bluuebunny/crossref_metadata_2025_split huggingface dataset:
3163 Laparoscopic Transgastric ERCP for Choledocholithiasis After Roux-en-Y Gastric Bypass: A Different Approach to ERCP
Authors: Wojtkowski Antoni , Pandit Sarbagya , Atia George , Chalise Shyam 
Published: October 2019

INTRODUCTION:
With bariatric procedures becoming more prevalent, performing an ERCP becomes a challenge with patients who have had bariatric surgeries.

CASE DESCRIPTION/METHODS:
A 60 year old male with a past medical history of hypertension, diabetes mellitus type 2, and Roux-en-Y gastric bypass surgery developed abdominal pain 3 days prior to admission and was admitted for a laparoscopic cholecystectomy. Pre-operative MRCP did not show any significant common bile duct obstruction (a small non-obstructing stone was noted). Intraoperatively, the stone was found to be obstructing the common bile duct after a cholangiogram was performed. A laparoscopic trans-gastric ERCP was scheduled. The ERCP was scheduled for the next day. After a laparoscopic gastrostomy, the ERCP scope was advanced through the gastrostomy and the stone was removed with standard biliary sphincterotomy and balloon extraction without complications. The gastrostomy site was closed, and the procedure finished without complications. The patient was discharged in good condition 2 days after the procedure.

DISCUSSION:
An ERCP in a Roux-en-Y gastric bypass patient requires careful planning with surgery. Nonetheless, the time of the procedure is shortened considerably compared to the older double-balloon approach and shorter anesthesia overall is associated with better outcomes for the patient. One surgical approach to these patients is a transgastric approach through gastrostomy (either laparoscopic or open surgical approach). The open approach is achieved by creating an opening in the abdominal wall, and attaching the gastric wall to the opening, then opening it for the ERCP scope to be advanced through. In this particular case, a laparoscopic gastrostomy was performed in the distal area of the stomach, and cannulated with a 15 mm cannula through an umbilical port. An 11 mm ERCP scope was then inserted through the trocar directly into the stomach, and advanced to the pylorus where the gastroenterologist was able to cannulate the common bile duct. A stent was not placed in this particular case, as it would require repeat surgery to remove it. The gastrostomy was then closed by a mini laparotomy. Alternative approaches to GI procedures will become more common with the growing prevalence of bariatric procedures.
3164 The Unhelpful Biopsy: Autoimmune Hepatitis in a Young Woman With Kikuchi Fujimoto Disease
Authors: Magee Jared S. , Lindholm Phillip C. 
Published: October 2019

INTRODUCTION:
Kikuchi Fujimoto disease (KFD), also known as histiocytic necrotizing lymphadenitis, is a rare, immune-mediated condition usually seen in young Asian females. There are only two reported cases of autoimmune hepatitis (AIH) in a patient with KFD. Systemic lupus erythematosus (SLE) has a strong association with KFD and introduces diagnostic uncertainty in differentiating AIH and SLE-hepatitis. We present a challenging case of acute hepatitis in a woman with KFD, positive rheumatologic signal and bland liver biopsy.

CASE DESCRIPTION/METHODS:
A 33-year-old female presented with non-bloody emesis. Her history was significant for KFD and exam was notable for jaundice and a diffuse maculopapular rash involving palms and soles. She had normal vitals and was previously known to have a positive ANA (1:640) and anti-dsDNA. Labs were notable for ALT 843, AST 646, alkaline phosphatase 173, total bilirubin 10.6 with direct bilirubin 8.6. Given her elevation in transaminases, additional serologies and imaging were performed demonstrating a mildly elevated transferrin, no sign of viral hepatitis and a right upper quadrant ultrasound and MRCP with nonspecific hepatitis. She was admitted for expedited workup and further laboratory evaluation was notable for a mildly elevated IgG and negative for abnormalities in ASMA as well as p-ANCA, Anti-LKM1, and ALC-1. Serologies were overall consistent with a probable diagnosis of AIH and a liver biopsy was planned to secure a definitive diagnosis. However this demonstrated non-specific necrosis and cholestasis, inconsistent with AIH. After a prompt response to steroids and a negative antiribosomal P antibody, probable AIH was suggested and she recovered uneventfully.

DISCUSSION:
Diagnosis of AIH can be made with clinical presentation, laboratory evaluation and biopsy. Our patient presented with a probable diagnosis of AIH (score of 14 by AASLD guidelines), yet a negative ASMA, bland biopsy and a positive SLE signal (though not meeting formal diagnostic criteria) were significant confounders. Treatment response to steroids suggested AIH by AASLD scoring, yet SLE hepatitis is also steroid responsive. Negative anti-ribosomal P antibody may suggest decreased likelihood of SLE hepatitis, and this distinction is critical given the more benign course of SLE-hepatitis. This is a rare case of KFD associated, probable AIH, yet there remains much overlap with SLE-hepatitis. We recommend additional research to determine clinical or laboratory criteria to differentiate these diagnoses.
3168 Acute Liver Failure, Rhabdomyolysis, and Acute Kidney Injury Secondary to Influenza A Infection
Authors: Ghanim Marcel , Ghazaleh Sami , Nehme Christian , Awad Mohammed , Nesheiwat Zeid , Nawras Ali 
Published: October 2019

INTRODUCTION:
Influenza A is considered a self-limiting pulmonary infection with a constellation of respiratory symptoms. However, it is sometimes associated with unfortunate complications with high morbidity and mortality. We present a case who suffered from rhabdomyolysis, acute kidney injury, and acute liver failure secondary to influenza infection.

CASE DESCRIPTION/METHODS:
A 22-year-old male presented with red urine for one day associated with muscle pain in the thighs, back, neck, and extremities. He also had fever, chills, sore throat, and dry cough for 4 days. Past medical and surgical histories were unremarkable. Family history was insignificant. He did not take medications. He denied cigarette, alcohol, or IV drug use. He denied headache, nausea, vomiting, diarrhea, chest pain, hematemesis, or hemoptysis. On exam, the patient was in no acute distress. Vital signs were within normal limits. Abdominal exam showed a soft, non-tender, and non-distended abdomen without organomegaly. Initial testing revealed an elevated creatinine of 2.02 mg/dL. Urinalysis was significant for the presence of blood, but RBC count was 0/HPF. CK was elevated at 407,176 U/L and myoglobin elevated at 33,673 ng/ml. AST was elevated at 1540 U/L and ALT at 286 U/L. Respiratory pathogen panel was positive for influenza A. The patient's acute kidney injury was believed to be secondary to rhabdomyolysis. Extensive testing to look for the cause of elevated liver enzymes came back negative including viral hepatitis, iron studies, HIV, liver ultrasound, and abdominal CT. Similarly, no cause for rhabdomyolysis was found and autoimmune workup was negative. The patient's labs continued to worsen over his hospital course. His creatinine peaked at 8.69 mg/dL and he eventually needed dialysis. His CK continued to trend up and peaked at 1,271,160 U/L. His liver enzymes also trended up with AST peaking at 4100 U/L and ALT at 1043 U/L. Eventually, his liver enzymes and CK trended down to normal levels and he did not require liver transplantation. Unfortunately, his kidney function did not completely recover, and he still required dialysis.

DISCUSSION:
Although rare, extrapulmonary involvement of influenza A infection can happen and rhabdomyolysis is exceedingly rare. In our case, rhabdomyolysis was believed to be due to influenza A infection. As a result, he developed acute kidney injury requiring dialysis. His acute liver failure was believed to be multifactorial secondary to influenza infection and/or rhabdomyolysis.
3176 Sickle Cell Intrahepatic Cholestasis Following Choledocholithiasis: A Case Report
Authors: Zafar Yousaf , Gondi Keerthi , Muthukumar Varsha 
Published: October 2019

INTRODUCTION:
Sickle Cell Intrahepatic Cholestasis (SCIC) is an acute manifestation of Sickle Cell Disease (SCD) characterized by occlusive sickling in the liver, causing biliary obstruction. We present a case of a patient in vaso-occlusive crisis with SCIC following choledocholithiasis.

CASE DESCRIPTION/METHODS:
A 23-year-old male presented with severe abdominal pain after having a complicated stay for choledocholithiasis one week prior. Total bilirubin level was 42.2 mg/dL, and transaminases were elevated. Abdominal ultrasound did not demonstrate repeat biliary duct blockage. Magnetic Resonance Cholangiopancreatography revealed intrahepatic biliary duct dilation and scattered wedge-shaped enhancements peripherally. The patient underwent plasma exchange transfusion. Afterwards, patient rapidly recovered with reduction in bilirubin level and resolution of pain and jaundice. He was discharged without complication.

DISCUSSION:
SCIC is a rare and potentially fatal sequela of vaso-occlusive crisis in SCD. Our patient may have been predisposed to developing SCIC due to a prior complicated admission for choledocholithiasis which may have damaged the biliary system to induce SCIC. Plasma exchange transfusion results in rapid recovery and should be initiated quickly in these patients.
3177 Splenomegaly in an Adult Female With Sickle Cell Disease
Authors: Benjaram Sindhuri , Rahim Usman , Ehrinpreis Murray N. 
Published: October 2019

INTRODUCTION:
A mutation in the beta globin chain of hemoglobin results in Sickle type of Red blood cells. To remove the sickle shaped red blood cells, the spleen becomes hyperactive and enlarged. These red cells have more affinity to the vascular endothelial membrane resulting in Vaso-occlusive phenomenon. Repeated episodes of this cause thrombosis, infarction leading to fibrosis and Autosplenectomy. This is generally complete by the age of 5 and for more than 80% in their first decade. Existence of spleen in adolescents and adults with sickle cell disease in uncommon. Here we present such a case.

CASE DESCRIPTION/METHODS:
A 22-year-old female with known history of homozygous sickle cell disease presents with abdominal pain. She started to have generalized body pains, later localized to all quadrants of the abdomen. She described it as achy type constant pain associated with nausea. She denies any emesis, changes with bowel or bladder habits and association with food intake. CT imaging done revealed an enlarged spleen with scattered densities and a 2 cm splenule in the inferior aspect. The enlarged spleen 14 × 5 × 15 cms was present in prior ultrasound imaging study done 4 years ago. Further laboratory work including complete blood counts with differential, reticulocyte count & index were consistent with sickle cell pain crisis.

DISCUSSION:
Although the presence of echogenic lesions increases the risk of sequestration crisis, increased Hemoglobin F levels and alpha thalassemia may cause splenomegaly, but the patient did not have either. Hemoglobin Electrophoresis showed Hb F 1% and Hb S of 70%. Some studies conclude splenic enlargement in adulthood may imply less severe form of the disease. With no other possible cause identified, this adult female with Sickle cell HbSS disease has Splenomegaly.
3184 A Case of Alcoholic Hepatitis With Unusual Leukamoid Reaction
Authors: Lakkasani Saraswathi , Barham Shaker , Depasqule Joseph , Abusalah Wala 
Published: October 2019

INTRODUCTION:
Leukemoid reaction is defined by predominantly neutrophilic leukocytosis with a total leukocyte count >50,000 cells/µl, after excluding leukemia. Leukemoid reaction is seen in various conditions. It is very rare in alcoholic hepatitis (AH). Herein, we present a case of a young alcoholic male who was admitted with alcoholic hepatitis and leukemoid reaction. He underwent extensive workup to rule out other etiologies and subsequently improved after glucocorticoid therapy.

CASE DESCRIPTION/METHODS:
28-year-old male with history of alcohol abuse presented with a two-week history of abdominal pain, distention, jaundice and vomiting. On exam, the patient had a fever and tachycardia. He was also found to be icteric and had ascites. Investigations revealed a bilirubin of 9.4 mg/dl. WBC of 42,000 cells/µl with a left shift. Ultrasound showed enlarged fatty liver. MDF was 61 and MELD was 37. Septic workup was negative including ascitic fluid cell count and culture. He was started on prednisolone 40 mg. Hematologic workup including peripheral smear ruled out neoplasm. Leukocyte alkaline phosphatase was elevated at 249. The patient was discharged on prednisolone and was followed as an outpatient. He improved after four weeks and his WBC count normalized.

DISCUSSION:
Leukemoid reaction is a very rare event in AH and is a poor prognostic marker. The pathophysiology is likely due to the increased levels of granulocyte colony stimulating factor (G-CSF) released by the damaged hepatocytes. The release of excessive amounts of tumor necrosis factor-alpha has been postulated to be instrumental in the causation of leukemoid reaction in alcoholic patients as well. However, Arguelles-Grande et al. reported a patient in which the cytokine profile did not demonstrate increased amounts of TNF-a. In their patient, levels of IL-18 and IL-1b were increased. IL-1b stimulates the proliferation and maturation of neutrophils in the bone marrow both directly by the induction of granulocyte-macrophage colony-stimulating factor and G-CSF; thus the postulated pathogenic sequence for LR: increased IL-18 produces increased IL-1b, which along with increased IL-8 produces neutrophilia. In this setting, corticosteroids may play a role by their reported inhibition of IL-1b transcription. Hematologic evaluation in these cases is necessary to rule out underlying neoplasm. If patients with severe alcoholic hepatitis are found to have leukemoid reaction, treatment with steroids should be considered after excluding sepsis and neoplasm.
3189 Portal Vein Thrombosis Without Cirrhosis: A Case Report
Authors: Lopez Paola , Torres Victor , Morales Ahmed , Di Marco Anna , Ayala Alfredo 
Published: October 2019

INTRODUCTION:
PVT is a rare entity in the absences of liver cirrhosis, malignancy, prothrombotic disorder or an intra-abdominal inflammatory state. In some cases, no clear etiology can be found and it can be triggered by a combination of factors. We report a case of non-cirrhotic woman with a symptomatic and progressive PVT in the setting of low antithrombin activity and liver lesions.

CASE DESCRIPTION/METHODS:
48 year old female without past medical or family medical history, was brought to the ED with diffuse abdominal pain. For the past ten weeks, she has experienced post-pandrial abdominal pain associated with nauseas and two episodes of non-bloody vomiting. She denied diarrhea, recent abdominal infections, drug use or OCP use. Patient has not undergone abdominal surgery. Her physical exam was unremarkable except for mild diffuse abdominal pain, no Murphy's sign, no guarding or rebound signs. CBC, BMP, lipase and liver function panel was unremarkable. Recent mammography, EGD and colonoscopy displayed no signs of malignancy or portal hypertension. MRA showed no stenosis or obstruction of arteries. CAT-scan of abdomen and pelvis with IV contrast showed extensive thrombosis of main portal vein, right portal vein, left portal vein and the portosplenic confluence. Also showed collateral vessels extending from the portosplenic confluence into the bilateral retroperitoneum, bilateral renal hilum and extending across the ovarian veins into the pelvis. There were multiple indeterminate hypodense liver lesions. Additional laboratory tests were ordered and samples collected before starting anticoagulation. Laboratory tests showed decrease antithrombin activity, which is a risk factor for PVT. She was admitted on low-molecular weight heparin (LMWH) until stabilization, and then discharged on oral anticoagulation. In this case, outpatient follow up evaluation by hemato-oncology was scheduled to rule out other coagulation disorders and malignancy.

DISCUSSION:
PVT in a healthy and young patient is not common. The prevalence of PVT is low in patients with cirrhosis; it is even lower in patients non-cirrhotic and without malignancy. It has been estimated that in non-cirrhotic PVT, hypercoagulable states account for 40%-60% of cases. The American Association for the Study of Liver Diseases (AASLD) guidelines recommend treatment with anticoagulation to prevent thrombi extension and to restore blood flow in occluded vessels. The outcome for non-cirrhotic, non-malignant PVT is good if the diagnosis and treatment occurs early.
3192 Sealing the Diagnosis of Celiac Disease in Pregnancy
Authors: Nahar Ritu , Amin Avani , Moleski Stephanie 
Published: October 2019

INTRODUCTION:
Celiac disease (CD) is an immune-mediated disease that results from a reaction to dietary gluten and primarily affects the small intestine. The diagnosis of CD can be challenging in those that do not present with the classic gastrointestinal symptoms, and the diagnosis can further be complicated in pregnancy.

CASE DESCRIPTION/METHODS:
A 28-year-old G1P0 woman presented with hypertension and at 15 weeks gestation. Initial workup for the patient's transaminase elevation was remarkable only for hepatic steatosis on abdominal ultrasound, with normal liver size, echogenicity and echotexture. She was diagnosed with chronic hypertension with superimposed preeclampsia complicated by transaminase elevation. However, her transaminase elevation persisted postpartum prompting re-evaluation. Further testing revealed a weakly positive anti-tissue transglutaminase antibody (IgA tTG) of 6 units/mL. Biopsy at the time of esophagogastroduodenoscopy revealed duodenal mucosa with intraepithelial lymphocytosis and focal moderate villous blunting consistent with CD.

DISCUSSION:
While the prevalence of CD is approximated to be one percent of the American population, it can be as high as four percent in those with cryptogenic transaminase elevation.1,2 Untreated CD during pregnancy predisposes patients to increased rates of intrauterine growth restriction (IUGR), low birth weight, and preterm birth.3 Establishing a diagnosis of CD during pregnancy can be challenging. However, prenatal screening for CD in high risk populations can lead to more cost effective care as well as improved maternal and fetal outcomes.
3195 Autoimmune Hepatitis With Primary Biliary Cirrhosis: An Overlapping Syndrome of the Liver
Authors: Jobanputra Hardik , Shrimanker Isha 
Published: October 2019

INTRODUCTION:
Autoimmune liver diseases consist of Primary Biliary Cirrhosis (PBC), Autoimmune Hepatitis (AIH) and Primary Sclerosing Cholangitis (PSC). Overlap syndromes are defined when there are characteristic features of AIH along with PBC and PSC. We report the presentation and management of an AIH-PBC overlap syndrome.

CASE DESCRIPTION/METHODS:
A 60-year-old Asian female with a past history of hypertension, presented with fatigue, myalgia, nausea, vomiting, and icterus for ten days. She denied the use of illicit drugs, alcohol consumption or family history of liver disease. On arrival, she had a temperature of 38.2°C, a pulse of 110 beats/minute, blood pressure of 100/70 mm Hg, and oxygen saturation of 97% on room air. Physical exam revealed icterus 1+, and mild tenderness in the right hypochondriac area. Laboratory investigations revealed leukocyte count of 15.2 K/ul, alanine transaminase of 1107 U/l, aspartate aminotransferase of 1010 U/l, alkaline phosphatase of 685 U/l, total bilirubin of 10 mg/dl with the direct component of 9 mg/dl, and gamma-glutamyl transferase of 666 U/l. Further workup revealed anti-nuclear antibody titer of 1:1000, antimitochondrial antibody (AMA) titer of 1:80 with negative peripheral antineutrophil cytoplasmic antibody and hepatitis serology. Ultrasound of the abdomen showed common-bile duct (CBD) stricture formation. The patient underwent endoscopic retrograde cholangiopancreatography with sphincterotomy and stenting. Liver biopsy showed interface hepatitis with portal tract inflammation. Brush border sampling from the CBD revealed lymphocytic and neutrophilic infiltrate. A diagnosis of AIH-PBC overlap syndrome was made. She was started on piperacillin/tazobactam 4.5 gm and metronidazole 400 mg along with with ursodeoxycholic acid (UDCA) 300 mg, thrice a day. After a month, the stent was removed and there was a resolution of symptoms with normalization of liver enzymes.

DISCUSSION:
The minimum criteria required for the diagnosis of AIH-PBC overlap syndrome include positive AMA and histology showing bile duct abnormality in an otherwise classical AIH (Table 1). Management is usually with UDCA, immunosuppressants, and corticosteroids. It is prudent to maintain a modest index of suspicion of overlap syndromes in patients such as ours. Early diagnosis and appropriate management are of paramount importance.
3196 A Rare Occurrence of Tricuspid Valve Histoplasma Endocarditis in a Patient With NASH Cirrhosis and No Intravenous Drug Use
Authors: Abraham Fiyinfoluwa , Subramanian Sruthi K. , Singh Khushboo , Machicao Victor 
Published: October 2019

INTRODUCTION:
Bacterial endocarditis not commonly seen in patients with cirrhosis, while culture-negative endocarditis in the setting of cirrhosis is rarely seen at all. We present a case of Histoplasma endocarditis diagnosed in Nonalcoholic Steatohepatitis (NASH) cirrhosis.

CASE DESCRIPTION/METHODS:
A 66-year-old Caucasian female with a history of atrial fibrillation on rivaroxaban, diastolic heart failure, and decompensated NASH cirrhosis with controlled ascites presented with two weeks of weight gain, bilateral lower extremity swelling, and dyspnea. No history of intravenous drug use (IVDU). She had anasarca on physical examination and was admitted for diuresis. A transthoracic echocardiogram (TTE) five months before these symptoms described moderate tricuspid regurgitation. Due to acute anasarca, a repeat TTE was obtained which showed a left atrial thrombus, moderate to severe tricuspid regurgitation (Table 1) with anterior leaflet prolapse, and an echodensity (1.12 × 0.7 cm) seen on the tricuspid valve (Figure 1). A follow up transesophageal echocardiogram (TEE) was done 7 days later. It confirmed the tricuspid vegetation and severe tricuspid regurgitation (Table 1). Blood cultures returned negative. She was treated empirically with IV vancomycin, ceftriaxone, and doxycycline for infective endocarditis and switched to warfarin from rivaroxaban. The patient was later discharged; however, she had two more admissions for similar symptoms of dyspnea and anasarca. Repeat blood cultures remained negative; however, serology for Histoplasma antibody returned positive (1:8). The patient was started on Isavuconazonium and had improvement of symptoms upon outpatient follow up. She was not a surgical candidate for aortic/tricuspid valve replacement due to underlying liver disease; however, to re-evaluate surgical candidacy, she underwent a liver biopsy to confirm cirrhosis. A separate sample was sent for fungal culture in the setting of diagnosed Histoplasma endocarditis – currently pending.

DISCUSSION:
In the general population, fungal endocarditis is uncommon, but Histoplasma endocarditis is an infrequent manifestation of disseminated Histoplasmosis. It is frequently missed and usually involves prosthetic valves. The presence of Histoplasma endocarditis in a cirrhotic has been described in three other patients in a case series by Riddell et al. where two patients had hepatitis C-related cirrhosis. Our case describes an atypical occurrence Histoplasma endocarditis in NASH cirrhosis without prior IVDU.