehmood Asif 
Published: October 2019

INTRODUCTION:
Amiodarone is a lipophilic structure with a half-life of 25-100 days. Long term oral amiodarone is associated with photosensitivity, thyroid dysfunction, pulmonary, and hepatic toxicity. Hepatic toxicity varies from an asymptomatic and transient rise of serum aminotransferases that resolves after dose reduction or withdrawal, to severe liver disease. Acute hepatotoxicity is a rare but lethal complication of amiodarone use.

CASE DESCRIPTION/METHODS:
A 60-year-old male with a past medical history of hypertension and atrial fibrillation admitted for shortness of breath. He was taking Lopressor 25 mg twice a day and apixaban 5 mg twice a day at home. On exam, blood pressure was 130/70 mmHg, saturation 92% on room air, respiratory rate 13, and heart rate 145, which was irregular. ECG showed atrial fibrillation with a rapid ventricular rate. He was treated with diltiazem bolus and infusion but became hypotensive, so diltiazem infusion was discontinued. Amiodarone 150 mg bolus was given, followed by continuous amiodarone infusion of 900 mg over 24 hours. Blood work performed 24 hours later showed a sudden rise in aminotransferases (aspartate aminotransferase 3254 U/L, alanine aminotransferase 1643 U/L), and direct bilirubin (5.12 mg/dL). International normalized ratio, Gamma-GT, and alkaline phosphatase were normal. Extensive workup like abdominal ultrasonography, viral hepatitis serologies (hepatitis B and C, cytomegalovirus, Epstein-Barr, HIV and herpes zoster viruses) and autoimmune markers (antinuclear antibody, anti-smooth muscle antibody, anti-liver/kidney microsomal antibody type 1) were unremarkable. Amiodarone was discontinued about 50 hours after its beginning and his liver enzymes improved with normalization in 7 days. He was started on oral Lopressor and diltiazem, and his heart rate was well controlled.

DISCUSSION:
Acute intravenous amiodarone-induced hepatotoxicity is a rare but potentially lethal side effect so physicians should be aware of it and check for its occurrence by performing serial liver tests. The exact mechanism for intravenous amiodarone-induced acute liver failure is not well defined, but the hypotensive effect attributable to polysorbate 80 present in intravenous amiodarone is a compelling hypothesis. Treatment is mainly supportive. A recent study favored the use of N-acetylcysteine in acute liver injury beyond acetaminophen intoxication. Liver injury does not recur upon reintroduction of amiodarone by the oral route.
2384 Unusual Cause of Encephalopathy in an Immediate Post Transplant Patient
Authors: Humphrey Kyle , Henderson Phillip 
Published: October 2019

INTRODUCTION:
Brain abscesses are a rare complication post liver transplantation. They can present as a wide array of symptoms that can include fever, headache, focal deficits, or altered mental status. Immunosuppression makes transplant patients more susceptible to a wide array of microorganisms. We present a case of Nocardia farsinica brain abscess in a patient 4 months after liver transplantation.

CASE DESCRIPTION/METHODS:
A 76-year-old male with known cirrhosis from fatty liver disease, and recent liver transplant presenting with acute encephalopathy. Four months earlier, the patient received a liver transplant secondary to Nash cirrhosis. His post-operative course showed no infectious complications. He did have issues with mobility and was placed in a rehab facility. He was on tacrolimus as well as azathioprine for immunosuppression. He had hyperkalemia at rehab and his trimethoprim–sulfamethoxazole was held. The patient's family brought him to the hospital for changes in mental status. The patient met sepsis criteria on admission. CT of the head showed multifocal hypoattenuation lesions. MRI with contrast was obtained which showed multiple peripherally enhancing lesions. On peripheral history he had fallen at rehab and developed a hematoma of his thigh. The fluid collection on his thigh which was aspirated. Culture results were concerning for Nocardia. Patient was presumed to have cerebral nocardiosis and was started on imipenem and trimethoprim–sulfamethoxazole. The culture confirmed Nocardia farcinica. During his hospital stay, patient's mental status gradually improved. He was discharged on imipenem and Bactrim. Repeat MRI one year later showed complete resolution of lesions.

DISCUSSION:

Nocardia intracranial abscesses represent a rare complication post liver transplantation; although, infection is a common cause of mortality following liver transplantation. Opportunistic infection prophylaxis is vital and his lapse was likely cause of this infection. Patients that present with fever require expansive evaluation for the common and uncommon infectious causes. Any transplant patient with new or changing headache or altered mental status require imaging of the CNS as well as a lumbar puncture. Imaging, physical exam, cultures and serologies can then further delineate the cause. Brain abscesses have high morbidity and mortality; therefore, prompt diagnosis and treatment is vital.
2389 Nivolumab-Induced Hepatitis: A Rare Side Effect of Programmed Cell Death-1 (PD-1) Inhibitor
Authors: Kang Gurjeet , Ghanekar Dilip , Orpiano Christopher L. , Quinn Michael , Staffetti Joseph , Venu Lakshminarasimhan 
Published: October 2019

INTRODUCTION:
Nivolumab is a human immunoglobulin G4 (IgG4) monoclonal antibody that blocks the function of programmed cell death (PD-1) activity by binding to the PD-1 receptor. This prevents suppression of T-cell activity, which can lead to T-cells targeting cancer cells. Unfortunately, these medications induce various types of immune related adverse events including colitis, pneumonitis, endocrinopathies and hepatitis. We report rare case of of nivolumab-induced hepatitis.

CASE DESCRIPTION/METHODS:
An 86-year-old female with history of metastatic melanoma and was started on nivolumab 3 mg/kg every 3 weeks. Patient noted to have abnormal liver chemistries, nausea and yellowing of skin after 6 months of nivolumab. On presentation she was found to have a total bilirubin of 7.79 mg/dL, INR 1.3, AST 885 IU/L and ALT 999 IU/L. Physical examination was significant for mild scleral icterus only. An ultrasound of liver was notable prominent left lobe of liver but no focal hepatic masses and s/p cholecystectomy with no bile duct dilation. Infectious etiologies were unrevealing for viral hepatitis and acute EBV. Her autoimmune serologies were negative for anti-smooth muscle antibody and anti-mitochondrial antibody. Work up was negative for herbal supplements, illicit substance or other medications. The most likely culprit for her hepatitis was due to nivolumab. Patient was started on prednisone at 1 mg/kg daily for a total of 100 mg prednisone daily and her nivolumab dose was held. On discharge her total bilirubin was 2.45, INR 1.2, AST 62, ALT 249 and Alk Phos 252. Patient continued prednisone taper over 30-day period and by end of the month her liver chemistries had normalized and patient was asymptomatic.

DISCUSSION:
Nivolumab-induced hepatoxicity is rare and accounts for 3-6% of all immune-related adverse effects. The median time of onset was 3.3 months (range: 6 days to 9 months). In addition to systemic corticosteroid, alternative immunosuppressive therapies may be employed if symptoms continue after 3-5 days. Etiologies of liver dysfunction such as viral infection, obstruction and other forms of autoimmune hepatitis must be excluded. In such an event, oral mycophenolate mofetil 500 mg every 12 hours can be used for treatment. Our patient showed rapid improvement in liver chemistries and had minimal physical side effects. Healthcare provides managing patients with liver injury should be able to recognize and treat prior to development of fulminant hepatitis.
2390 Trenbolone-Induced Liver Injury
Authors: Kang Gurjeet , Venu Lakshminarasimhan , Orpiano Christopher L. , Quinn Michael , Staffetti Joseph , Ghanekar Dilip 
Published: October 2019

INTRODUCTION:
Anabolic-androgenic steroid abuse has been steadily increasing in the general population. According to a 2014 study, approximately 1 in 50 students in the 12th grade reported using anabolic steroids. Trenbelone acetate is a synthetic anabolic androgen which is an agonist of the androgen receptor and most often used in cattle.

CASE DESCRIPTION/METHODS:
A 23 year old male with no significant past medical history presented with complaints of jaundice and generalized weakness which began 10 days prior to presentation. Patient endorsed weekly IM trenbelone 1000 mg weekly over the last 8 weeks. Physical examination was remarkable for icterus and appropriate mentation. Initial investigations reflected a total bilirubin of 13.44 mg/dL, AST 159 IU/L, ALT 425 IU/L, PT 11.0, INR 1.0, and Alk Phos of 142. Serologies were negative for viral hepatitis, anti-mitochondrial antibody, anti-smooth muscle antibody and ANA of 1:40. A liver ultrasound reported normal liver size without biliary obstruction. Patient's liver chemistries improved over the next three days and he was discharged with total bilirubin of 12.54 mg/dL, AST 135 IU/L, ALT 320 IU/L, PT 11.0, INR 1.0 and Alk Phos of 121. Patient advised to abstain from any future use of trenbelone. On repeat labs in 10 days, his total bilirubin of 29.50 mg/dL, AST 78, ALT 123, PT 20.1, INR 1.85 and Alk Phos 242. Physical examination noted worsening jaundice overall along with icterus but mentation remained appropriate. Patient denied any new medications and no further use of trenbelone since discharge. Patient's liver chemistries remained stable and he underwent MRI abdomen which was unremarkable. Patient was discharged home on ursodiol 300 mg BID. Patient's liver chemistry improved in one week and returned to baseline in one month.

DISCUSSION:
Anabolic steroids have been linked to four different forms of liver injury including an acute cholestatic syndrome such as in our patient, elevation in serum enzymes, chronic vascular injury and hepatic tumors including adenomas and hepatocellular carcinoma. Mechanism of cholestatic syndrome is not well defined in this type of injury. Urosdiol has been used in the past for treatment however efficacy has not been shown in a study. Healthcare provides managing patients with elevated liver chemistries should able to recognize anabolic induced liver injury given increasing use and ease of availability of such performance enhancing drugs.
2392 Not so Safe for All: A Case of Statin-Induced Autoimmune Hepatitis and Primary Biliary Cholangitis Overlap
Authors: Hang Thuy-Van , Taborda Cesar , Barrett Amanda , Xue Yue , Vora Ravi 
Published: October 2019

INTRODUCTION:
Hydroxymethylglutaryl coenzyme A reductase inhibitors, or statins, are widely used and typically well tolerated. They are rarely associated with severe hepatotoxicity and several randomized trials have demonstrated no significant difference in incidence of persistently elevated liver function tests (LFTs) between statins and placebo. We present an interesting case of drug induced liver injury from atorvastatin resulting in autoimmune hepatitis (AIH) and primary biliary cholangitis (PBC) overlap.

CASE DESCRIPTION/METHODS:
A 70 year old woman with a history of stroke with residual dysarthria presented with generalized weakness and decreased appetite for one week, found to have AST of 1347, ALT 807, ALP 230, bilirubin 10.2, INR 1.47, and ferritin 221,358. She did not take any herbals or over-the-counter medications, but was on atorvastatin. Four months before presentation, she had LFTs in the 400-500s, which was attributed to atorvastatin 80mg daily. This was stopped and her LFTs normalized. One month before admission, she was started on atorvastatin 40mg daily, which was discontinued on admission. Hepatitis A, B, and C and HIV were negative, and her right upper quadrant ultrasound was unremarkable. Her workup was significant for positive ANA, dsDNA Ab, anti-centromere Ab, anti-Smith Ab, RNP Ab, F-actin Ab, and smooth muscle Ab, as well as IgG of 5,599. She underwent liver biopsy, which demonstrated panlobular active hepatitis and portal inflammation with ductitis. TPMT was normal, so she was started on azathioprine and prednisone taper for AIH/ PBC overlap. Her labs dramatically improved and on discharge, AST was 375, ALT 641, ALP 184, bilirubin 3.2, and ferritin 2784. She has continued to do well and LFTs and ferritin normalized one month after discharge.

DISCUSSION:
While statins generally have infrequent significant side effects, they can cause hepatocellular injury that does not improve with dose reduction. There have been case reports of statins causing AIH, but in this patient’s unusual case, atorvastatin caused an autoimmune hepatitis/ primary biliary cholangitis overlap. It is important to recognize that in patients who develop LFT elevations more than three times ULN, it may not be safe to restart statins, even at a lower dose. In addition, statin-induced AIH can cause a hyperinflammatory response with significant elevations in multiple acute phase reactants, as well as lead to numerous auto-antibodies such as in the case described.
2393 A Unique Case of Liver Disease in Pregnancy
Authors: Rana Prachi , Han Hyosun 
Published: October 2019

INTRODUCTION:
Pregnancy-related liver disease is seen in up to 3% of all pregnancies. Pregnancy-related etiologies include hyperemesis gravidarum, pre-eclampsia, HELLP, intrahepatic cholestasis of pregnancy, and acute fatty liver of pregnancy (AFLP). Given the significant morbidity and mortality associated with these conditions, there is a need for early recognition. Here we present a unique case of pregnancy-related liver disease in an asymptomatic patient. Despite a thorough evaluation for liver and non-liver related causes, her lack of symptomatology and associated laboratory findings made establishing a definitive diagnosis difficult.

CASE DESCRIPTION/METHODS:
30 year-old woman G1P0 at 29 weeks gestation with dichorionic triamniotic triplets presented with generalized weakness. Her past medical and surgical histories were otherwise non-contributory and her only medication included prenatal vitamins. The physical exam was unremarkable except for a gravid uterus. Throughout her hospital course, she remained normotensive. Admission labs were significant for an abnormal liver profile: AST 200 U/L, ALT 349 U/L, ALP 121 U/L, and total bilirubin 0.5 mg/dL, compared to a previous normal baseline. Complete blood count and renal function were normal. Abdominal ultrasound (US) showed increased liver echogenicity consistent with fatty liver disease. Additional work-up revealed a normal coagulation profile, fibrinogen, lactate dehydrogenase, and haptoglobin. Urinalysis was negative for proteinuria. Serologies for viral and autoimmune hepatitis were negative. Total bile acids were mildly elevated at 9.3 umol/L (normal < 6.8umol/L) and 24-hour urinary copper was normal. Though she remained asymptomatic, liver enzymes continued to uptrend. On day 16 she underwent urgent C-section due to rising liver enzymes and evidence of fetal distress. Liver enzymes continued to rise until POD1 before rapidly declining.

DISCUSSION:
This was a unique case of pregnancy-related liver disease of unknown etiology, but most consistent with an early manifestation of AFLP. We suspected AFLP based on the steatosis noted on US, however, since we could not check her children for LCHAD deficiency a definitive diagnosis could not be made. Surveillance US showing resolution of steatosis would have helped confirm the diagnosis however the patient was lost to follow up. This was an interesting presentation of AFLP as most cases are discovered in women presenting with acute liver failure; this case was unique in that it was discovered unexpectedly.
2401 A Case of Hepatitis B Reactivation
Authors: Haddadin Sadam H. , Martinez Beatriz , Ravendhran Natarajan 
Published: October 2019

INTRODUCTION:
It is estimated that more than two billion people around the world have been infected by hepatitis B virus (HBV). Several immunosuppressive agents have been associated with HBV reactivation (HBVr). We present a case of HBVr in a patient with ulcerative colitis (UC) treated with tofacitinib.

CASE DESCRIPTION/METHODS:
A 57-year-old female with UC on tofacitinib presented to the emergency department with flu-like symptoms for 2 months after being switched from azathioprine to tofacitinib. She was HBV surface antigen (HBsAg) negative, anti-HBV core antibody (anti-HBcAb) and anti-HBV surface antibody (anti-HBsAb) positive and had normal liver enzymes before initiation of tofacitinib. On initial evaluation she was febrile, hypotensive, and had lower extremity edema. Laboratory data was significant for total bilirubin 2.5 mg/dL, AST 1601 U/L, ALT 1013 U/L, positive HBsAg, anti-HBsAb, total anti-HBcAb and HBeAg, HBV DNA 10,354,246 IU/m; she had negative HBeAb, IgM antibody to HBcAg, hepatitis A, C and E antibodies. She was diagnosed with HBVr and was started on tenofovir disoproxil fumarate. Over the next two days her enzymes continued to rise and peaked at day 5. At day 7 liver enzymes started to trend down. She was later discharged on tenofovir. At the 2 month follow up liver enzymes had normalized and HBV DNA was down to 30 IU/m.

DISCUSSION:
Tofacitinib is a kinase inhibitor extensively studied in patients with rheumatoid arthritis and has been shown to be generally safe in multiple clinical trials. In patients with UC the data is limited. Most clinical trials excluded patients with chronic HBV infection, therefore the risk of HBVr among tofacitinib-treated patients remains unknown. HBVr is defined as an increase in HBV DNA of more than 100-fold in patients with previously detected HBV DNA, detection of HBV DNA in patients that previously had undetectable titers or when reverse seroconversion or development of detectable HBsAg occurs. In this case, the reactivation of HBV was most likely induced by tofacitinib and its suppression of various kinase signaling pathways essential for controlling immune activation and proliferation the cells responsible of preventing HBV replication. In conclusion, in patients with resolved HBV infection who are HBsAg negative and anti-HBcAb positive, periodic HBV DNA monitoring should be considered as HBVr is possible and the exact risk of reactivation remains unknown.