bluuebunny/crossref_metadata_2025_split huggingface dataset:
3154 Severe Shock as the Initial Presentation of Inflammatory Bowel Disease Unclassified
Authors: Rashed Laila Abu 
Published: October 2019

INTRODUCTION:
Age dependent immune modulation plays a major role in the late uncovering of inflammatory bowel disease (IBD). 1/3 of IBD occurs in elderly, yet the diagnosis is delayed by 6 years on average when compared to younger peers who have a 2-year delay. Subtle and unconventional symptoms plus comorbidities play a major role in this.

CASE DESCRIPTION/METHODS:
A 61-year-old veterinarian female with a long-standing history of constipation presented with acute sharp abdominal pain associated with bloating, nausea and non-bilious vomiting. Vital signs were within the normal range. Physical examination showed a slender female in mild distress, with a soft but distended abdomen that was tender to palpation mainly in the left lower quadrant. Pertinent laboratory tests showed bands 24%, WBC 7 × 103/µL, platelets 47103/µL, lactic acid 4.6 mmol/L, and alkaline phosphatase 216 IU/L. A computed tomography (CT) of the abdomen showed segmental narrowing of the body of the stomach and stool impaction. She was admitted for observation for possible early sepsis; over the course of the next 6 hours she developed severe diarrhea and shock and required admission to the ICU where she was treated empirically for a gastrointestinal infection. She was worked up extensively, but the only significant finding was a positive serum Salmonella IgM. She improved with medical management and eventually antibiotics were deescalated, she completed a 10-day course; however, diarrhea persisted and eventually became bloody. Given her history of chronic constipation the possibility of Celiac disease was entertained but work up was negative. Sigmoidoscopy with biopsy was suggestive of ischemic colitis. The hematochezia resolved by itself and apart from the ongoing diarrhea she was doing well; she was discharged home. At follow up 2 months later she was back to her baseline constipation, her calprotectin level was found to be high and upper and lower endoscopy with biopsies showed minimal active chronic colitis concerning for idiopathic IBD.

DISCUSSION:
The products of genetic mutations related to IBD are involved in antigenic recognition and the modulation of humoral and cell-mediated immunity, at times this leads to loss of self-tolerance, normal flora tolerance or tolerance to antigens that are present at low concentrations or in immune privileged locations and this event is now considered the trigger that unleashes IBD.
3158 Sacral Osteomyelitis Secondary to Crohn's Disease
Authors: Khorsandi Pedram J. , Thaker Sarang , Carroll Robert 
Published: October 2019

INTRODUCTION:
Increased ostomy output and abdominal pain can be concerning symptoms for patients with underlying gastrointestinal pathology such as Inflammatory Bowel Disease (IBD). While the acute etiology is often directly related to said underlying condition, alternative causes should remain on the differential diagnosis. The following is a case of sacral osteomyelitis as a result of direct extension from the gastrointestinal tract.

CASE DESCRIPTION/METHODS:
A 43 year old male with Crohn's disease complicated by recurrent fistula/abscess status post multiple colectomies with ileostomy and blind colostomy presented from a rehabilitation facility due to increased non-bloody watery ileostomy output and abdominal pain. He also presented with chronic rectal ulcers that appeared stable with scant purulent drainage. Vital signs were notable for hypotension and tachycardia that responded to fluids and empiric vancomycin and imipenem. Labs were notable for significantly elevated inflammatory markers, negative stool infectious panel, negative clostridium difficile, negative lactoferrin, white blood cell count of 23.9, and negative blood/urine cultures. Ileoscopy revealed colonization of the ileum and no source of high ostomy output was identified. Ileal biopsy revealed acute Crohn's enteritis. MRI pelvis fistula protocol revealed S5 osteomyelitis which was confirmed clinically by visualization in the OR. However, bone biopsy was negative in the setting of empiric antibiotic therapy. Patient was treated with approximately six weeks of vancomycin and ceftriaxone. He then followed up with Infectious Disease and had resolution of the infection and significant improvement in rectal ulcer drainage.

DISCUSSION:
Determination of the source of infection in patients with IBD can be challenging due to the inflammatory nature of the disease. Patients often present with systemic symptoms and non-specific complaints that could be mistakenly attributed to the underlying chronic disease. In any patient with fistulizing Crohn's presenting with sepsis, clinicians should have a high level of suspicion for osteomyelitis, especially in chronically debilitated patients with non-healing wounds. If routine infectious evaluation is unrevealing, clinicians should consider musculoskeletal infections due to direct extension from organic intra-abdominal processes. A broad differential diagnosis should be maintained for these Crohn's patients as multiple organ systems may be affected both directly and indirectly.
3160 The Medicaid Coverage Gap and IBD Care
Authors: Wade Francis , Srour Maria , Odufalu Florence-Damilola , Clarrett Danisa M. , Schroeder Katie S. 
Published: October 2019

INTRODUCTION:
Medicaid expansion is a key provision of the 2010 Affordable Care Act (ACA) that bolsters healthcare access for Inflammatory Bowel Disease (IBD) patients. Prior to the ACA, Medicaid was guaranteed only to specific patient populations whose income falls within certain limits of the federal poverty level (FPL). Medicaid expansion ensures eligibility for all adults aged 18-65 years with incomes up to 138% of the FPL regardless of age, family, or health status. 17 states, including Missouri, have not expanded Medicaid which has created a coverage gap for low-income adults who do not qualify for Medicaid nor the ACA's Marketplace subsidies. We present a case of a young Missourian within the Medicaid coverage gap who was unable to gain healthcare access for severe fistulizing Crohn's disease until his incarceration.

CASE DESCRIPTION/METHODS:
A 27-year-old man with Crohn's disease presented from a correctional facility with enterocutaneous fistulae and abdominal wall abscesses. He was uninsured with limited healthcare access and unable to afford the recommended biologic therapy. Once incarcerated, he qualified for Department of Corrections healthcare coverage and sought care. Surgery with temporary colostomy was recommended due to his advanced disease. The patient did not want to have an ostomy in prison so instead opted for treatment with infliximab, complete bowel rest, and total parenteral nutrition. His hospital course was complicated by drug-induced liver injury from infliximab which extended his admission to 107 days. The correctional facility eventually enacted a compassionate release which paradoxically terminated his healthcare coverage and jeopardized further access to care. The patient was enrolled in Missouri Medicaid due to disability and underwent surgery but not before suffering significant morbidity from preventable complications of Crohn's disease.

DISCUSSION:
The Medicaid coverage gap in non-expansion states limits healthcare access for non-disabled, low-income IBD patients. Our patient's case exemplifies challenges to providing healthcare to IBD patients within the Medicaid coverage gap in non-expansion states. Healthcare costs for IBD patients are more expensive than for those without IBD, increasing the importance of maximizing healthcare coverage for this patient population. Policy change in non-expansion states would improve access to healthcare coverage which may reduce hospitalizations and improve outcomes for low-income IBD patients.
3166 Autoimmune Hepatitis: When You Cannot Blame the Gallbladder Anymore
Authors: Janssens Laurens , Penrice Daniel , Kashiwagi Deanne 
Published: October 2019

INTRODUCTION:
Autoimmune hepatitis (AIH) is a chronic liver disease with varying degrees of onset severity often presenting with nonspecific symptoms such as abdominal pain, fatigue, jaundice and nausea. Although initial reports have suggested that AIH has a bimodal age distribution (with the second peak between 40 and 50 years), the condition has increasingly been recognized in all age groups, including the elderly.

CASE DESCRIPTION/METHODS:
A 70-year-old woman was admitted to our medical center with a 2-month history of abdominal discomfort, anorexia and fatigue. Past medical history was notable for hyperlipidemia. Five weeks prior to admission, the patient had presented to her primary provider with similar complaints and was found to have significantly elevated liver enzymes, as shown in Table 1. The patient denied alcohol use. At the time of admission, work-up showed similar transaminases with an increase in bilirubin (Table 1). Abdominal ultrasound revealed cholecystolithiasis and possible cholecystitis without intra- or extrahepatic ductal dilation. ERCP confirmed cholecystolithiasis without visualization of intraductal stones on cholangiogram or after sweeping of the biliary tree. Laparoscopic cholecystectomy was performed and pathology results revealed chronic cholecystitis. Despite these interventions, the patient was readmitted one week later for ongoing jaundice and malaise. She had no ascites on exam. Laboratory work-up showed persistently elevated liver tests (Table 1). Anti-smooth muscle antibodies (ASMA) were elevated at 1:80. Viral hepatitis panel was negative. Liver biopsy revealed marked panacinar hepatitis with cholestasis without hemosiderin deposition. The patient was diagnosed with autoimmune hepatitis and initiated on steroids with rapid resolution of symptoms. Transaminases and bilirubin decreased significantly one week after initiation of steroids and normalized after 6 weeks.

DISCUSSION:
The clinical presentation of AIH is often nonspecific and highly variable. Most patients present with insidious symptoms, but the spectrum of symptomatology can range from asymptomatic to severe acute disease. Acute AIH can mimic other conditions such as acute viral hepatitis and choledocholithiasis resulting in delayed diagnosis and sometimes unnecessary interventions such as ERCP and cholecystectomy. In the absence of an obvious alternative diagnosis, acute transaminitis warrants work-up that includes ASMA testing since AIH can present in virtually any age category, as highlighted in this case.
3169 Drugs! A New Mimicker of Primary Sclerosing Cholangitis
Authors: Kagihara Jaclyn E. , Kalathil Sumodh C. , Lopez Kristi T. 
Published: October 2019

INTRODUCTION:
In the United States, drug-induced liver injury (DILI) is the most common cause of acute liver failure necessitating liver transplantation. DILI can be characterized biochemically based on specific patterns of injury - hepatocellular, cholestatic, or mixed. Detection of bile-duct strictures on magnetic resonance cholangiopancreatography (MRCP) is uncommon in DILI, and nearly pathognomonic for primary sclerosing cholangitis (PSC). Here we present two cases of “PSC-like DILI.”

CASE DESCRIPTION/METHODS:
Patient 1: A 68-year-old man with type 2 diabetes mellitus (T2DM) and hyperlipidemia was admitted for sepsis secondary to methicillin-sensitive staphylococcus aureus right wrist abscess, and subsequently started on cefazolin. He developed acute hepatitis with aspartate transaminase (AST) 665, alanine aminotransferase (ALT) 367, and alkaline phosphatase (ALP) 2317. Extensive work-up, including ferritin, anti-nuclear antibody (ANA), anti-mitochondrial antibody (AMA), anti-smooth muscle antibody (SMA), and viral serology, was unremarkable. MRCP showed multi-focal areas of intra-hepatic biliary ductal dilation and mild strictures without evidence of stones or malignancy, consistent with PSC. Liver biopsy was non-specific, demonstrating portal and lobular hepatitis with mild bile duct injury, and mild steatosis without steatohepatitis. Colonoscopy did not show inflammatory bowel disease. DILI with drug-induced PSC-phenomenon was suspected. The patient's liver function tests (LFTs) normalized within 24 hours of stopping cefazolin. Patient 2: A 63-year-old woman with T2DM was found to have AST 229, ALT 186, and ALP 652, 5 months after starting atorvastatin for stroke. MRCP revealed abnormal appearance of the central intrahepatic bile ducts (Figure 1). Ferritin, alpha-1 anti-trypsin, ceruloplasmin, and viral serology were unremarkable. ANA, SMA, and immunoglobulin G were elevated, suggestive of an immunologic process. Anti-liver-kidney-microsomal antibody and AMA, however, were negative. The patient was presumed to have a drug-induced autoimmune and cholestatic reaction with PSC-cholangiographic findings. LFTs normalized within 2-months after cessation of the statin.

DISCUSSION:
DILI with concurrent findings of bile-duct strictures on MRCP has yet to be described in the literature. The first case suggests cefazolin as the culprit, while the second points to atorvastatin as the suspected trigger for DILI and an “autoimmune-PSC overlap syndrome.” Clinicians should be aware that DILI can mimic PSC.
3171 Amoxicillin-Clavulanate Related Mixed Cholestatic-Hepatocellular Injury
Authors: Vaishnani Devin , Vekaria Pratikkumar , Patel Ravish , White Megan , Vaishnani Marvin , Raiyani Tejas 
Published: October 2019

INTRODUCTION:
Recognition of Drug-induced Liver Injury (DILI) may be challenging as it is often diagnosis of exclusion, unavailability of diagnostic test and variability in presentation. Many antibiotics can cause DILI but Amoxicillin-Clavulanate has rare adverse reaction causing mixed cholestatic-hepatocellular injury. Since amoxicillin alone does not induce liver injury, combination of amoxicillin and clavulanic acid could be responsible for this adverse reaction. It can be due to metabolic idiosyncrasy or hypersensitivity mechanism.

CASE DESCRIPTION/METHODS:
64-year-old female with no pertinent PMH presented to ER with abdominal pain and jaundice. She had abdominal pain for 4-5 days. Abdominal pain was constant and located at right upper quandrant and epigastric region. She had associated complaint of nausea, vomiting, metallic taste and chills. Patient had been avoiding eating in fear of vomiting. She also had pale colored stool. Patient did not have any history of gall stones, hepatitis or alcohol use. On further inquiry, she reported being on Amoxicillin-Clavulanate for 4 days, for dental abscess, before onset of symptoms. She stopped taking antibiotic as soon as she started having above-mentioned symptoms. Patient was not on any other new medications during this time-period. On initial evaluation, patient was found to have elevated liver enzymes with T.bilirubin 6.4, AST 218, ALT 288, ALP 331. Due to broad differentials associated with elevated liver enzymes with abdominal pain, further workup was done. Abdominal CT scan and MRCP results were unremarkable. Hepatitis panel was also negative. Patient was provided with supportive care and hydration with IV fluids. Repeat labs done on 4th day after admission showed down trending LFTs – T.bill 3.8, AST 152, ALT 141, ALP 253.

DISCUSSION:
Amoxicillin-Clavulanate can cause hepatocellular, cholestasis or mix type of liver injuries depending upon genetic factors or pre-existing liver conditions. Early recognition and removal of offending medication is the initial mainstay of treatment along with supportive care. This case signifies proper history taking and review of medications could avoid unnecessary and expensive diagnostic tests for diagnosis. Our case emphasis importance of early recognition of this reversible condition due to Amoxicillin-Clavulanate or other medications to prevent worsening of liver faliure and its complication.
3180 Previously Undiagnosed Hepatocellular Carcinoma Presenting as Cardiac Mass Causing Decompensated Right Heart Failure and Subsequent Multi-Organ Failure
Authors: Higley Cory , Nadella Sandeep , Badoghaish Waleed , Lalos Alexander 
Published: October 2019

INTRODUCTION:
Hepatocellular carcinoma (HCC) is the most common primary malignancy of the liver. Some patients may present with early stage disease due to HCC surveillance however widespread adoption of screening recommendations in this country is lacking. Therefore, many cases present with locally advanced or metastatic disease. We present the case of a patient whose initial manifestation of HCC was an unusual presentation of respiratory failure and an intracardiac mass. This case should emphasize the protean manifestations of metastatic HCC.

CASE DESCRIPTION/METHODS:
The patient was a 65-year-old male with past medical history significant for hepatitis C who had achieved a sustained virologic response (SVR) three years prior to presentation. He had not been previously diagnosed with cirrhosis according to family members and was not undergoing HCC surveillance. He presented to our hospital with a complaint of shortness of breath for one week and was noted to have significant dyspnea necessitating intubation. Laboratory results of significance are summarized in Table 1. An echocardiogram noted a large echodensity spanning both the right atrium and right ventricle, measuring 8 cm × 4 cm (Figure 1) and a CT angiography of the chest, abdomen and pelvis revealed a large heterogeneous, multiseptated right lobe liver mass measuring 11.5 cm by 8.6 cm by 12.2 cm in the setting of a cirrhotic liver (Figure 2). Due to extent of disease, there were no meaningful treatment options available and the patient expired 48 hours later following a family meeting and compassionate extubation.

DISCUSSION:
Cardiac metastases of HCC are rare, with rates estimated between 1.2% and 6%, and signify a late manifestation of HCC. As such, it often has a poor prognosis with median and mean survival times of 102 and 161 days, respectively, after diagnosis. A literature review did yield some cases of patients with HCC who eventually developed metastases to the heart, however none have described the presence of cardiac metastases at time of diagnosis of HCC which we believe makes our case particularly unusual. This is in part explained by underutilization of HCC surveillance in this country. This case highlights the associated morbidity of hepatocellular carcinoma and necessitates ongoing adherence to surveillance recommendations to reduce advanced stages of HCC.
3183 Explanted Liver Confirming Hereditary Hemochromatosis in an African American Male
Authors: Abraham Fiyinfoluwa , Subramanian Sruthi K. , Singh Khushboo , Younes Mamoun , Machicao Victor 
Published: October 2019

INTRODUCTION:
Hereditary hemochromatosis (HH) is a disorder in which intestinal iron absorption leads to iron overload. It is associated with mutations in the HFE gene. Most commonly seen in Caucasian individuals; however, it is infrequent to see it present in those of African descent.

CASE DESCRIPTION/METHODS:
A 52-year-old African American male with a history of decompensated alcoholic cirrhosis with ascites, portosystemic encephalopathy (PSE), and non-bleeding esophageal varices presented to hepatology clinic with a MELD score of 16. He quit drinking ten years before the presentation. He was evaluated for a liver transplant, was subsequently deemed a candidate, and placed on the list. As a part of transplant evaluation, an MRI of the abdomen was obtained approximately which showed cirrhotic liver morphology with no hypervascular liver lesions, but the presence of diffuse T2 hypointensity suggestive of iron overload and fibrosis, located in the liver, pancreas and myocardial tissue (Figure 1). A dedicated cardiac MRI with iron protocol was done to confirm findings and give quantification, which showed iron overload with an iron concentration of 1.8 mg/g of dry weight. Serology showed serum iron 125 ug/dL (normal), ferritin 1281 ng/mL (very high), 95% transferrin saturation (very high), and total iron binding capacity of 132 ug/dL (very low). Hereditary hemochromatosis (HH) was suspected, and genetic testing was conducted. The patient was found to be negative for HFE mutations C282Y, H63D, and S65C. Two months following the serological workup, he underwent a liver transplant with an ABO identical allograft liver. The explanted liver (Figure 2) showed severe iron overload in the hepatocytes confirmed by iron stain with pericanalicular accentuation (Figure 3). The diagnosis was confirmed to be HH.

DISCUSSION:
HH was confirmed when the presence of multi-organ iron overload was seen in imaging, serology showed significant ferritinemia with 95% transferrin saturation, and biopsy showed the presence of severe iron overload in the hepatocytes. While genetic testing for C282Y, H63D, and S65C was negative, this does not mean HH can be ruled out. Identifying these mutations is not necessary for the diagnosis of HH, but the mutations are predominantly positive in Caucasians. For other ethnicities, including Africans, there are rare HH mutations that can return positive but were not tested. This case describes a rare phenomenon of biopsy proven HH found in an African American male.
3185 An Unusual Cause of Abdominal Pain and Elevated Liver Chemistries
Authors: Dave Isha , Dailey Francis , Turse Erica , Tahan Veysel 
Published: October 2019

INTRODUCTION:
Nonalcoholic fatty liver disease (NAFLD) is a spectrum ranging from simple steatosis to cirrhosis. It is present in 33% of the general adult population and is more prevalent in overweight and diabetic patients. This can be explained by abnormal lipid metabolism with stressed conditions such as Cushing's disease (CD). In CD, glucocorticoids act synergistically with insulin to increase lipid accumulation. The incidence of NAFLD in CD is not well described but is thought to be greater than the general population. CD is less commonly labelled as a culprit of elevated liver chemistries. Here, we present a case of a young woman with uncharacteristically elevated liver tests found to be due to CD.

CASE DESCRIPTION/METHODS:
A 35-year-old woman was admitted for abdominal pain, nausea, and vomiting. Her medical history included a pituitary adenoma with subsequent CD status post three resections, diabetes insipidus, diabetes mellitus type 2, bipolar disorder, and symptomatic cholelithiasis status post cholecystectomy. Admission labs showed total bilirubin 3.70 mg/dL, ALP 480 U/L, AST 681 U/L, ALT 992 U/L, lipase 25 U/L. Workup was negative including viral hepatitis including hepatitis E, autoimmune hepatitis, hemochromatosis, alpha-1 anti-trypsin deficiency were negative. Abdominal ultrasound and MRCP showed hepatic steatosis. Liver biopsy revealed 70-80% macrovesicular hepatic steatosis and prominent cholestasis. Her liver function tests transitioned to a cholestatic pattern with total bilirubin 7.07 mg/dL, ALP 1019 U/L, AST 273 U/L, and ALT 519 U/L. She was started on ursodiol 15 mg/kg resulting in immediate symptomatic improvement. One month following hospitalization while on treatment, labs were AST 21 U/L and ALT 30 U/L.

DISCUSSION:
NAFLD is diagnosed by adiposity within the liver on imaging or histopathology and remains the most common cause of abnormal liver chemistries. Patients with CD have been shown to have a higher incidence of NAFLD, as much as 20%. This is thought due to an increase in visceral fat rather than a direct effect of cortisol, as often the BMI is not particularly elevated. While a majority of patients with NALFD may have normal transaminases, a study by Shirin et al found that patients with higher elevations in cholestatic enzymes were more likely to have advanced liver disease. Thus, clinicians should have a high suspicion when a patient has comorbidities predisposing them to hepatic steatosis, including metabolic syndromes such as CD.