Introduction: Esophageal epidermoid metaplasia (EEM) is a rare premalignant condition seen in middle aged men with history of alcohol and tobacco use. EEM has been reported in association with esophageal squamous cell carcinoma, as well as GERD, Barrett’s esophagus, lichen planus, and esophageal adenocarcinoma. Case Description/Methods: A 75-year-old man with history of gastroesophageal reflux and tobacco use (1 pack per day) presented to clinic for evaluation of odynophagia and unintentional weight loss. He reported a history of oral Candidiasis and dysphagia that had empirically been treated with fluconazole on multiple occasions in previous years. The patient was underweight, 104 lbs, BMI = 15.4. Labs were significant for an iron deficiency anemia – hemoglobin= 9.0 g/dL, mean corpuscular volume = 82 fL, iron = 23 ug/dL (low), total iron binding capacity = 469 ug/dL (high) and transferrin saturation = 5% (low), ferritin = 59 ug/L (low normal). EGD showed a focal nodular lesion,< 1 cm, in the middle third of the esophagus that was resected and more diffuse verrucous patches proximal to the nodules (Figure 1A), from which biopsies were obtained. Histology of the resected focal nodular area showed high grade squamous dysplasia. The more diffuse verrucous areas revealed squamous mucosa with epidermoid metaplasia and reactive epithelial changes (Figure 1B). A follow up surveillance EGD performed 4 months later showed segmental moderate mucosal changes characterized by discoloration, nodularity and altered texture in the mid and distal esophagus (Figure 1C). Repeat surveillance biopsies revealed squamous mucosa with marked active inflammation and reactive changes with identification of superimposed Candida. Discussion: Endoscopically, EEM can vary in appearance including white plaques, keratotic patches,granularity, nodularity, furrows, and lacy appearance. Histological features include hyperorthokeratosis and a pronounced granular cell layer. This case showed high grade squamous dysplasia, which has been previously described but also demonstrated as association with esophageal Candidiasis, which has not been previously described. It is unclear why the patient had chronic Candidiasis and whether the chronic fungal infection played a role in the pathogenesis of EEM. Treatment of EEM with endoscopic resection of focal lesions and/or radiofrequency ablation of more diffuse disease has been reported. Given that EEM has been associated with esophageal cancer, close monitoring with endoscopic surveillance seems prudent.Figure 1.: A: Narrow Band Imaging demonstration few tiny mucosal nodules, hyper-keratosis, and linear furrows with a patchy distribution in the middle third of the esophagus. B: Histology of the biopsies taken from the verrucous patches showing hypergranulosis and hyperorthokeratosis consistent with Epidermoid Metaplasia. C: Segmental verrucous keratotic focal and broad linear mucosal changes noted in the mid and distal esophagus.

Michael Kurin: NO financial relationship with a commercial interest

Introduction: Pelvic inflammatory disease (PID) is an infection of the upper genital tract, including the uterus, fallopian tubes, and/or ovaries. Neisseria gonorrhea, Chlamydia trachomatis, and Mycoplasma genitalium are the most frequently isolated pathogens. Case Description/Methods: A 25-year-old female presented with an 8-day history of lower abdominal pain associated with fevers, chills, vomiting, and non-bloody diarrhea. Patient denied recent travel, changes in her diet, family history of Inflammatory Bowel Disease. Her abdomen was diffusely tender. Routine laboratory testing was unremarkable. CT scan of the abdomen and pelvis (Figure 1) showed focal small bowel mural thickening, concerning for gastroenteritis. COVID PCR, HIV antigen/antibody, blood cultures, Clostridium difficile toxin and stool pathogen PCR panel were all negative. Patient was presumed to have viral gastroenteritis and was discharged home. She was readmitted two days later for worsening nausea and vomiting. Laboratory testing was significant for WBC 12.7 x 109/L, potassium of 2.8 mEq, INR 1.7, CRP 19.24 mg/dL. A repeat CT abdomen and pelvis (Figure 2) showed a re-demonstration of marked wall thickening of the small bowel most consistent with enteritis, and the development of large loculated ascites in the mid abdomen and pelvis with peritoneal thickening and enhancement. Diagnostic paracentesis showed PMNs 990, RBCs 4000, SAAG < 1.1, total protein 3.7 g/dl, glucose 29 mg/dl, and LDH 1609 U/L. Peritoneal cultures grew Neisseria gonorrhea. Patient was discharged home on a two-week course of IV ceftriaxone, metronidazole and doxycycline with improvement in clinical symptoms. Repeat diagnostic imaging showed interval improvement and resolution of ascites. Discussion: Acute symptomatic PID presents with lower abdominal pain associated with fevers, chills, nausea, vomiting, vaginal discharge and/or intermenstrual bleeding. PID may present with RUQ pain in the setting of liver capsular inflammation, also known as perihepatitis i.e. Fitz-Hugh Curtis Syndrome. Perihepatitis occurs in about 10% of woman with acute PID. However, the development of ascites as a presenting complication of PID is very rare. In this case, the ascites fluid studies were not consistent with portal hypertension with a SAAG < 1.1. In addition, PMNs > 250 cells suggested bacterial peritonitis. Furthermore, per the Runyon’s criteria, this pattern resembled secondary bacterial peritonitis with a total protein >1 g/dL, glucose < 50 mg/dL, and LDH > upper limit of normal serum.Figure 1.: CT abdomen and pelvis on presentation showing small bowel mural thickening and enhancement.Figure 2.: CT abdomen and pelvis on representation showing large volume ascites with continued small bowel mural thickening and enhancement.

Introduction: Acute Esophageal Necrosis (AEN) is a rare condition that presents with an upper gastrointestinal bleed. It is characterized by blackened esophageal mucosa usually affecting the distal esophagus. Etiology of AEN remains unclear; however, it has been proposed to result from an inciting ischemic injury to the esophagus, which is further aggravated by acidic gastric contents. Case Description/Methods: A 56-year-old male with no medical history presented to the hospital with a 2-day history of abdominal pain associated with fevers, chills, night sweats, and loss of appetite. The patient reports a one month history of weight loss and fatigue. On presentation, he had an acute onset of coffee ground/black emesis. Vital signs revealed a respiratory rate of 25 breaths/min and were otherwise normal. Physical exam was notable for jaundice, distended abdomen and diffuse tenderness with no peritoneal signs. Laboratory testing was significant for white blood count of 24.3 x109/L, hemoglobin 11.5 g/dL, platelet count 116 x109/L, potassium 5.2 mEq, BUN 88 mg/dL, creatinine 2.61 mg/dL, AST 215 IU/L, ALT 632 IU/L, ALP 494 IU/L, direct bilirubin 5.5 mg/dL, INR 2.0, uric acid 12.9 mg/dL, lactate 11.5 mmol/L. CT scan of the chest, abdomen, and pelvis demonstrated mediastinal and hilar lymphadenopathy, hepatomegaly, ascites, multiple liver lesions, and numerous sclerotic bone lesions concerning for metastases. Serum tumor markers were elevated (carcinoembryonic antigen 793, cancer antigen 19-9 27,414). An EGD revealed severe esophagitis with blackened mucosa in the middle third and distal esophagus without stigmata of a recent bleed and a distal esophageal mass (Figure 1 and 2). Brush cytology of the distal esophageal mass showed atypical epithelioid cells suggestive of malignancy. Liver biopsy showed poorly differentiated adenocarcinoma. The patient’s condition deteriorated and he passed away in the setting of multi-organ failure. Discussion: AEN has been associated with underlying malignancy, infections, broad spectrum antibiotic use, gastric volvulus, paraesophageal hernia, hyperglycemia, diabetic ketoacidosis, Stevens-Johnson syndrome, cocaine use, alcoholic hepatitis, and lactic acidosis. Diagnosis is usually incidental in patients undergoing EGD for evaluation of an UGIB. Mortality rates range from 13% to 35%, with a case-fatality rate of 6% typically secondary to the underlying disease. In our case, the patient had an underlying malignancy likely triggering the occurrence of AEN.Figure 1.: Evidence of necrotic mucosa in the middle third of the esophagus. Figure 2: Necrotic mucosa and mass in the distal esophagus.

INTRODUCTION: Olmesartan enteropathy is a well-documented uncommon cause of diarrhea. However, olmesartan induced colitis is an under-recognized entity. We report a case of olmesartan enteropathy and colitis in a patient on olmesartan for hypertension for over a year who presented with chronic diarrhea. CASE DESCRIPTION/METHODS: A 69-year-old man, with history of hypertension, on olmesartan for 1.5 years presented with 5 weeks of 4-5 daily episodes of watery, non-bloody diarrhea associated with nocturnal fecal incontinence, nausea, and vomiting. He had no abdominal pain, melena, weight loss, NSAIDs use, or recent travel. Patient had had multiple admissions for dehydration, and suspected infectious etiology for which he was given empirical antibiotics without clinical improvement. On exam he was afebrile, hemodynamically stable, with unremarkable physical exam. Laboratory testing revealed WBC of 10.8 × 103/ul, hemoglobin of 14.5 g/dL, creatinine of 1.53 mg/dL, and potassium of 2.8 mEq/L. Inflammatory markers and liver function test were not elevated. Stool PCR and C. Difficiletoxin were negative, as was anti-TTG with normal IgA levels. A CT abdomen and pelvis was unrevealing. EGD revealed blunted duodenal mucosa with biopsy showing chronic enteritis with villous shortening, crypt hyperplasia, and increased intraepithelial lymphocytes (Figure 1). Colonoscopy demonstrated multiple scattered non-bleeding aphthous ulcers in the entire colon (Figure 2). Colonic pathology showed focally active colitis and intraepithelial lymphocytes without granulomas (Figure 3). Olmesartan enteropathy was suspected and the medication was discontinued. The patient’s diarrhea resolved two weeks after olmesartan was discontinued. DISCUSSION: Olmesartan enteropathy can manifest with diarrhea, weight loss, iron deficiency anemia, dehydration, hypokalemia, and renal insufficiency. It mimics celiac disease clinically and microscopically, with the presence of villous atrophy in the small intestine biopsy. A negative celiac disease serology helps to distinguish between these two entities. In addition, drug-induced colitis has also been reported in patients on olmesartan. The presence of lymphocytic infiltrate, preserved architecture, and absence of granuloma on colon biopsy helps differentiate this entity from IBD or infectious colitis. Symptoms of olmesartan enteropathy may develop months or years after the initiation of therapy. However, mucosal changes in small and large intestine will resolve after discontinuation of olmesartan.

INTRODUCTION: Hepatic sinusoidal obstructive syndrome (SOS) occurs when sinusoidal endothelial cells are damaged leading to occlusion of hepatic venules. Causes include hematopoietic stem cell transplantation, chemotherapy, toxins, and radiation. Here, we report the case of a man with blinatumomab induced SOS. CASE DESCRIPTION/METHODS: A 39-year-old male with a recent history of drug induced liver injury presented with relapsed t (9;22) negative ALL and was started on blinatumomab therapy. On clinical examination, the patient was jaundiced with a distended abdomen. Prior to starting blinatumomab the patient’s aspartate aminotransferase (AST), alanine aminotransferase (ALT) and total bilirubin were 162 U/l, 71 U/L, and 12.3 mg/dL respectively. These levels rose over the next several weeks (ALT, 100 U/L; AST, 364 U/L; total bilirubin, 28.4 mg/dL). Abdominal CT showed large volume ascites, gastric varices, and hepatomegaly with numerous hypodense lesions (Figure 1). Transjugular liver biopsy (Figure 2) revealed SOS as well as cholestatic liver disease, consistent with sepsis. The patient’s condition progressed despite treatment with defibrotide, and he died of multiple organ failure 1 month after starting blinatumomab. DISCUSSION: Hepatic SOS occurs when hepatic terminal venules and sinusoids become obstructed. SOS is commonly seen in the setting of hematopoietic stem cell transplantation, but also occurs after chemotherapeutic agents, radiation therapy, liver tumor embolization and transplantation. The incidence of SOS varies widely between studies. Pre-existing liver disease, patients age, and prior radiation therapy are known risk factors. Clinical features of SOS include RUQ pain, jaundice, and ascites as well as elevated ALT, AST, and bilirubin. In severe disease, PT and platelet counts may also be abnormal. SOS is a clinical diagnosis, and imaging studies, such as an abdominal US, are frequently done during initial evaluation. Liver biopsy is not commonly used for diagnosis, but will show dilated and congested liver sinusoids with RBCs. Although SOS has been previously reported in the setting of chemotherapy, blinatumomab induced SOS is rare. Moreover, even though hepatotoxicity in the setting of blinatumomab has been documented, the mechanism of liver injury remains unknown. Further studies can explore whether SOS could relate directly to the method of liver injury in the setting of blinatumomab.