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SummaryBackgroundNeoplasia detection rate, the proportion of Barrett's oesophagus patients with high‐grade dysplasia or oesophageal adenocarcinoma detected at index surveillance endoscopy has been proposed as a quality metric. However, the correlation between neoplasia detection rate and a clinically relevant outcome like post‐endoscopy Barrett's neoplasia remains unknown. Post‐endoscopy Barrett's neoplasia refers to the rate of high‐grade dysplasia or oesophageal adenocarcinoma on repeat endoscopy within one year of an index screening examination revealing non‐dysplastic Barrett's oesophagus or low‐grade dysplasia.AimTo assess correlation between neoplasia detection rate and post‐endoscopy Barrett's neoplasia.MethodsWe performed a systematic search of multiple databases from date of inception to June 2021 to identify cohort studies reporting both neoplasia detection rate and post‐endoscopy Barrett's neoplasia. Data from each study were pooled using a random effects model, and their correlation assessed using meta‐regression. Heterogeneity was assessed and a priori planned subgroup analyses were conducted.ResultsTen studies with 27 894 patients with Barrett's oesophagus were included. The pooled neoplasia detection rate and post‐endoscopy Barrett's neoplasia were 5.0% (95% CI: 3.4%‐7.1%, I2 = 97%) and 19.6% (95% CI: 10.1%‐34.7%, I2 = 96%), respectively. Meta‐regression revealed a statistically significant inverse relationship between the two variables (coefficient −3.50, 95% CI: −4.63 to −2.37, P < 0.01). With every 1% increase of neoplasia detection rate, post‐endoscopy Barrett's neoplasia decreased by 3.50%. Heterogeneity was high despite adjusting for study quality and performing several subgroup analyses.ConclusionWe observed a statistically significant inverse correlation between neoplasia detection rate and post‐endoscopy Barrett's neoplasia. Additional studies are needed to further validate this correlation.

5017 Background: HDCT/ASCT represents a curative salvage treatment for patients with GCT but is rarely used for other solid tumors. Patients undergoing HDCT/ASCT for hematologic neoplasms require revaccination for their childhood immunizations. Whether this is necessary in patients with GCT is unknown. Methods: In this prospective longitudinal study, patients with GCT undergoing HDCT-ASCT from 11/2010 to 5/2018 had serologies for Measles, Mumps, Rubella, Diphtheria, Tetanus, Polio, and Varicella Zoster measured before HDCT and at 3, 6, and in a subset, 12+ months after the last HDCT with results at these timepoints compared using descriptive statistics. In addition, titer levels at ≥6 months post-transplant were matched 1:1 for age and gender with HL patients who underwent HDCT/ASCT during the same time period. Immunity was compared between cohorts using the Cochran-Mantel-Haenszel test. Results: Of 80 patients with GCT (median age 30, 84% nonseminoma), 91% received 3 sequential transplants and 68 had repeat titers at ≥6 months. Immunity at baseline was >95% for Diphtheria, Tetanus and Polio and 89% for Varicella Zoster but lower for Measles (74%), Mumps (85%), and Rubella (83%) (Table). Compared to baseline, proportional immunity for all infections was similar at 3, 6, and 12 months post-transplant in the GCT population (≥6 months shown in Table). Matching resulted in 58 GCT-HL pairs. One-year immunity was numerically lower for most infections in the HL vs. GCT patients and significantly decreased for Measles and Rubella (Table). Conclusions: To our knowledge, this is the first study to assess vaccine titers following HDCT/ASCT for GCT. We demonstrate that HDCT/ASCT does not result in loss of immunity to childhood vaccines and that GCT patients retain protective titers more frequently than those with HL. However, 15-31% of GCT patients lack MMR immunity at baseline and at 1-year post-ASCT. Therefore, we recommend checking MMR titers at 1-year post-ASCT with revaccination of those lacking immunity. Titer evaluation and revaccination is not necessary for other childhood immunizations.[Table: see text]

INTRODUCTION: Esophageal epidermoid metaplasia (EEM) is a rare disease. METHODS: Patients with EEM diagnosed between 2014 and 2020 were reviewed. RESULTS: Forty EEM cases were identified. EEM occurred in 9 (23%) patients before, concordant, or after esophageal squamous cell carcinoma (ESCC). EEM was associated with previous esophageal lichen planus in 5 patients, Barrett's esophagus 7, and esophageal adenocarcinoma 1. EEM was focal in 28 (70%) or diffuse in 12 (30%) and not detected in 45% on recent previous endoscopy. DISCUSSION: EEM is a premalignant underrecognized condition associated with multiple conditions. Close follow-up or endoscopic treatment may be warranted because of its ESCC association.

INTRODUCTION: Varicella Zoster Virus (VZV) is a DNA virus that leads to two clinical syndromes: varicella (primary) and herpes zoster or shingles (secondary). Disseminated infection is most common in immunocompromised hosts and can lead to multi-organ involvement including hepatitis, pneumonitis, encephalitis and others. Here, we describe a case of a young woman with human immunodeficiency virus (HIV) and primary varicella infection leading to VZV hepatitis. CASE DESCRIPTION/METHODS: A 35-year-old woman presented with a 1-week history of fevers, right upper quadrant and epigastric pain, and a non-pruritic, non-painful rash. Her past medical history was significant for a diagnosis of HIV 5 years prior, not currently on treatment. Upon presentation, vital signs were within normal limits except for a fever of 38.8°C. Physical examination was notable for multiple crusted erosions and papules present on her face, trunk and extremities (Figures 1 and 2). Laboratory evaluation was notable for alanine aminotransferase level 291 U/L, aspartate aminotransferase level 260 U/L, alkaline phosphatase level 135 U/L, total bilirubin 0.4 mg/dL, leukocytes 8 × 10 9 /L, and platelet count 132 × 10 9 /L. CD4 count was 118 cells/mcL and HIV-1 RNA 4,120,000 copies/mL. Computed tomography abdomen/pelvis demonstrated diffuse heterogeneity of the hepatic parenchyma (Figure 3). She underwent liver biopsy and pathology demonstrated hepatic parenchyma with portal and lobular inflammation but no necrosis. VZV polymerase chain reaction (PCR) from the liver and facial lesion swab returned positive. She was treated with 4 days of IV acyclovir with improvement in her fevers and transaminitis and then transitioned to oral valacyclovir. HAART was also initiated two days after the start of IV acyclovir. DISCUSSION: The differential for fever and widespread rash in an immunocompromised individual is broad, and includes disseminated herpes simplex virus, VZV, secondary syphilis, disseminated gonococcal infection, parvovirus, cryptococcosis and others. While uncomplicated VZV can be treated with supportive care or oral antivirals, such as acyclovir, valacyclovir, or famciclovir, an immunocompromised host with disseminated VZV should typically be admitted to the hospital for intravenous acyclovir. Biopsy proven VZV hepatitis is rare and is associated with a high mortality. Notably, our patient's VZV IgM and IgG were negative, indicating the need for a high degree of suspicion if the clinical scenario is consistent with VZV.

INTRODUCTION: Recurrent pancreatitis with pseudocyst can present with gastric outlet obstruction. Endoscopic evaluation should be utilized in certain contexts, especially to exclude more sinister causes of this presentation. CASE DESCRIPTION/METHODS: A 43-year-old woman with a history of alcohol use disorder presented with a gastric outlet obstruction. This was felt secondary to a pancreatic pseudocyst given multiple episodes of recurrent pancreatitis, the last being 1 week prior to her current admission. On presentation, physical exam was significant for ascites and epigastric tenderness. Labs were notable for AST 214 U/L, ALT 99 U/L, alkaline phosphatase 147 U/L, lipase of 203 U/L, and negatives serum alcohol. Notably, Ca 19-9 was elevated to 154 IU/mL during admission 2 weeks prior. Computed tomography chest and abdomen revealed bilateral pleural effusions, pseudocyst, and abdominal ascites. A thoracentesis and paracentesis were performed with cytology for both peritoneal fluid and pleural fluid confirming metastatic adenocarcinoma. Given her refractory symptoms, an esophagogastroduodenoscopy (EGD) was performed which showed an obstructing tumor at the gastric outlet with biopsies revealing poorly differentiated gastric adenocarcinoma. A gastric stent was placed; however, she had continued nausea and vomiting. Repeat EGD showed gastric stent failure and subsequent endoscopic gastrojejunostomy with Axios stent was placed. The patient's functional status declined rapidly as a result of her advanced malignancy and on hospital day 8 she suffered a cardiac arrest, passing shortly after being transitioned to comfort cares. DISCUSSION: The patient's prior history of alcohol use disorder, recurrent pancreatitis, and imaging consistent with pancreatic pseudocyst made this case prone to numerous cognitive errors initially obscuring the etiology of her gastric outlet obstruction and pancreatitis. By reframing the presentation, we were able to question pancreatic pseudocyst as the sole source of the gastric outlet obstruction. Traditionally, Ca 19-9 is associated with pancreatic adenocarcinoma. It also can be elevated in the setting of other gastric malignancies and acute pancreatitis. In pancreatitis, absolute value and trends of Ca 19-9 can help differentiate between pancreatitis and malignancy. The diagnostic uncertainty around this patient's presentation with recurrent pancreatitis, pseudocyst, and gastric outlet obstruction required endoscopic evaluation to ultimately diagnose metastatic gastric adenocarcinoma.

INTRODUCTION: Eosinophilic gastrointestinal diseases (EGIDs) are a set of inflammatory diseases subclassified according to the site(s) of abnormal accumulation of eosinophils (eos) in the gastrointestinal (GI) tract such as eosinophilic esophagitis (EoE), gastroenteritis (EGE), and colitis. These conditions often decrease quality of life due to debilitating symptoms. While the pathogenesis of EGIDs is primarily thought to be driven by eos, there is increasing evidence for the involvement of mast cells (MCs). AIM: To characterize symptomatic patients (pts) with suspected EG/EGE who did not meet histopathologic entry criteria for mucosal eosinophilia for a Phase 2 randomized, double-blind, placebo-controlled study of AK002, an anti-Siglec-8 antibody. METHODS: To undergo screening endoscopy for this study, pts were required to report an average symptom score ≥3 (0 to 10 scale) for abdominal pain, nausea, and/or diarrhea on a daily patient-reported outcome questionnaire for ≥2 weeks and have no other known cause for GI symptoms. During the screening endoscopy, biopsies were systematically obtained from the stomach and duodenum, and read by a single pathologist. Eos counts (eos/hpf; hpf area = 0.237 mm 2 ) were assessed on H&E slides. To quantify MCs, immunohistochemistry for tryptase was performed. We quantified eos and MCs in the stomach and duodenum. Histopathologic entry criteria for the randomized study was ≥30 eos/hpf in 5 hpfs in the stomach (EG) and/or ≥30 eos/hpf in 3 hpfs in the duodenum (EGE). A literature review was conducted to determine normal MC counts in the GI tract. RESULTS: Eighty-eight pts underwent screening endoscopy based upon suspected EG/EGE and active symptoms, and 72 pts met histopathologic eos criteria. All pts whose eos did not meet entry criteria (n = 16) were found to have elevated MC counts (Figure 1; reported normal range = 12-19 MCs/hpf). In these pts, the mean gastric eos count was 6 eos/hpf in 5 hpfs and mean duodenal eos count was 15 eos/hpf in 3 hpfs. In contrast, these pts exhibited a mean gastric MC count of 47 MC/hpf in 5 hpfs and a mean duodenal MC count of 49 MC/hpf in 3 hpfs. Almost all symptomatic pts screened (87/88; 99%) had elevated MC counts. CONCLUSION: Data from this large randomized EG/EGE study showed that symptomatic pts with suspected EG/EGE had increased mucosal MCs with or without mucosal eosinophilia. These data suggest that MCs may play a role in pts with suspected EG/EGE and raise the possibility of a unique clinical presentation driven by MCs.