bluuebunny/crossref_metadata_2025_split huggingface dataset:
2242 I'm Starving: A Rare Case of Liver Autophagocytosis Secondary to Anorexia Nervosa
Authors: Rozenshteyn Frederick , Rastogi Neelesh , Collins Kelsey , Nagirimadugu Ankita , Ascunce Gil 
Published: October 2019

INTRODUCTION:
Anorexia nervosa is a common eating disorder associated with fear of gaining weight and when severe can cause life-threatening complications. While mild elevations in liver enzymes can occur in anorexia, severe liver injury is rarely reported. Autophagy is a liposomal catabolic pathway that is crucial for cell survival under stressful conditions. We present the case of a young female with anorexia nervosa with severe malnutrition found to have significantly elevated liver enzymes concerning for autophagocytosis of the liver.

CASE DESCRIPTION/METHODS:
A 19-year-old female with a history of severe anorexia nervosa (BMI 11.5) presented with 3 days of abdominal pain. Basic lab testing was done which revealed significant elevations in LFTs in a hepatocellular pattern with both AST and ALT above 1000. The patient underwent abdominal imaging with no major abnormalities found and viral, drug-induced, and autoimmune causes were also ruled out. However, her LFTs continued to uptrend with a peak AST of 6328 and ALT of 5606 and her hospital course was complicated by hypotension requiring ICU care. Due to severe nutritional deficits and inability to tolerate oral intake, the decision was made to initiate supplemental nutrition first with TPN and subsequently with enteral feeding through a PEJ. Following nutrition initiation, the patient’s liver enzymes started to down-trend and ultimately normalized within a couple weeks of nutritional support. Therefore, it was determined that the patient’s acute liver elevations and abdominal pain were likely secondary to liver autophagocytosis in the setting of severe starvation from anorexia nervosa. Due to the normalization of her LFTS, liver biopsy was not pursued. The patient improved and was discharged to a specialized eating disorder rehabilitation center.

DISCUSSION:
Autophagy is a physiologic process the body activates under episodes of severe stress which can include severe malnutrition. While mild liver enzyme elevation can occur, there are only a few reported cases of profound LFT elevation such as in this patient. Initiation of enteral/parenteral nutrition appears to improve liver injury and stop autophagy. Therefore, careful implementation of nutritional support and close monitoring of LFTs is essential in anorexic patients with liver injury to help treat the underlying condition, avoid unnecessary invasive diagnostic testing, and prevent further autophagy.
2244 Getting to the Root of the Matter: A Case of Valerian Root-Induced Hepatitis and Pancreatitis
Authors: Bergagnini Isabella , Kadosh David , Nguyen Andrew , Swaminath Arun 
Published: October 2019

INTRODUCTION:
The use of herbal supplements has increased substantially in recent years for amelioration of common ailments. Valerian root, a common over-the-counter supplement (OTC) used for insomnia and anxiety, has been in rare instances linked to hepatotoxicity and pancreatitis, as depicted in the case below.

CASE DESCRIPTION/METHODS:
A 36-year-old gentleman with no significant medical history presented with worsening burning abdominal pain, nausea and vomiting for one day with similar symptoms three months prior. Labs were notable for elevated AST/ALT 682/619, GGT 100, and lipase 220. Abdominal ultrasound showed mildly echogenic liver with no intrahepatic or extrahepatic ductal dilatation or cholelithiasis, and patent hepatic and portal veins. CT abdomen and pelvis demonstrated acute edematous interstitial pancreatitis with a small heterogeneous area concerning for necrosis. The patient revealed routine use of multiple OTC supplements including Driftoff and Epi-dry, and Valerian root, each of which contain Valerian officinalis. The remaining workup was negative for infectious, autoimmune, and other toxic etiologies. On day two, AST/ALT peaked at 2398/3132 and N-acetylcysteine (NAC) was initiated. Labs and symptoms improved and he was discharged home on day four. At follow-up in 2 weeks, he was asymptomatic, remained off supplements, with normalization of his transaminases.

DISCUSSION:
Valerian officinalis is increasingly used for its sleep aid properties and anxiolytic effects. Its interaction with gamma-aminobutyric acid (GABA) receptor produces effects similar to benzodiazepines though clinical data is scant. Presentation of valerian root induced hepatotoxicity varies, ranging from no symptoms to overt jaundice, with abdominal pain as the most common symptom. Liver enzyme elevation is of hepatocellular or hepatocellular-cholestatic pattern with aberrancies seen 3-12 weeks later. While the mechanism of hepatotoxicity remains unknown, the literature suggests gallstone formation may be responsible for valerian root induced pancreatitis unlike our case which suggests a drug induced injury. Effects are self-limited though abstaining from the causative agent is paramount. Management often remains supportive. Although data is limited, NAC has been used in non-acetaminophen induced hepatotoxicity and aided in improvement in liver injury in our patient. We present this case to raise awareness of this potential toxin and consider this in the differential when evaluating concomitant hepatitis and pancreatitis.
2245 Thoracic Neuroendocrine Tumor With Hepatic Metastases: An Ideal Case for Radioembolization
Authors: Kolli Sindhura , Aamar Ali , Etienne Denzil 
Published: October 2019

INTRODUCTION:
This rare case of a thoracic neuroendocrine tumor (NET) metastasizing to the liver is meant to bring attention to the lag in diagnosis until symptoms from the metastases become discernible. It also acknowledges recent literature on radioembolization efficacy in disease control rate as well as symptom resolution for NET with liver metastases, in particular.

CASE DESCRIPTION/METHODS:
A 56-year-old male patient with cirrhosis secondary to hepatitis C s/p treatment presented with RUQ abdominal pain, fever, chills, and fatigue. Labs show elevated AST/ALT/ALP of 64/72/227, respectively. A CT abdomen and MRCP demonstrated a cirrhotic liver with multiple hypodense ill-defined hepatic lesions with portocaval lymphadenopathy. An EGD discovered 4 non-bleeding esophageal varices and hypertensive portal gastropathy (Figure 2). EUS-guided liver and periportal lymph node biopsies returned positive for a high grade poorly differentiated metastatic NET with greater than 50% positive for KI-67. Octreotide scan was negative. PET scan indicated the primary source as possibly thoracic given mediastinal involvement. Currently, patient is receiving cycles of carboplatin and etoposide.

DISCUSSION:
NETs arise from neurological and hormonal cells within any organ system and are classified by their anatomical location. Incidence is 5/100,000 with total prevalence 35/100,000, with the highest proportion reported in African Americans. Genetically, they are associated with MEN1, VHL, and tuberous sclerosis. Symptoms are present for 5-7 years before finally being diagnosed and include abdominal pain, diarrhea and fatigue. They are detected sooner if they are functional tumors that secrete hormones, such as serotonin, causing carcinoid syndrome. A majority, however, are non-secretory or non-functional and found incidentally. For diagnosis and staging, a CT or MRI and Ki-67 IHC staining. An octreotide scan is sensitive for a well-differentiated NET, whereas a PET scan is more sensitive for poorly differentiated or high grade tumors. Treatment entails laparoscopic removal or debulking, local hepatic ablation via radiofrequency, cryotherapy or electroporation, or embolization of the hepatic artery. For those with metastases or poor surgical candidates, chemotherapy with cisplatin and streptozocin are widely used. A recent study showed that radioembolization for NETs with hepatic metastases had a 91% disease control rate and 79% had resolution of NET-related symptoms.
2248 Primary Malignant Mesothelioma of Liver: A Rare Liver Tumor
Authors: Ghimire Subash , Yang Tsujung , Shah Harshil , Srivatana Ukorn , Sarker Ashit 
Published: October 2019

INTRODUCTION:
Primary malignant mesothelioma of liver is an extremely rare condition. Less than twenty cases have been reported so far in literature. This presents as liver mass and differentials include primary and secondary tumors of the liver. We describe the case of a 70-year-old male with asbestos exposure who was incidentally found to have primary malignant mesothelioma of liver in screening CT scan.

CASE DESCRIPTION/METHODS:
A 70-year-old non-smoker, nonalcoholic male with past medical history of pulmonary asbestosis (had a stable calcified pleural plaques, no evidence of metastatic disease in the chest) being followed with annual low dose CT scan for asbestosis exposure management was found to have an incidental liver mass in the CT scan. He did not have icterus, itching of the skin or change in his stool color or weight loss. Upon examination, he was found to be hemodynamically stable, there was no jaundice. There was no right upper quadrant tenderness on palpation. CT scan of abdomen with contrast was obtained that showed an 8 cm mass involving the right lobe of liver predominantly the segment 6 (Figure 1). This mass was highly concerning for liver malignancy. A bone scan was obtained for metastatic workup which did not reveal any metastatic disease. CT scan of the chest was done that did not show any evidence of hematogenous metastasis or mesothelioma in the thorax. His hepatitis panel, AFP level were negative. There was no elevation of liver enzymes. The patient underwent partial hepatectomy (segments V/VI), diaphragm resection and cholecystectomy. Biopsy of the liver mass showed a poorly differentiated malignancy, showing areas of epitheloid and spindle cell morphology. The tumor cells were positive for keratin AE1/AE3, keratin CAM 5.2, WT1, calretinin, CK20 and D2-40. Tumor cells were negative for arginase, CK 5/6, ERG, mucicarmine, MOC 31, BerEp4, desmin, S–100, and albumin in situ hybridization. The overall morphology as well as immunohistochemical staining pattern were most consistent with malignant mesothelioma. The patient was started on adjuvant chemotherapy with Pemetrexed and Cisplatin.

DISCUSSION:
Primary malignant mesothelioma of liver is an extremely rare condition. This presents a solitary lesion in the liver. Treatment includes surgical resection followed by adjuvant chemotherapy with Pemetrexed and Cisplatin. It should be considered as a differential in patients with solitary liver mass.
2249 Rectus Sheath Hematoma Post Abdominal Paracentesis: A Rare Complication
Authors: Laoveeravat Passisd , Tikue Alay M. , Thavaraputta Subhanudh , Suchartlikitwong Sakolwan , Mingbunjerdsuk Thammasak , Thongtan Thanita , Nugent Kenneth 
Published: October 2019

INTRODUCTION:
Rectus sheath hematoma (RSH) is a very rare complication after abdominal paracentesis especially in patients who do not take antiplatelet or anticoagulants. We presented a case of rectus sheath hematoma post paracentesis in a patient without obvious risk factors.

CASE DESCRIPTION/METHODS:
A 56-year-old male with past medical histories of chronic diastolic congestive heart failure and end-stage renal disease (ESRD) on hemodialysis presented with abdominal pain after abdominal paracentesis for ascites. 4.3 L of yellow ascitic fluid was drained in the first attempt of ultrasound-guided paracentesis. Abdominal distension on the right flank was also noticed. Vital signs were stable. Abdominal exam showed moderate tenderness on right flank, no guarding, no rebound tenderness, no bruising. ESRD was believed to be the cause of ascites. He received hemodialysis one day prior to the procedure. He is not on any antiplatelet or anticoagulation therapy. Computed tomography scan of abdomen showed right rectus sheath hematoma 14 × 9 cm (Figure 1). Labs on admission showed Hemoglobin (Hb) of 9.2 g/dL (compared to baseline Hb of 10.8 g/dL), Platelet count 192000 /uL, PT 13.9 secs, PTT 34.6 secs, and INR 1.22, BUN 42 mg/dL, Creatinine (Cr) 5.6 mg/dL (similar to baseline Cr). Interventional radiologist was emergently consulted and performed embolization which found extravasation from the right iliolumbar artery (Figure 2). Coil embolization was done successfully. On post-embolization day 3, Hb continued to drop to 5.7 g/dL. He developed hypotension. Surgery team was notified and brought the patient to operation room for exploratory laparotomy. Intraoperative findings revealed that 2 L of hematoma was evacuated from the patient’s rectus sheath. No active bleeding was immediately noted. Upon the exploration of the anterior wall toward the medial side of the incision, a small bleeding vein was noted and ligated. Vital signs became stable after the operation. He was discharged without postoperative complications.

DISCUSSION:
Large RSH is a rare complication of paracentesis. It can also develop in a patient without obvious bleeding risk factors. Clinicians should watch for this potential complication when a patient presents with an abdominal mass or abdominal pain without other particular symptoms after paracentesis. RSH is a self-limited condition; however, our case suggests that RSH may take an unpredictable course and may not be successfully managed with a conservative approach.
2252 From Lungs to Liver: Acute Budd-Chiari Syndrome Secondary to Small Cell Lung Carcinoma
Authors: Weismiller Scott , Ganapini Vincent , Ramasamy Kovil 
Published: October 2019

INTRODUCTION:
Budd-Chiari syndrome (BCS) is any process that inhibits hepatic venous outflow. It is caused by malignancy in 10% of all cases, either through hepatic vein / inferior vena cava (IVC) thrombosis and / or vascular compression due to mass effect. Clinical suspicion should remain high when abdominal pain, jaundice, and hepatomegaly are present with elevated transaminases, alkaline phosphatase, and bilirubin. This is a rare case of acute BCS caused by metastatic small cell lung carcinoma (SCLC) compressing the IVC.

CASE DESCRIPTION/METHODS:
A 61 y/o male with hypertension, dyslipidemia, asthma, and nonalcoholic fatty liver disease presented to the ED for URI symptoms refractory to antibiotics and steroids. He denied weight changes, hemoptysis, nausea, abdominal pain, sick contacts, and recent travel. The patient reported 22 years of second-hand smoke exposure as a police officer. He denied alcohol, tobacco, or illicit drug use. On exam he had a firm, distended abdomen. Laboratory exam showed: WBC: 18.8 103/µL, lactate: 2.8 mmol/L, BUN: 25 mg/dL, Tbili: 3.0 mg/dL, AST: 637 U/L, ALT: 606 U/L, ALP: 362 U/L, and LDH: 11173 U/L. Autoimmune, infectious, and toxicology workup was negative. Abdominal US and CT revealed hypoechoic liver masses and hilar / mediastinal lymphadenopathy. His liver biopsy identified a primary small cell carcinoma. The patient developed severe elevation of transaminases and acute kidney injury. RUQ tenderness, hepatomegaly, and jaundice correlated with worsening liver and kidney tests (Figures 1, 2). Abdominal CT revealed extra-luminal tumor compression of the IVC (Figure 3). The oncologist began carboplatin / etoposide in the ICU with rapid improvement of his labs and symptoms. The final diagnosis was stage IV SCLC complicated by BCS. The patient expired six months later.

DISCUSSION:
BCS caused by primary lung carcinoma (PLC) is rare; less than a dozen cases are reported in the literature. Prompt diagnosis of PLC allowed for targeted chemotherapy, which reduced tumor burden, improved symptoms, prevented acute liver and renal failure, and prolonged life. Rapid treatment may have prevented ascites by restoring hepatic venous pressures. Clinical suspicion of BCS should be based on physical exam and lab findings even with negative doppler US or CT. Past cases showed post-mortem tumor invasion of hepatic vasculature despite negative imaging. The overall prognosis for stage IV SCLC is poor, making early immunohistochemical analysis, tumor identification, and treatment method paramount.
2255 Acute on Chronic Hepatic Failure From Primary Amyloidosis (AL): A Fatal Complication
Authors: Rashid Mamoon Ur , Khan Muzammil Muhammad , Ullah Waqas , Zafar Hammad , Hussain Ishtiaq , Hasan Badar , Ur Rehman Fnu Asad , Hurairah Abu 
Published: October 2019

INTRODUCTION:
Hepatic involvement in primary amyloidosis (AL) is common but rarely causes severe cholestasis. We are here reporting a case of acute on chronic hepatic failure from amyloidosis leading to a severe decline in patient’s clinical status and fatality.

CASE DESCRIPTION/METHODS:
44 years old man was initially seen for persistent cough and recurrent right-sided pleural effusion. Thoracentesis showed exudative effusion. A right VATS with decortication was done. Pathology showed extensive caseating granulomas and tissue cultures came back positive for MTB. Initial labs showed elevated LFT’s with a cholestatic pattern. The patient was started on levofloxacin, rifabutin and ethambutol due to less hepatotoxic profile. During hospitalization, patient LFTs kept on worsening. Medications were stopped and a liver biopsy was done. There was significant involvement of the liver by amyloidosis (AL). Patient further workup included a bone marrow biopsy which revealed 30-40% cellularity, 5-10% plasma cells, amyloidosis AL (Kappra type) consistent with multiple myeloma. Oncology team recommended chemotherapy with CyborD (Bortezomib, dexamethasone and cyclophosphamide) for multiple myeloma. In spite of chemotherapy patient hepatic, renal and cardiac functions were worsening. Patient developed abdominal pain, moderate ascites and hypotension with elevated INR and bilirubin of 30. He was ultimately transferred to ICU where he developed cardiac arrest and could not survive.

DISCUSSION:
Primary amyloidosis (AL) is the most common form of systemic amyloidosis with mean age of diagnosis 65 years and less than 10% of patients being 50 years of age. As compared to myeloproliferative disease, leukemias and lymphomas, hepatic involvement is less common in multiple myeloma (32%). Amyloid deposits may be seen in the liver with hepatomegaly and normal to mild elevation of hepatic enzymes but serious manifestations such as hepatic failure and portal hypertension are rare. Previously in literature very few cases of acute hepatic failure from AL amyloidosis have been reported. Diagnosis is made by biopsy of the involved site showing amyloid deposits. There has been reported limited success for liver transplantation as the disease progression is unchanged in the presence of plasma cell dyscrasias. In the literature combined approach with autologous stem cell transplant and liver transplant have been suggested but the prognosis still remains poor.
2257 Hepatic Dysfunction as a Result of Multiple Myeloma
Authors: Taborda Cesar , Barrett Amanda , Li Shiyong , Vora Ravi 
Published: October 2019

INTRODUCTION:
Plasma cell infiltration of the liver can be detected in up to 45% of patients with multiple myeloma (MM) at autopsy. However, only a few cases have been reported of plasma cell infiltration of the liver leading to plasmacytoma formation and non-obstructive cholestasis with progression to liver failure.

CASE DESCRIPTION/METHODS:
A 53-year-old African American male with history of IgG multiple myeloma status post AlloimmuneStem Cell transplant (ASCT) in 2010 was admitted for intermittent epistaxis, hemoptysis and fatigue found to have relapse. Patient was started on salvage therapy with bortezomib, dexamethasone, cyclophosphamide, etoposide and cisplatin (VDCEP). Physical exam revealed an alert and lethargic male in no acute distress but with asterixis. Sclera were icteric. Abdominal exam revealed marked hepatomegaly without tenderness. Laboratory data showed an ALT of 60 IU/L, total bilirubin of 11mg/dL and normal AST and ALP . INR was 3.0, platelets 38 × 103 mcL, Hgb 7.6gm/dL and WBC 1.6 × 103 mcL. Factor VIII activity was 311.1%. Ammonia levels were 67mcmol/L. Imaging with MRI showed an enlarged liver measuring 22.4cm without mass lesions. A transjugular liver biopsy was then performed revealing atypical mononuclear cell infiltration with positive stain for CD138 and MUM1 consistent with patient’s known history of labda-restricted plasma cell neoplasm (Figures 1 and 2). His clinical course deteriorated with worsening total bilirubin, hepatic encephalopathy and coagulopathy consistent with liver dysfunction and acute liver failure. Eventually there was development of multiorgan failure and death. Autopsy confirmed presence of myeloma cells in the liver forming a subcapsular plasmacytoma with associated extensive cholestasis and hepatocyte necrosis.

DISCUSSION:
Hepatic involvement of multiple myeloma most commonly presents with hepatomegaly and portends poor prognosis. It is important to recognize that patients may present with a cholestatic pattern of liver injury which can lead to severe hepatic dysfunction and liver failure such as the case of our patient. The histological pattern of liver involvement in MM can be in the form of light chain deposition disease, extramedullary plasmacytoma, amyloidosis, or a diffuse infiltrative pattern. Liver biopsy is thus an imperative way of diagnosis particularly to differentiate it from other entities causing similar pattern of injury such as sinusoidal occlusive syndrome or drug induced liver injury.
2259 Severely Jaundiced Body Builder: A Case of Acute Cholestatic Syndrome With Anabolic Androgenic Steroid Use
Authors: Flores Estefania , Fu Damon , Attar Bashar M. , Palacios Pedro , Vohra Ishaan , Demetria Melchor V. 
Published: October 2019

INTRODUCTION:
Illicit use of anabolic androgenic steroids (AAS) has been growing among athletes and bodybuilders for cosmetic and performance purposes. We report a case of one of the possible hepatic complications of AAS, acute cholestatic syndrome (ACS), in a male with anabolic steroid abuse.

CASE DESCRIPTION/METHODS:
27-year-old Polish man with no past medical history presented with jaundice, itching of the body, dark-colored urine, clay-colored stools for 5 weeks. No abdominal pain was reported. Patient reported taking for 4 months 4 types of AAS (testosterone, oxandrolone, methasterone and trenbolone) for body building, which he stopped taking 6 weeks prior to initial presentation due to fatigue. Vitals were normal, and on exam he appeared to be a muscular, jaundiced male with scratch marks on his skin. Abdominal exam revealed a non-tender, non-distended abdomen, with difficulty palpating the liver edge due to the muscularity. Laboratory tests were significant for total bilirubin of 34.8 mg/dL with direct of 23.5 mg/dL, AST 55 U/L, ALT 70 U/L, ALP 212 U/L, GGT 57 U/L, INR 1, creatinine 1.1 mg/dL. Liver ultrasound showed hepatomegaly with no biliary dilation and patent hepatic and portal veins. A liver biopsy was obtained showing portal neutrophil predominant inflammation with occasional eosinophils, mild portal fibrosis and cholestasis, suggestive of drug-induced hepatotoxicity. Liver function tests normalized after 4 months of cessation of AAS use, with resolution of his jaundice and pruritis.

DISCUSSION:
Body builders usually prefer polydrug use of AAS to maximize the desired effects and hypothetically reduce side effects at the same time. But contrary to their belief, the concomitant use of different illicit AAS may be a factor in their toxicity, making difficult to link an adverse effect with a specific substance. Acute cholesta tic syndrome, has been associated with use of the 17α – alkylated anabolic steroids ( i.e. oxandrolone, methasterone), thought related to an increase of reactive oxygen. This leads to prolonged direct toxic effects and intrahepatic cholestasis, though the pathophysiology remains unclear. ACS usually occurs 1-4 months after steroid initiation presenting with nausea, fatigue, pruritis; later, jaundice, dark urine, with significantly elevated total bilirubin and ALP but mild aminotransferase elevation can be seen. Management consists of stopping anabolic steroid use, supportive care and symptomatic treatment of pruritis.