bluuebunny/crossref_metadata_2025_split huggingface dataset:
2243 Abdominal Pain Born From Migrating IUD to the Liver
Authors: Pacha Faris , Matsuzak Francis , Skrove Jamie L. , Paniker Linoj , Sobrado Javier , Rana Zaid 
Published: October 2019

INTRODUCTION:
The use of intrauterine devices are a core of contraception practiced globally. There are several different types and brands that are FDA Approved for use in the United States. The advantages include their length of efficacy, one cost, and safe for breastfeeding. The risks of using IUDs include infection and migration. These risks have been as high as 3% but more consistently at one to two percent. Usual mechanisms for migration include erosion through uterine tissue or expulsion from vaginal canal. Once migrated the device is removed and another is placed as efficacy drops.

CASE DESCRIPTION/METHODS:
Patient is a 43-year-old female Hispanic American who presented to the hospital with complaints of generalized abdominal pain and low back pain for one year. The patient has no past medical history and does not take any medication besides ibuprophen for minor aches and pains. The patient has a surgical history of copper IUD placed five years prior. The patient mentions at a recent appointment with her primary care doctor her “liver tests” were “a tad elevated.” The patient has no family history of cancer or gastrointestinal history. Labs were performed and were WNL other than moderately elevated transaminases. Imaging demonstrating the patient’s intrauterine device had migrated to the anterior portion of the liver.

DISCUSSION:
There have been less than three cases including this one where an IUD migrated to the liver. The migration of the copper IUD was causing the transaminitis and general abdominal pain. This Case was chosen because it demonstrates a complication that is less than one percent. There have been very limited cases of an IUD migrating to the liver and even lower causing transaminitis. The mechanism of the migration in this case is unknown and thus makes this case very unusual. The proposed mechanism is erosion through the uterus and migration to the anterior portion of the liver.
2247 Transfusion Associated Babesiosis: An Uncommon Cause of Acute Liver Failure
Authors: Brandt Daniel R. , Balasubramanian Manjula , Navarro Victor J. , Kalman Richard 
Published: October 2019

INTRODUCTION:
Babesiosis is a zoonotic disease caused by obligate intracellular protozoa that reproduce in erythrocytes. We present a case of transfusion-transmitted babesiosis (TTB) leading to acute liver failure (ALF). Whereas mild liver chemistry abnormalities are common in babesiosis, to the authors’ knowledge this is the first case of TTB directly leading to ALF.

CASE DESCRIPTION/METHODS:
A 79-year-old man from New Jersey with end stage renal disease presented with two weeks of flu-like illness and was found to have profound liver function abnormalities consistent with ALF. Six weeks prior the patient was hospitalized for a diverticular bleed at which time he received multiple packed red blood cell transfusions and recovered to his baseline health. At that time, liver chemistries were normal. On arrival, he was afebrile and normotensive. He was oriented but lethargic. Skin exam notable for pallor. His abdomen was benign. Initial investigations revealed AST 3497 IU/L, ALT 2719 IU/L, ALP 259 IU/L, TB 5.2mg/dl, DB 3.6mg/dl. INR was 4.1, Hgb 8.7g/dL, and fibrinogen 252mg/dl. LDH 2003 IU/L with haptoglobin < 8.0mg/dl. Peripheral smear revealed ring-shaped intra-erythrocytic trophozoites (Figure 1). Babesia microti PCR was positive. Atovaquone and azithromycin were started and exchange transfusion performed. Fevers and worsening encephalopathy progressed despite directed treatment. Multi-system organ failure developed and care was withdrawn. Further testing determined our patient was a recipient of babesia microti contaminated transfusion.

DISCUSSION:
Babesiosis is a world-wide emerging disease caused by intra-erythrocytic protozoa that are transmitted primarily through Ixodes ticks but also through blood transfusion. TTB is often severe in presentation with a mortality rate of approximately 20%. Marked hemolytic anemia, disseminated intravascular coagulation, and adult respiratory distress syndrome may develop. Case series have established that patients with babesiosis exhibit abnormal liver chemistries with median values notable for ALT of 59 IU/L and AST 79 IU/L. A literature review reveals just one published case of babesiosis presenting as ALF, and no such cases when babesia is transmitted through transfusion. Babesiosis should be considered in the differential diagnosis of ALF in patients living in or having recently travelled to an endemic area or who have recently received transfusions. In such patients, we recommend performing blood smear to prevent delay in treatment.
2253 Is There a Role for TAVR in Cirrhotics With Severe Aortic Stenosis? A Case Report
Authors: Hyder Jeffrey , Srinivasan Sachin , Tofteland Nathan , Salyers William , Fanari Zaher 
Published: October 2019

INTRODUCTION:
Patients with cirrhosis requiring transplant are usually fraught with co-existing co-morbidities that make them poor surgical transplant patients. One such common co-morbidity is severe aortic stenosis. Trans-catheter aortic valve replacement (TAVR) is a promising alternative to surgical aortic valve replacement (SAVR) in patients at intermediate to high surgical risk. A recent meta-analysis by the above authors (Srinivasan, Fanari et al) has shown improved medical and surgical outcomes in patients undergoing TAVR. We here describe the case of a patient with cirrhosis and severe aortic stenosis who had significantly improved outcomes post-TAVR.

CASE DESCRIPTION/METHODS:
A 73-year-old white male with past medical history significant for CAD status post-CABG, congestive heart failure with reduced ejection fraction (EF 30%), end-stage renal disease on dialysis (EGFR- 20 mL/min per 1.73 m2 ) and cirrhosis secondary to hepatitis C (MELD-24) presented to the clinic for increased shortness of breath and fluid retention over the past two days. Most recent ECHO demonstrated severe aortic stenosis (AS), moderate to severe mitral valve regurgitation, and atrial fibrillation. The patient had a balloon valvuloplasty one-year prior for his AS. On CT, the aortic valve was found to be tricuspid and have bulky calcifications of the aortic valvular leaflets with a calcium score of 2000. He was deemed a poor surgical candidate given his co-morbidities and it was discussed that he might benefit from TAVR. He underwent the procedure without any complications. Post-procedure ECHO demonstrated no evidence of aortic stenosis or para-valvular leak. The patient’s mitral valve regurgitation was reduced from severe to mild to moderate. His LVEF was increased mildly to 35%. One day after the procedure the patient’s EGFR increased to 50 mL/min per 1.73 m2 and the patient no longer needed dialysis. The patient’s MELD score significantly decreased from 24 to 11. His calculated MAYO post-operative mortality risk at 7, 30, and 90 days decreased from 22%, 65%, and 81% to 4%, 15%, and 24% respectively. The patient tolerated the procedure well and was discharged to home two days post-operatively.

DISCUSSION:
Patients with cirrhosis and co-existent co-morbidities (esp. AS) are poor surgical candidates. TAVR in such patients could significantly improve their post-operative mortality risk and potentially improve their candidacy for liver transplantation.
2254 A Rare Case of Valproate-Induced Encephalopathy Requiring Hemofiltration
Authors: Myat Thin , Win Min 
Published: October 2019

INTRODUCTION:
We present a rare case of acute encephalopathy due to Valproate induced hyperammonemia required Hemofiltration (HF).

CASE DESCRIPTION/METHODS:
45-year-old male was brought in by caregiver to the hospital with acute altered mental status, somnolent but arousable. PMHx of CP, Epilepsy, Left sided hemiplegia, Mental retardation, Abscess of thigh and wrist. Medications were Valproate and Phenytion. PE showed stable vitals, confused, was spitting to staff required restraints. Pupils equal, reactive to light. Neurological exam- left sided hemiplegia. Lab showed Na 140, K 4.0, HC03 30, BUN 7, Cr 1.18, Glucose 101, Osmolarity 287, ALT 24, AST 24, T Bil 1.1, Albumin 3.5, Al phos 79, Mg 2.0, lactic 1.2. WBC 6.9, hemoglobin 15.2, platelet 291, INR 1.2, Ammonia 402. Blood & urine culture and toxicology were negative. Acute hepatitis panel was non- reactive, Ceruloplasmin 32, ferritin 33.7, AMA < 20.1, Smooth muscle antibody < 1:40. Valproic acid level 125 mcg/ml (therapeutic level-50-100 mcg/ml). ECG was normal. Head CT showed no acute abnormality. Ultrasound showed fatty infiltration & Cholelithiasis. Unremarkable EGD. Lactulose & xifaxan were given for hyperammonemia, recurrent seizures occurred.

RESULTS:
Valproate was discontinued. L-carnitine 100 mg/kg IV loading dose was given. Received HF for 3hrs , and supportive care. Ammonia at 2hours post HF was 80. Patient’s mental status improved back to baseline over 24 hours.

DISCUSSION:
Acute encephalopathy due to valproate induced hyperammonemia required Hemofiltration is very rare. The incidence of valproate-induced hyperammonemia in the general population of patients taking VPA (Valproate acid) is not well established. Most cases of Valproate acid- toxicity are rather benign and resolve with supportive therapy. It is generally accepted that serum level >180 mcg/ml represents a high risk of toxicity. Our case was a first patient without chronic liver disease and valproate level was below high risk for toxicity who presented with acute encephalopathy due to valproate induced hyperammonemia and required Hemofiltration. Care of patients depends upon recognition of those at increased risk, anticipation & prevention, and appropriate response when they occur. Discontinuation of Valproate may require. L-carnitine has a significant mortality benefit in patient severe Valproate toxicity. HF is reserved for severely ill patients who have not responded to less invasive treatment.
2258 Cascara Sagrada: A Dangerous Herbal Stool Softener: A Case Report and Literature Review
Authors: Flores Estefania , Mbachi Chimezie , Randhawa Tejinder , Vohra Ishaan , Agrawal Rohit , Mba Benjamin 
Published: October 2019

INTRODUCTION:
The percentage of drug-induced liver injury due to the use of herbal supplements has exponentially increased over the last decade from 7% to about 20%. Liver injury attributed to supplement use is associated with more deaths than cases attributed to anabolic steroid use or even allopathic medications.

CASE DESCRIPTION/METHODS:
53-year-old female presented with jaundice, pruritus, fatigue, clay-colored stools and dark-colored urine for 4 days. She reported taking an herbal supplement called cascara sagrada for constipation over an 8-week period. On physical examination she appeared jaundiced, abdomen was non-tender, non-distended, and there was no hepatomegaly. Laboratory tests were significant for total bilirubin 8.2 mg/dL, direct bilirubin 5.5 mg/dL, ALP 459 U/L, GGT 733 U/L, AST 1274 U/L, ALT 1711 U/L, INR 0.97, ferritin 1409 ng/ml, transferrin saturation 59%, viral hepatitis antigens and antibodies were negative and an autoimmune panel was unremarkable. Liver ultrasound revealed coarse echotexture with no hepatomegaly and no biliary dilatation. Patient was discharged with close follow up. Five days after discharge, total bilirubin was 19 mg/dL with worsening symptoms necessitating re-admission. Further workup with liver biopsy showed marked portal and lobular chronic inflammatory infiltrate and focal bile duct injury and cholestasis; iron stain showed minimal Kupffer cell iron deposition but no hepatocellular deposition. Patient improved clinically and biochemically after discontinuation of cascara sagrada, with normalization of liver function tests after 3 months of the initial presentation.

DISCUSSION:
Cascara Sagrada is a herbal medication used for short term treatment of constipation, generally well tolerated but is known to cause liver injury when used in higher doses than recommended. Anthraquinone derivatives are the active laxative components; promoting peristalsis and inhibiting reabsorption of water and electrolytes. Cascara is slightly absorbed, and typical recommended courses are for less than 7 days. The mechanism of liver injury is not well understood but it has been hypothesized that it is mediated by the direct toxicity of anthraquinone derivatives. Liver injury can present with a pattern of serum enzyme elevation that can be either hepatocellular or cholestatic and ranges in severity from mild transaminase elevation to severe hepatitis with associated portal hypertension and ascites. Nevertheless, injury is usually self-limited and typically reversible upon discontinuation.
2262 Too Much TAE: A Case of Tumor Lysis Syndrome After Repeat Transarterial Embolization of Hepatocellular Carcinoma
Authors: Henry George 
Published: October 2019

INTRODUCTION:
Hepatocellular carcinoma (HCC) is the sixth most common cancer in the world & the second highest cause of cancer-related deaths globally. In the US, HCC incidence has almost tripled since the 1980s & has become the fastest rising etiology of cancer-related deaths. Tumor lysis syndrome (TLS) is a condition that results when malignant cells release their intracellular contents, either spontaneously or in response to cytoxic treatment. The cellular contents result in hyperuricemia, hyperkalemia, hyperphosphatemia, & hypocalcemia; these disturbances can lead to arrhythmias, AKI & death. TLS is common in leukemias & lymphomas but is rare in solid tumors.

CASE DESCRIPTION/METHODS:
A 50-year-old female with biopsy proven HCC without cirrhosis was admitted for planned transarterial chemoembolization (TACE) of her large right lobe & medial left lobe HCC, measuring 13.3 × 17.9 × 21.8 cm (Image 1), as too advanced for surgical resection or transplant & she had large liver-lung shunt preventing radioembolization treatment. Interventional Radiology (IR) placed two vials of LC beads containing doxirubicin 100mg & bland transarterial embolization (TAE) via 2.5 vials of Embospheres into right hepatic artery. Afterwards, she had acute drop in Hgb with CTA revealing multiple areas of active bleeding in the liver & new hematoma centrally in the mass. IR performed complete embolization of the right hepatic artery using coils & gelfoam to achieve hemostasis; patient was transferred to ICU. She received blood products & lab monitoring, the latter demonstrated new hyperkalemia of 5.5 mmol/L, previously normal. Creatinine increased from 0.55mg/dL to 1.23, thought to be multifactorial. Additional workup revealed uric acid of 12.5mg/dL, calcium 6.9mg/dL & phosphorous 7.4mg/dL. TLS was diagnosed & treated with intravenous fluids for dilution, rasburicase for hyperuricemia, furosemide for renal dysfunction & minimal urine output, & insulin for hyperkalemia.

DISCUSSION:
HCC is a growing health burden, & advanced tumors that are not candidates for surgical resection are commonly treated with radiofrequency ablation, TACE, TAE, & chemotherapy. Early recognition of TLS is key for treatment & involves awareness of the propensity for development of TLS in large tumor burdens, rapidly dividing tumors, multiple treatment sessions, & pretreatment renal dysfunction. Oliguria after IR treatment of HCC should raise the suspicion for possible TLS & not be easily dismissed as the common but less fatal contrast induced nephropathy.
2264 Hyperammonemia Secondary to an Acquired Urea Cycle Disorder in a Patient With Metastatic Hepatocellular Carcinoma
Authors: Sen Ahana , McNutt Markey , Singal Amit G. , Lee William M. , Rich Nicole E. 
Published: October 2019

INTRODUCTION:
Urea cycle disorders are rare but critically important to consider in the differential diagnosis of hyperammonemia. Delayed treatment may result in disastrous neurologic consequences.

CASE DESCRIPTION/METHODS:
A 45-year-old woman with past history of gastric sleeve, no known liver disease, and biopsy-proven hepatocellular carcinoma (HCC) with peritoneal metastases on sorafenib presented with acute onset confusion and seizures. She was found to have severe hyperammonemia to 331 µMol/L. Labs were also notable for normal urine organic acids and low plasma citrulline (Table 1). She started on emergent dialysis as well as levetiracetam, lactulose, rifaximin, citrulline, and a low protein diet; sorafenib was discontinued. Her ammonia levels and mentation gradually improved over 3 days. She underwent genetic testing for 14 genes associated with primary urea cycle defects and further testing for another 72 genes associated with secondary hyperammonemia, all of which were negative.

DISCUSSION:
Urea cycle disorders (UCDs), whether genetic or acquired, can lead to life-threatening hyperammonemia. While classically seen in children, an increasing number of late-onset genetic UCDs have been reported. Ornithine transcarbamylase (OTC) deficiency in particular is X-linked and late-onset, and mild forms are more common than in other genetic UCDs. Individuals may also develop acquired urea cycle defects, with symptoms and lab results consistent with the genetic forms but without an identifiable mutation, as seen in this patient. Acquired UCDs have been reported secondary to tyrosine kinase inhibitors such as sorafenib, and a few cases described in untreated fibrolamellar-type HCC (Table 2). Whether these are primary acquired deficiencies in the setting of hypermetabolic states, as seen in advanced tumors, or an unmasking of an underlying genetic predisposition remains unknown. Further, this patient’s bariatric surgery could have resulted in nutritional deficiencies, revealing an occult UCD. Regardless of etiology, treatment for UCDs includes aggressive ammonia control with nitrogen scavengers, amino acid supplements, and appropriate dietary protein intake. Suspected offending agents should be stopped immediately and emergent hemodialysis initiated if hyperammonemia does not improve with conservative measures. Empiric therapy should be initiated even without confirmation of the diagnosis, as prolonged exposure to high ammonia can lead to irreversible neurological ramifications.
2265 Umbilical Hernia Rupture Complicated by Enterocutaneous Fistula in 63-Year-Old Female With Decompensated NASH Cirrhosis
Authors: Kloska Michal , Sullivan Matthew J. , Peyton Adam , Adeel Waqas 
Published: October 2019

INTRODUCTION:
Spontaneous umbilical hernia rupture, known commonly as Flood syndrome, is a rare complication of severe ascites in end stage liver disease. Leakage of ascitic fluid leads to skin ulceration and necrosis which poses a threat of infection in addition to risk of evisceration or incarceration of bowels. Surgical repair is often deferred due to high mortality risk in decompensated cirrhosis which further complicates management.

CASE DESCRIPTION/METHODS:
A 63-year-old female with decompensated NASH cirrhosis, type 2 diabetes, atrial fibrillation, chronic heart failure, and morbid obesity was admitted after she developed sudden rupture of umbilical hernia with large amount of fluid discharge after defecation. She was afebrile and normotensive and was found to have ulcerated, ruptured umbilical hernia with active leakage of yellow fluid. Labs were significant for thrombocytopenia (115 × 10^3/µL), mild creatinine elevation (1.11 mg/dl), hyperbilirubinemia (2.8 mg/dl) and hypoalbuminemia (2.2 mg/dl). CT of the abdomen and pelvis revealed large abdominal wall hernia containing large and small bowels with questionable low-grade partial small bowel obstruction. General Surgery was involved but as she didn’t want to undergo any invasive treatment and due to high surgical risk, conservative treatment was recommended. Two days later she became febrile and hypotensive, accompanied by acute kidney injury (1.40 mg/dl) and worsening bilirubin (3.5 mg/dl). Due to high likelihood of SBP, diuretics were held, and ceftriaxone and albumin were initiated. Her INR increased to 6.3 and thrombocytopenia progressed (56 × 10^3/µL). Blood cultures showed no growth, but ascitic fluid cultures revealed polymicrobial flora including Bacteroides fragilis raising concerns of enterocutaneous fistula. Fortunately, she improved with conservative management and was safely discharged.

DISCUSSION:
Flood syndrome is caused by increased intraabdominal pressure during coughing, vomiting or defecating, like in our patient. Treatment is challenging as surgical repair is associated with high mortality despite known benefits of hernia repair in cirrhotic patients, however, these studies did not include decompensated cirrhosis. Patients are at increased risk of intraperitoneal infection, which was likely the case in our patient, however formation of enterocutaneous fistula is extremely rare.
2268 Rituximab for the Treatment of Refractory Autoimmune Hepatitis
Authors: Lourdusamy Vennis , Kemmer Nyingi , Albers Christopher , Syed Rashid , Malespin Miguel , Agrawal Saurabh 
Published: October 2019

INTRODUCTION:
Autoimmune hepatitis can be refractory to steroids and traditional immunosuppressant agents especially in the setting of coexisting autoimmune conditions. We describe a patient with autoimmune hepatitis and Neuromyelitis Optica with elevated liver enzymes who was refractory to the traditional immunosuppressant management, but responded to therapy with Rituximab.

CASE DESCRIPTION/METHODS:
Our patient is a 57-year-old male who was diagnosed with Autoimmune hepatitis after he presented with elevated liver enzymes. Just prior to being evaluated for autoimmune hepatitis, he was diagnosed with Neuromyelitis Optica after extensive investigation when he presented with recurrent symptoms of diffuse paresthesia and muscle weakness distributed all over the body. His liver enzymes at the time of presentation were ALT (1688), AST (656), ALP (193), Bilirubin (1). Autoimmune work up was positive for NMO IgG antibody and ANA, but negative for AMA and ASMA. Liver biopsy was consistent with autoimmune hepatitis showing interface hepatitis with necroinflammatory activity and presence of plasma cells with lobular disarray. Work up for other chronic liver diseases was negative. He initially improved with pulse dose of IV steroids and was later transitioned to maintenance therapy with oral prednisone and Imuran. But, he continued to have moderately elevated liver enzymes with relapses of both autoimmune hepatitis and neurological symptoms on combination of prednisone and Imuran, and also experienced adverse effects from Imuran. He was later transitioned from Imuran to Cellcept without significant improvement. He was finally started on Rituximab infusion due to severe neurologic symptoms with complete normalization of liver enzymes and remission of Neurological manifestations.

DISCUSSION:
Rituximab is an anti CD 20 monoclonal antibody that depletes B cells. It has been shown to improve many autoimmune conditions and should be considered in refractory cases of autoimmune hepatitis especially in the setting of coexisting autoimmune conditions. Although prior case reports and case series have demonstrated the efficacy and safety of Rituximab in difficult to treat autoimmune hepatitis, it is not currently FDA approved for this purpose and payers will usually deny coverage. Prospective clinical trials of Rituximab in refractory autoimmune hepatitis should be considered for further validation.