bluuebunny/crossref_metadata_2025_split huggingface dataset:
3054 Getting to the Bottom of Incessant Diarrhea
Authors: Kulkarni Mayuri , Saxena Rovin , Ponna Pramod , Cosma Cecilia 
Published: October 2019

INTRODUCTION:
Clostridium difficile infection (CDI) is a common cause of recurrent diarrhea. Up to 35% of patients experience recurrent infection after initial therapy. Patients with recurrent CDI are occasionally treated empirically with antibiotics. There has been an increase in recurrence in CDI over recent years. In fact, there is a 50-60% chance of a repeat recurrence. Persistent diarrhea is also caused by microscopic colitis, which occurs 7.9 per 100,000 person years. It has been associated with the use of NSAIDs and proton-pump inhibitors (PPI). We present a case of a patient with recurrent CDI who was eventually diagnosed with microscopic colitis.

CASE DESCRIPTION/METHODS:
A 41-year-old male with a history for DM type 1, renal failure, GERD presented with persistent diarrhea for the past 5 years. His temperature was 98.3 F, HR 87 bpm, BP 123/89 mmHg, and RR was 20 per minute. Physical exam was unremarkable. Laboratory studies were insignificant. CT with contrast was negative for any pathologies. Initial stool testing was negative for CDI. A colonoscopy with biopsy was performed which showed no abnormal findings. He was treated with IV fluids and loperamide. His symptoms persisted and repeat stool was positive for Clostridium difficile toxin. According to guidelines at the time of presentation, he was started on metronidazole and his PPI was discontinued. His symptoms resolved over 48-72 hours and he was discharged. Two weeks later, he presented again with CDI and was treated with oral vancomycin and discharged. He presented with diarrhea 2 months later and was treated empirically with metronidazole, showing minimal to no improvement of his symptoms. Stool studies were negative for Clostridium difficile toxin. A repeat colonoscopy with biopsy showed lymphocytic infiltrates within the colonic mucosa, confirming the diagnosis of lymphocytic microscopic colitis. He was started on budesonide with a good clinical response and was discharged. Follow-up at our clinic showed near-resolution of his symptoms.

DISCUSSION:
Recurrent diarrhea is a bothersome symptom. Our patient's microscopic colitis was overshadowed by his history of CDI. He was treated empirically for CDI, exposing him to antibiotics and delaying appropriate treatment. Antibiotics may create iatrogenic consequences such as antibiotic resistance. Clinicians must be aware that patients with history of recurrent CDI may have other underlying etiologies for persistent diarrhea.
3083 Campylobacter coli bacteremia: How Common Is It?
Authors: Pisipati Sindhura , Zafar Yousaf , Elkafrawy Ahmed A. , Ullah Waqas 
Published: October 2019

INTRODUCTION:
Campylobacter species are known to cause enteritis, usually self-limited, but with the risk of developing Guillain Barre Syndrome. However, over the past 40-50 years, there have been reports of varying presentations, such as cellulitis, spondylodiscitis, and bacteremia. Of the Campylobacter species, C. jejuni is the most common culprit for causing bacteremia, however, C. coli bacteremia is becoming more prevalent. Here we discuss an unusual case of C. coli bacteremia in a patient with decompensated liver cirrhosis.

CASE DESCRIPTION/METHODS:
59 y/o with history of cirrhosis secondary to alcohol abuse complicated by esophageal varices, who presented with black, watery stools in the previous one week with concurrent scrotal swelling. Vital signs were stable with temperature of 97.6 degrees F, heart rate 84 bpm, respiratory rate 16, blood pressure 117/72, and oxygen saturation 99% on room air. Physical exam was remarkable for voluntary guarding, and right upper quadrant tenderness. Lab tests revealed a white blood count of 2300/cm2, hemoglobin 9.9 g/dL, alkaline phosphatase 132 IU/L, aspartate aminotransaminase 65 U/L, alanine aminotransaminase 26 U/L, lactic acid 5.0 mmol/L, magnesium 1.2 mg/dL, and phosphorus 2.2 mg/dL. Computed tomography abdomen/pelvis with contrast showed findings of colitis. Ultrasound of the scrotum showed possible scrotal cellulitis. Stool culture returned positive for Campylobacter antigen, for which doxycycline was initiated. Blood cultures resulted with gram negative rods, which were later confirmed to be C. coli. Blood cultures continued to grow the bacteria and antibiotics were switched to imipenem until the day of discharge. Unfortunately, the patient left the hospital against medical advice and was sent home with ciprofloxacin to complete a total antibiotic course of 2 weeks after the last negative blood culture. Patient was seen at his primary care physician's office 4 days after leaving the hospital and reported complete resolution of his symptoms.

DISCUSSION:
Campylobacter bacteremia is rare. We must be aware of the possibility of a Campylobacter bacteremia and consider this organism when choosing empiric antibiotics. Additionally, once confirmed of a Campylobacter bacteremia, we must be mindful of resistance and choose treatment wisely. As Campylobacter infections have a wide array of presentations, it is imperative that cases are shared amongst the medical community so that prompt recognition, diagnosis, and treatment can be offered.
3099 Endoscopic Botulinum Toxin Injection for Tacrolimus-Induced Achalasia in a Renal Transplant Recipient
Authors: Campos Marilia , Matlock Jake 
Published: October 2019

INTRODUCTION:
Multiple medications have been associated with secondary achalasia. Here we present a patient who developed dysphagia 4 days after his renal transplant and was found to have achalasia thought to be due to his tacrolimus; he was successfully treated with botulinum injection. To our knowledge, this is the first case of tacrolimus-induced achalasia ever reported in a renal transplant patient; it is also the first case in a transplant patient to be treated endoscopically with botulinum injection.

CASE DESCRIPTION/METHODS:
A 58 year old man with a history of end stage renal disease secondary to focal segmental glomerulosclerosis presented with progressive renal failure and underwent deceased kidney transplant without complications. At clinic, follow-up on post-operative day #4, the patient reported difficulty in swallowing since post-operative day two. A modified barium swallow study (Figure 1) demonstrated severe esophageal dysmotility and lower esophageal sphincter dysfunction concerning for achalasia. Upper endoscopy (Figure 2) one week later revealed a dilated esophagus with mild edema but without focal lesions or ulcerations. Esophageal manometry (Figure 3) evidenced outflow obstruction of the esophagogastric junction and weak peristalsis in the esophageal body, confirming the diagnosis of achalasia. Surgical therapy and changing his calcineuron inhibitor for achalasia were considered too high risk in this patient so shortly after transplant. The patient ultimately underwent therapy with endoscopic botulinum toxin injection (100 units) of the lower esophageal sphincter. He had excellent results with immediate and complete resolution of dysphagia.

DISCUSSION:
The proposed mechanism for CNI induced changes in esophageal motility involves inhibition of nitric oxide synthase by CNIs. Nitric oxide (NO) is responsible for esophageal peristalsis as well as relaxation of the lower esophageal sphincter (LES). Although it is unclear why switching between different CNIs would lead to symptom resolution, individual variation in the reaction to the different chemical structures of tacrolimus and cyclosporine has been proposed. Botulinum toxin can be considered as a therapeutic option in those patients who are not candidates for a change in their immunosupression. To our knowledge, this is the first case of botulinum induced achalasia reported after a kidney transplant and also the first successfully treated with botulinum toxin injection.
3102 Atrio-Esophageal Fistula Presenting as Odynophagia: A Rare but Fatal Complication of Cardiac Ablation
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:
Atrio-esophageal fistula is one of the challenging complications of catheter ablation. The clinical presentation is unpredictable but rapid diagnosis and surgical treatment may prevent fatality. We are here reporting a case of a patient who initially presented with odynophagia and was diagnosed later with atrio-esophageal fistula.

CASE DESCRIPTION/METHODS:
43 years old male presented to ED with complaints of retrosternal chest pain and odynophagia s/p cardiac ablation for AF 4 days ago. Initial investigation were normal. Patient on upper GI series had focal contrast collection at the distal esophagus. Patient underwent EGD and it was found that patient had linear deep mid esophageal perforation for which 6 hemostatic clips were used for closure patient was discharged on TPN. After 2 weeks patient presented again for shortness of breath and chest discomfort. On examination patient had loud pericardial friction rub suspicious and stat Echo showed pericardial effusion with early signs of cardiac tamponade. Patient underwent emergent pericardiocentesis. After pericardiocentesis patient became febrile and blood cultures were growing Lactobacillus. CT chest (pulmonary veins) revealed Atrio-esophageal fistula, pericardial effusion and left sided pleural effusion suspected for empyema. Patient underwent thoracotomy, decortication of empyema, repair of inferior pulmonary vein/atrial margin, esophageal repair, G/J tube placements, and omental transfer. Patient eventually improved and was discharged home.

DISCUSSION:
The estimated incidence of atrio-esophageal fistula is less than 0.1% – 0.25% after AF ablation procedures. Potential culprit is direct heat of radiofrequency ablation causing damage to already susceptible epithelial esophageal mucosa. After esophageal mucosal necrosis, fistula formation and mediastinitis can occur. Pericardial effusion/tamponade, sepsis and cardioembolic stroke can also occur. Patient may present with fever, nausea, vomiting, dysphagia, odynophagia, hematemesis and melena. CT scan of the chest with intravenous contrast is considered by many as the diagnostic modality of choice as it can identify the leak along with any signs of pneumomediastinum and pneumopericardium. Endoscopy should be avoided as blowing of air inside can result in dislodging of the large embolus to the brain resulting in stroke or death. Treatment options include open surgical repair of fistula via thoracotomy with placement of tissue/omentum between esophagus and left atrium or esophageal stenting.
3173 Spontaneous HBsAg Seroclearance in a Patient With Chronic Hepatitis B: Do We Need Surveillance?
Authors: Singh Khushboo , Subramanian Sruthi K. , Abraham Fiyinfoluwa , Machicao Victor 
Published: October 2019

INTRODUCTION:
Hepatitis B virus (HBV) infection is a global health problem despite an effective vaccination program, routine antenatal screening, and perinatal care. Among the individuals infected with the HBV, about 5 % of adults and 90% of children become chronic carriers. A small percentage of carriers undergo spontaneous seroclearance of Hepatitis B surface antigen (HBsAg). We present a case of spontaneous HBsAg seroclearance in a chronic hepatitis B carrier.

CASE DESCRIPTION/METHODS:
A 60-year-old Hispanic male with a history of chronic hepatitis B presented to the hepatology clinic for regular follow-up. He was asymptomatic with no stigmata of chronic liver disease. He had been followed in the clinic for nine years. He was HBsAg positive, hepatitis B surface antibody detectable at 6.9 mIU/ml, hepatitis B e antigen (HBeAg) negative, hepatitis B e antibody positive, undetectable HBV DNA levels, and alpha-fetoprotein 17.2 ng/ml. He persistently had normal liver enzymes. Five months after the last positive HBsAg, routine serology showed loss of HBsAg. CT Abdomen with contrast liver protocol showed no evidence of cirrhosis and hepatocellular carcinoma (HCC). The liver biopsy showed no evidence of fibrosis. The patient is on surveillance with a follow-up in 6 months for repeat serology.

DISCUSSION:
Chronic hepatitis B carriers are at risk of developing decompensated liver cirrhosis and hepatocellular carcinoma. The rate of HBsAg spontaneous seroclearance is estimated to be 1–3% per year. The long-term outcome after HBsAg seroclearance is excellent if there is no pre-existing cirrhosis or viral superinfection. HBsAg carriers who are negative for HBeAg or negative for HBV DNA are more likely to clear HBsAg from serum. AASLD guidelines recommend HCC surveillance in chronic hepatitis B infection, but its usefulness in patients after HBsAg seroclearance without any liver injury remains controversial. Few retrospective studies recommend surveillance in high-risk patients, which include male patients, patients with cirrhosis, HCV superinfection, age ≥50 years at the time of seroclearance and family history of HCC. Surveillance in patients who do not have any risk factors may not be cost effective as the incidence of adverse liver events among them is rare. Our patient had chronic hepatitis B for nine years and underwent spontaneous seroclearance of HBsAg with negative HBeAg and undetectable HBV DNA. He has no evidence of cirrhosis or viral superinfection, thus having a favorable long-term prognosis.
3181 Intravenous Amiodarone: An Uncommon Culprit of Reversible Hyper-Acute Liver Injury
Authors: Ramachandran Rajarajeshwari , Bongu Ramachandra , Ajluni Allison , Jani Niraj 
Published: October 2019

INTRODUCTION:
Amiodarone is a commonly used anti-arrhythmic agent and it is important that physicians are familiar with the toxicity profile. We are reporting a case of intravenous (IV) amiodarone induced hyper-acute liver injury.

CASE DESCRIPTION/METHODS:
62-year-old man with history of atrial fibrillation, non-ischemic cardiomyopathy and tobacco abuse, was admitted with atrial fibrillation and rapid ventricular response related to medication non-adherence. Patient was given IV amiodarone (total of 1050 mg) over 24-hour period, following which patient developed marked elevation of aspartate aminotransferase/AST (4021 U/L) and alanine aminotransferase/ALT (3000 U/L) with mild elevation of alkaline phosphatase/ALP (218 U/L) and total bilirubin (2.0 mg/dL). International Normalized Ratio (INR) - 5.3. Viral hepatitis panel, acetaminophen and drug toxicology screen - negative. Ceruloplasmin – normal. Ultrasound abdomen – normal liver and CBD diameter 4 mm. Portal venous duplex – no thrombosis. Patient denied use of over the counter medications or herbal supplements. No hypotensive episodes or evidence of cardiogenic shock. Due to the temporal relationship between the use of intravenous amiodarone and the development of liver injury, amiodarone-induced liver injury was suspected. Amiodarone was immediately discontinued and patient was given IV N-acetylcysteine (NAC). 24 hours later, AST fell by 50% to 2167 U/L. Liver enzymes continued to decrease and on day 4 (day of discharge), AST and ALT levels were 212 U/L and 929 U/L. After the liver enzymes normalized, our patient was started on oral amiodarone without recurrence of liver injury.

DISCUSSION:
IV amiodarone is typically used as a short-term therapy for various arrhythmias and is primarily eliminated by biliary excretion. Acute hepatitis due to parenteral therapy is extremely rare and can develop within 1 day of administration. Amiodarone should be immediately discontinued in those cases. The different mechanisms suspected to cause acute liver toxicity due to IV amiodarone are ischemic liver injury due to relative hypotension, hypersensitivity reaction, toxicity of the vehicle (polysorbate-80), and idiosyncratic toxicity. Limited evidence is available about the use of NAC in amiodarone induced liver injury.
3198 An Unusual Case of Severe Hypertriglyceridemia in an Alcohol Naïve Patient
Authors: Baseer Yaseen 
Published: October 2019

INTRODUCTION:
Hypertriglyceridemia (HT) is a metabolic disorder due to an altered synthesis of lipoproteins. Although HT is often asymptomatic, acute cases can result in pancreatitis and chronic elevations of HT can lead to the development of atherosclerotic disease. HT is most commonly caused by obesity, diabetes mellitus and excess alcohol intake. Alcohol-induced HT is due to increased very-low-density lipoprotein secretion and impaired lipolysis. Previous research has shown an association of severe HT with chronic alcohol use. Here, we present an unusual case of new onset severe HT in a patient who recently began drinking alcohol.

CASE DESCRIPTION/METHODS:
A 42 year old female with a history of anxiety presented to the hospital with a primary complaint of suicidal ideation. Patient was subsequently admitted to psychiatric inpatient ward and medical team was consulted after labs revealed triglyceride level of 3930. Patient was questioned about recent travel, recent drug use, and recent medication use and patient's answers were noted to be unremarkable for any concerning history in relation to her HT. She does admit to moderate alcohol use for the first time as an adult during the last week and her alcohol level on admission was slightly elevated at 45. Patient's vitals were reviewed and noted to be within normal limits and patient's laboratory values were also noted to be within normal limits including her CBC, CMP, urine drug screen and chest x-ray. Additionally, triglyceride levels obtained on prior visits have ranged from the 40's to the 120's with the most recent level one year prior to current admission being 47. CT abdomen and pelvis showed no signs of acute intra abdominal pathology. At time of exam, patient was resting comfortably in bed and her only complaint was anxiety. Patient's triglyceride level returned to normal during hospital stay after treatment with insulin and gemfibrozil.

DISCUSSION:
One of the most common causes of HT in the United States is alcohol abuse. More specifically, previous research has shown severe HT developing as a consequence of chronic alcohol use. This case highlights severe HT in a patient who is alcohol naïve and had previous normal triglyceride values. Additionally, her moderate consumption of alcohol during the previous week would not explain such high values of triglycerides. More research is needed to clearly identify the risk of severe HT in a patient who has limited history in drinking alcohol.
3220 Systemic Sclerosis Leading to Recurrent Small Bowel Pseudo-Obstruction
Authors: Kailas Shilpa D. 
Published: October 2019

INTRODUCTION:
Systemic sclerosis (SSc) is a chronic systemic disease defined by early microvascular obliterative changes, early activation of T and B-lymphocytes, and extensive fibrosis of the skin and internal organs. Although gastrointestinal involvment of SSc is common, severe intestinal disease manifested by malabsorption, recurrent pseudo-obstruction, or need for parenteral nutrition carries a poor prognosis and is seldom seen. We present the uncommon case of a patient with severe scleroderma bowel causing debilitating disease.

CASE DESCRIPTION/METHODS:
A 76-year-old female with history of atrial fibrillation, systemic sclerosis, achalasia s/p Botox injections, and duodenal bulb ulcer presented to our institution with vomiting of blood-streaked emesis, epigastric abdominal pain, and distension for two days. She had multiple hospitalizations for presumed obstructions in the past treated medically. Endoscopy 3 months prior revealed a large cratered duodenal ulcer located at the duodenal sweep with recent stigmata of bleeding (Forrest Class IIa) treated with epinephrine. Upon evaluation the patient was afebrile and normotensive. Physical exam was significant for mild diffuse abdominal tenderness and no gross blood on rectal exam. Labs were remarkable for Hgb 11.9, MCV 92.8, lactic acid 1.0, and lipase within normal limits. CT A/P showed multiple dilated small bowel loops with air-fluid levels and a fluid-filled patulous esophagus that was unchanged. Trauma surgery was consulted and we managed the patient conservatively with bowel rest, IV fluids, and continuation of her PPI. Her clinical course improved and she was able to pass flatus and stool. We attributed her recurrent symptoms to intestinal pseudo-obstruction precipitated by scleroderma.

DISCUSSION:
SSc is a chronic autoimmune condition commonly affecting the gastrointestinal tract. Major manifestations of small intestinal involvement are due to reduced peristalsis, causing abdominal distension and pain from dilated bowel loops. Acute intestinal pseudo-obstruction is a medical emergency that warrants hospital admission. Most patients have spontaneous resolution with conservative measures like bowel rest, nasogastric decompression, and intravenous hydration but may require frequent readmissions. Surgery is discouraged due to risk of prolonged ileus or anastomotic failure although “venting” jejunostomy allows for air aspiration in chronic pseudo-obstruction. Recurrent intestinal pseudo-obstruction in these patients thus poses a therapeutic challenge.
From the meaning triad to meaning holism: Unifying life’s meaning
Authors: Seachris Joshua 
Published: October 2019

Abstract
Claims that talk of life’s meaning is misguided, unmanageable or, worse, nonsensical, are overblown. Such claims especially track the cosmically focused the meaning of life. “The meaning of life” is perfectly intelligible, and is centered on a cluster of ideas encapsulated by what I call the “meaning triad.” One component of this triad—I-MEANING
—provides the hermeneutical and conceptual resources for understanding the question “What is the meaning of life?” as asking for a single thing, in contrast to amalgam and pluralist views. I will investigate the meaning triad en route to defending meaning of life holism.
Recent work on the meaning of “life’s meaning”: Should we change the philosophical discourse?
Authors: Metz Thaddeus 
Published: October 2019

Abstract
In this article I critically discuss English-speaking philosophical literature addressing the question of what it essentially means to speak of “life’s meaning”. Instead of considering what might in fact confer meaning on life, I make two claims about the more abstract, meta-ethical question of how to understand what by definition is involved in making that sort of enquiry. One of my claims is that over the past five years there has been a noticeable trend among philosophers to try to change our understanding of what talk of “life’s meaning” connotes. For example, whereas most philosophers for a long while had held that such talk is about a kind of value possible in the life of human beings, recently some have argued that certain non-human parts of nature can exhibit meaningfulness, which, furthermore, is not necessarily something valuable. The second claim I advance is that there is strong reason to reject this trend, and instead for philosophers to retain the long-standing approach.
Why the indifference of the universe is irrelevant to life’s meaning
Authors: Trisel Brooke Alan 
Published: October 2019

Abstract
When pessimists claim that human life is meaningless, they often also assert that the universe is “blind to good and evil” and “indifferent to us”. How, if it all, is the indifference of the universe relevant to whether life is meaningful? To answer this question, and to know whether we should be concerned that the universe is indifferent, we need a clearer and deeper understanding of the concept of “cosmic indifference”, which I will seek to provide. I will argue that the lives of many individuals are meaningful and that human life, in general, is somewhat meaningful, despite the indifference of the universe. Furthermore, I will seek to demonstrate that even if the universe cared about us, or had preferences for how we live our lives, that this likely would not enhance the quality of our lives.