bluuebunny/crossref_metadata_2025_split huggingface dataset:
3112 Eosinophilic Esophagitis (EE) Presenting With Severe Dysphagia Showing Dramatic Response to Oral Steroid Therapy
Authors: Miah Ma Rahim , Hossain M. Shamiul , Ghosh C.K. , Kamal M. 
Published: October 2019

INTRODUCTION:
During the last decade of clinical practice, a rapid increase of a “new” disease termed as “eosinophilic esophagitis (EE)” have been identified among patients who were thought to have gastroesophageal reflux disease (GERD) but did not respond to medical and/or surgical GERD treatment. Over the last decade eosinophilic esophagitis is increasingly being recognized in adults and children throughout the world. Population-based studies suggest the prevalence to be in excess of 1:1000 with a predilection for white males. The disease is very rare in Bangladesh.

CASE DESCRIPTION/METHODS:
A 40 years old house wife presented with one-year long history of severe dysphagia with significant weight loss; endoscopic evidence of a long linear ulcer with stricture involving almost the whole length of the esophagus; histopathologic evidences of eosinophilic esophagitis and a dramatic response to systemic steroid therapy.

DISCUSSION:
Diagnosis of Eosinophilic Esophagitis is based on (i) symptoms including but not limited to food impaction and dysphagia in adults and feeding intolerance and gastro-esophageal reflux symptoms in children; (ii) histological evidence of ≥15 eosinophils /HPF; (iii) exclusion of other disorders associated with similar clinical, histological, or endoscopic features, especially gastro-esophageal reflux disease. The overlapping symptoms of EE and GERD sometimes may delay or confuse the diagnosis of the disease in many cases. Most patients present with dysphagia and food impactions, atypical chest pain and heartburn that is refractory to PPI therapy. Fibrosis, narrowing of the lumen and stricture esophagus can occur with EE. Appropriate treatments include dietary approaches based upon eliminating exposure to food allergens, and topical/systemic corticosteroids. This patient presented with severe dysphagia with significant weight loss; endoscopic evidence of a long linear ulcer with stricture involving almost the whole length of the esophagus; histopathologic evidences of eosinophilic esophagitis and a dramatic response to systemic steroid therapy. In conclusion, although EE is a very uncommon disease in Bangladesh, the intent of this report is to grow awareness of the clinicians about this disorder to make early diagnosis and treatment of the disease with systemic steroid to prevent the development of complications like esophageal stricture or perforation.
3128 A Rare Case of a Gastroduodenal Ulcer Arising From Checkpoint Inhibitors
Authors: Raman Daya 
Published: October 2019

INTRODUCTION:
Ipilimumab and Nivolimuab are in a class of immune checkpoint inhibitors that are widely used in the treatment of advanced malignancies.
1
Immunotherapy with monoclonal antibodies targeting cytotoxic T lymphocyte-associated antigen 4 (CTLA4) and the programmed death-1 receptor (PD-1) and its ligand PD-L1 has become the standard of care for cancer treatment today.
1
Gastrointestinal (GI) toxicity from cancer immunotherapy is well described for anti-CTLA4 Abs, but less well studied in combination of anti-CTLA4 and anti-PD-1Abs. GI effects of these immunotherapies range from enterocolitis, pancreatitis, diarrhea, and ulcerations involving the sigmoid colon and rectum.
1

CASE DESCRIPTION/METHODS:
Here, we present the case of an 80 year old male with past medical history of renal cell cancer (RCC) that was diagnosed 3 months prior to admission, who presented with melenic stool for one day. The patient had been initiated on a chemotherapy regimen of Ipilimumab and Nivolimuab of which he received three rounds, the last dose one week prior to hospitalization. He had not been on any anticoagulation nor had he endorsed NSAID use. Patient's hemoglobin was closely trended. One day into admission, patient had a large melenic bowel movement with Hb change from 9.0 to 8.7 mg/dL with significant hypotension and tachycardia. Patient was emergently intubated for airway protection for an EGD. EGD revealed a large 4-5 cm ulcer in the second portion of the duodenum and found to have a large artery protruding from the ulcer base, likely the gastroduodenal artery. Endoscopic intervention was performed by placing 5 clips at the ulcer base in an effort to further prevent bleeding. Hemoglobin was trended closely following the procedure, however post-EGD bleeding continued and patient became acutely hypotensive, requiring vasopressor support. As further EGD intervention was considered to be high risk, Interventional Radiology was consulted for embolization with empiric embolization of gastroduodenal artery using a microcoil, which was successful. Hemoglobin continued to trend downwards despite control of bleeding and vasopressor support increased at which point patient was transitioned to comfort measures.

DISCUSSION:
This case outlines a rare case of immune checkpoint inhibitors as a cause of a gastroduodenal ulcer and the adverse outcomes with checkpoint inhibitors as treatment for malignancies.
3133 Bleeding Peptic Ulcer Disease in Polycythaemia Vera Patient
Authors: Al Yassin Sarmed , Fatakhova Karina , Al-Naqeeb Ghadah , Haggerty Gregory , Tofano Michael 
Published: October 2019

INTRODUCTION:
Polycythaemia vera (PV) is a myeloproliferative disease, characterized by hematopoietic proliferation, expressed as inappropriate increase in circulating RBCs. It affects middle-aged and elderly patients Gastrointestinal disorders are common in PV, mainly represented by peptic ulcers. Our case highlights a severe fatal presentation of GI bleeding in a patient with recent diagnosis of PV.

CASE DESCRIPTION/METHODS:
63 years old M presented with altered mental status. He was recently diagnosed with Jak2+ P. Vera & A. Fib, not on anticoagulation, he takes daily low dose Aspirin 81 mg. In ED, He went into hemorrhagic shock. Significant amount of coffee ground vomitus seen upon intubation. NGT drained a large volume of blood. Labs revealed leukocytosis (185.9 K/uL), thrombocytosis (606 K/uL), AKI (BUN/Cr 83/4.6). Hgb was 14.8 g/dL 2 weeks prior to presentation. On arrival Hgb was 10 g/dL and decreased to 8.5 g/dL within 2 hours. Resuscitation started with IV fluids, blood transfusions and PPI drip. Emergent EGD revealed a large bleeding pyloric channel ulcer, which was treated with epinephrine injections and three clips. Urgent hemodialysis was initiated for worsening acidosis. LFTs were elevated, AST/ALT of 2080/1167 U/L, Alk. Phos. 1510 U/L. CT abdomen revealed infarcted liver, kidneys and bowel. CT of the brain showed acute posterior circulation infarction involving bilateral occipital & emporal lobes Family decided to withdraw care and made patient comfort care.

DISCUSSION:
Peptic ulcer (PU) disease manifested in higher frequency in PV patients compared to population. Various pathogenetic mechanisms suggested for PU in PV, altered mucosal blood flow due to increased plasma viscosity, and/or increase histamine release, due to high basophil count, a study suggested high risk of H. pylori infection in PV patient compared with controls. Limited evidence regarding the prevalence of GI bleeding in PV due to the retrospective nature of studies. In the ECLAP trial, the rate of total & major bleeding were 2.9% and 0.8%/year. 4% of deaths were attributed to bleeding. GIB was the most common cause of major bleeding. hence both the thrombotic and hemorrhagic manifestations of myeloproliferative disorders depend on the platelet count. Typical pattern of GI bleeding has not been well reported in literature, but it's more evident in the setting of extreme thrombocythemia. It is important to underline that gastroduodenal lesions present in 77% of asymptomatic PV patients, suggesting the need for endoscopic examination in those patients.
3136 Complex Rebleeding Cameron Ulcer in a Young Male—A Case Report
Authors: Schieferdecker Nicola , Pasan Botheju Welathanthrige Savindu , Mehta Amit , Buffie Charlie , Wan David 
Published: October 2019

INTRODUCTION:
A Cameron lesion is a gastric ulcer or erosion located in a diaphragmatic hernia that can be a rare source of occult GI bleeding. These types of lesions are commonly missed during EGD and are believed to be caused by mechanical damage to the mucosa in a sliding hiatal hernia. Here, we report the case of a young man without risk factors, with a complex rebleeding Cameron ulcer.

CASE DESCRIPTION/METHODS:
A 31-year-old male with no significant medical history presented with two episodes of syncope resulting in head and chin lacerations. He reported worsening headaches, nausea, and black stools for 3 days. He was alert, oriented, in no distress, hemodynamically stable and afebrile when brought in by EMS. He denied use of NSAIDs, reported normal bowel movements, and stated he never had an EGD or colonoscopy. He admitted to social alcohol and smoking for 10 years. Physical exam was remarkable for melena on rectal exam. Initial blood work was notable for hemoglobin 7.5, WBC of 13.0, BUN/Crea ratio of 39, with otherwise unremarkable CBC, CMP, troponin, coags, and urine analysis. UGI series showed no abnormalities. The patient was transfused 1 unit packed RBCs and was admitted to medicine. An EGD was performed and showed a large type III hiatal hernia and a Cameron ulcer with visible vessel in hernia (Figures 1 and 2) that was treated with two mechanical clips (Figure 3). Pathology of ulcer margins showed no diagnostic abnormality. Ten days after discharge he again presented with black stools, and repeat EGD showed bleeding under previously placed clips. Clips were removed and the lesion was cauterized with hemostasis.

DISCUSSION:
Cameron lesions are an uncommon cause of upper GI bleed that occur predominantly in women due to their higher incidence of diaphragmatic hernias. Patients usually present with anemia or occult GI bleeding. Diagnosis is made endoscopically, and first line treatment includes common hemostasis techniques including clipping. In this case, the patient presented without evidence for a hernia on UGI series, which could demonstrate a sliding hernia. However, he showed significant recurrent bleeding with hemodynamic instability that required multiple interventions. In summary, Cameron lesions or ulcers can be a rare cause of severe upper GI bleed and surgical hernia repair should be strongly considered in complex cases.
3151 Ustekinumab Administration Prior to Week Eight Following Induction Improves Symptoms and Maintains Remission of Severe Crohn's Disease: A Case Series
Authors: Azam Mohammad U. , Koehler Tara , Jackson Christian , Vega Kenneth J. 
Published: October 2019

INTRODUCTION:
Ustekinumab is a recently approved immunosuppressive agent for management of moderate to severe Crohn's Disease (CD). In trials, dosing was determined at 6 mg/kg for induction with maintenance injection of 90 mg every 8 weeks. Approximately half of the patients in the UNITI Induction trials did not respond to ustekinumab treatment when assessed at 6-8 weeks, and were included in the Maintenance trial with ustekinumab provided at week 8 or 12. Only 30-40% of these patients continued to have remission at maintenance trial conclusion. We present a case series of two CD patients who were initiated on ustekinumab therapy but required a shortened maintenance dose interval to achieve/maintain remission.

CASE DESCRIPTION/METHODS:
Case 1: A 33 year old female presenting clinically with intermittent abdominal pain, diarrhea, occasional blood in stool & nocturnal symptoms was diagnosed with CD in 2017 via computed tomography of the abdomen combined with colonoscopy revealing terminal ileum aphthous ulceration. Previous therapies included budesonide, prednisone & adalimumab. Ustekinumab induction was initiated on 2/2/2018. However, on 3/20/2018, the patient developed severe abdominal pain consistent with a CD flare. Following, she has received ustekinumab injections every 4-6 weeks to maintain disease remission. Case 2: A 47 year old male initially diagnosed with CD at the age of 22, complicated by emergent colectomy with end ileostomy in 2014 presented with an acute flare consisting of abdominal pain, peristomal fistulas and increased ostomy output. Following evaluation, he underwent surgical correction of fistula, drainage of intraabdominal wall abscess & abdominal wall reconstruction in December 2018. Prior to this, he was treated with sulfasalazine, mercaptopurine, azathioprine along with immunomodulators including infliximab & certolizumab without adequate response. In January 2019, ustekinumab therapy was initiated with standard induction followed by injectable dosing every 4 weeks due to CD severity and physician recommendation. Following this schedule, the patient has had improved ostomy output and symptom control.

DISCUSSION:
In our experience, shortening the interval of injectable ustekinumab dosing to 4-6 weekly from 8 weeks has proven successful in maintaining remission for patients with severe CD. This subsegment of CD patients was excluded in trials and further investigation is needed to assess long term efficacy of shortened ustekinumab therapy intervals to maintain remission.
3152 Out of the Blue: Unexpected Urine Color After Colonoscopy
Authors: Pierre-Louis Marvah Hill , Wan David 
Published: October 2019

INTRODUCTION:
Chromoendoscopy combines endoscopy and staining as a diagnostic technique to identify pre- and cancerous lesions. Methylene blue, one of many stains used, is sprayed directly in the lumen. Here we report the case of a man who experienced blue urine after undergoing chromoendoscopy.

CASE DESCRIPTION/METHODS:
71-year-old man with a history of UC on sulfasalazine and colon cancer presented to the endoscopy suite for colonoscopy. He was diagnosed with colon cancer 2 years ago and underwent resection and chemotherapy, with PET scan 1 year later showing no evidence of disease. On surveillance colonoscopy a few weeks prior to current presentation, a malignant polyp was found in the rectum along with significant inflammation. He presented to the endoscopy suite for chromoendoscopy to evaluate for dysplasia. It showed residual high-grade dysplasia. Shortly after, the patient's urine color turned blue. Initially, he feared he was having a stroke or seizure, but his wife confirmed indeed his urine was blue. The patient had been on the same two medications for years: atorvastatin and sulfasalazine. The only new agent was methylene blue for his endoscopy. This led us to conclude the blue dye used during chromoendoscopy is the source of the blue urine.

DISCUSSION:
Methylene blue has few indications, one of which is endoscopic dysplasia screening especially in cases of IBD and Barrett's esophagus. The absorption of methylene blue by the colonic lumen is a known but rare side effect. In fact, we have not found any case reports of blue urine in humans as result of chromoendoscopy. There are case reports of blue-green urine but primarily due to blue dye added to enteral feeds and intravenous administration. Many patients undergo chromoendoscopy however without any changes in their urine color. In our patient, the active inflammation could have led to enhanced absorption of methylene blue. There are a few reports to suggest that intestinal mucosa permeability is increased in IBD, possibly correlating to the degree of inflammation, which could have led to increased absorption of methylene blue and ultimately urine excretion. We conclude that our patient with active ulcerative colitis who underwent chromoendoscopy with methylene blue had increased intestinal absorption of methylene blue and urine excretion. This effect was possibly enhanced by active inflammation causing damage to the intestinal lumen leading to enhanced permeability.
3162 Through the Scope Retrieval of a Migrated AXIOS Stent
Authors: Gollol Raju Narasimha Swamy , Mudireddy Prashant 
Published: October 2019

INTRODUCTION:
Endoscopic drainage of pancreatic fluid collections (PFC) is widely accepted modality of therapy due to its less invasive nature, shorter recovery time, lower cost and complication rates. Lumen apposing covered self-expandable metallic stents (LACSEMS) are increasingly utilized in the management of PFC. LACSEM have excellent safety profile and adverse effects are generally low. Rare migration of these LACSEMS has been described, noted at follow up, both in to the enteral lumen as well in to the cyst cavity. We here by present a case of AXIOS stent migration in to PFC that was successfully retrieved.

CASE DESCRIPTION/METHODS:
A 33 year-old Caucasian male with H/O ETOH related pancreatitis presented with 3 months of intermittent nausea and vomiting with nearly 100-pound weight loss. CT abdomen showed a 24 × 21 × 14 cms PFC causing GOO (Figure 1). Under EUS guidance, a 15 × 10 mm hot AXIOS stent (Xlumena Inc., Mountain view, CA, USA) was deployed by transgastric approach in to the cyst but the stent migrated in to the cavity. A second 15 × 10 mm hot AXIOS stent was successfully placed in to the cyst (Figure 2). The lumen of the AXIOS stent in good position was dilated to 15 mm using a wire guided CRE balloon. Large amount of necrotic material was visualized in the cyst cavity. Through the stent necrosectomy was performed. The migrated stent within the cyst was localized by fluoroscopy. Under endoscopic and fluoroscopic guidance, attempt at grabbing the migrated stent with forceps and removal through the stent in good position was unsuccessful. Few days later, migrated stent removal was attempted again. A therapeutic scope was advanced through the AXIOS in good position in to the WON cavity. The migrated stent was grabbed with a Rat-Tooth forceps and was pulled in to the working channel and successfully removed through the scope (Figure 3).

DISCUSSION:
In our case, the AXIOS stent migrated in to the WON cavity at the time of initial deployment necessitating a second AXIOS stent placement. Immediate removal of the migrated stent was not pursued due to risk of dislodging the second stent in good position. Subsequently, after endoscopic necrosectomies and improved WON size, the migrated stent was removed by intubating the WON with a therapeutic gastroscope through the AXIOS stent in good position and pulling the migrated stent in to the working channel of the gastroscope. To the best of our knowledge, retrieval of a migrated LACSEMS inside a WON through the scope via an AXIOS stent has not been previously described.
3165 The Great Masquerade
Authors: Balarajah Sharmili , Lin Valerie 
Published: October 2019

INTRODUCTION:
Syphilis is a sexually transmitted infection caused by T. pallidum. It is often described as “the great imitator,” affecting multiple organ systems, and has a wide variation in its clinical presentation. Syphilitic hepatitis is a rare and occurs in 0.2-3% of cases of secondary syphilis. We present a case of mixed hepatocellular and cholestatic hepatitis that led to the diagnosis of syphilis in a patient who presented with non-specific symptoms.

CASE DESCRIPTION/METHODS:
A 39-year-old homosexual male was referred for evaluation of worsening jaundice following a course of acyclovir for genital herpes 3 months prior. He reported non-specific symptoms including acute diarrhea, abdominal pain, myalgia, rash and weight loss with no change in mental status. He had no pertinent past medical or family history and denied any exposure to IV drugs or blood transfusions. Clinical exam showed scleral icterus, a soft and non-tender abdomen and macular rash in the extremities. Laboratory evaluation showed AST 209, ALT 617 and ALP 1195 (peaked at 2170). INR was 1.0 and albumin was 3.1. Viral hepatitis A, B, C, EBV and HIV testing were negative. F-actin IgG was positive (36) and ANA negative. MRI abdomen showed hepatomegaly without evidence of biliary obstruction. Liver biopsy showed moderate portal/periportal edema; mixed acute and chronic inflammation and pericholangitis with cholestasis. Syphilis immunostaining and Warthin-Starry staining were negative. Our patient was initially treated as presumed autoimmune hepatitis with prednisone. He had significant clinical and LFT improvement over 3-4 weeks but developed new-onset arthralgia in the midst of treatment. Rheumatological workup revealed positive rapid plasma reagin with T. pallidumreactivity. He completed a course of benzathine penicillin, following which he had complete resolution of his symptoms and normalisation of his LFTs.

DISCUSSION:
SH presents a diagnostic challenge in view of its infrequency and there are currently no standardised diagnostic criteria. Liver chemistry typically demonstrates a cholestatic picture with a disproportionately elevated ALP, likely secondary to pericholangiolar inflammation. However, in our patient, there was also moderate lobular activity with plasma cells, corresponding to a moderately elevated ALT. It is imperative that clinicians have a high index of suspicion for syphilis in view of the morbidity and mortality associated with a missed or late diagnosis and the availability of an effective treatment.
3172 A Rare Complication of Hepatic Cirrhosis: Nephrotic Syndrome in IgA Nephropathy
Authors: Jiyani Rucha , Patel Saumil , Patel Parth , Ghosh Sudeshna , Desai Jiten , Jacob Bobby 
Published: October 2019

INTRODUCTION:
There have been many documented cases of cirrhosis and associated Parenchymal renal disease (Ig-A nephropathy, glomerulonephritis). We discuss here rare case of hepatorenal syndrome type 2, in-patient with no clinically and imaging finding indicative of portal hypertension. Also, further interesting finding is to have nephrotic range proteinuria in nephritic syndrome.

CASE DESCRIPTION/METHODS:
56-Year-old Indian male with no past medical or surgical history presented with complaints of generalized weakness and occasional abdominal discomfort. He denied significant family history and alcohol, tobacco or illicit drug use. Ultrasonography (USG) abdomen showed cirrhotic changes. All work up including autoimmune panel negative, hence diagnosed with idiopathic liver cirrhosis. Patient managed with conservative approach, as there were no changes indicative of portal hypertension including Esophagogastroduodenoscopy. After about a year, on routine follow up he found to have his serum creatinine (Cr) progressed from 0.8 to 3.8 mg/dl. Repeat USG abdomen showed diffuse liver parenchymal disease with mild ascites and normal size of kidney with cortical thickness. Urine Microscopy revealed proteinuria and hematuria with 24 hour measured urinary protein 5 gm. Renal biopsy was performed and showed diffuse proliferative glomerulonephritis-Ig A Nephropathy (nephritic syndrome with nephrotic range proteinuria). Autoimmune profile was negative. Hospital course was complicated by septic shock and hemorrhagic cystitis. Patient was treated with inotropes, Pulse dose of intravenous methylprednisolone, albumin and other supportive approach. Decision was made not to continue cyclophosphamide due to hemorrhagic cystitis. Patient Cr later stabilized after peak of 4.3 mg/dl. Presently, is on diuretics and prednisone with Cr is stable around 1.3 mg/dl.

DISCUSSION:
Hepatorenal syndrome is divesting complication of liver cirrhosis, which can occur due to various mechanism one of which is described as in our case. Literature has focused mainly on mechanism of Ig-A nephropathy in portal hypertension. Our aim for this case report is to focus on monitoring renal function in cirrhotic patient even without no evidence of portal hypertension as there is no firm correlation between degree of portal hypertension and severity of IG A nephropathy. Thus, further studies can effect future era of hepatic transplant by more effectively understanding complex mechanism and managing complications.