BACKGROUND & AIMS: Endoscopic eradication therapy (EET) for Barrett's esophagus (BE) has unclear effects on the gastric cardia. We investigated the prevalence of intestinal metaplasia (IM) and dysplasia in the cardia after complete eradication of IM (CEIM) and the incidence of newly diagnosed cardia IM or dysplasia after EET. METHODS: We performed a prospective study, from 2013 through 2016, of patients with previously successful EET undergoing surveillance after CEIM (cross-sectional group) and treatment-naïve patients with BE undergoing EET (longitudinal group). Standard biopsies were collected from multiple levels in the cardia and analyzed histologically. We calculated the prevalence (crosssectional group) and the incidence (longitudinal group) of cardia IM or dysplasia after EET. RESULTS: Of the 116 patients in the cross-sectional group, 17 (15%) had cardia IM or dysplasia after CEIM: 12 patients had IM, 2 patients were indefinite for dysplasia, and 3 patients had low-grade dysplasia. Cardia IM or dysplasia were most commonly found at the tops of gastric folds. Among 42 subjects in the longitudinal group, the pre-treatment prevalence of cardia IM or dysplasia was 28.5% (3 with non-dysplastic IM, 9 with dysplastic IM, 1 indefinite for dysplasia, 2 with lowgrade dysplasia, 3 with high-grade dysplasia, and 3 with intramucosal cancer). All achieved CEIM. The incidence of cardia IM or dysplasia was 11.9% after 18 months of follow up. IM or dysplasia was more higher in the cardia after CEIM than in the tubular esophagus (P < .01). CONCLUSIONS: In a prospective study, we found that cardia dysplasia becomes less, not more, common, after successful EET; recurrence of IM or dysplasia was more frequent in the cardia than the esophagus. Patients with BE undergoing EET should have careful examination of the cardia, with a single set of surveillance biopsies at the top of the gastric folds.
INTRODUCTION: Poor bowel preparation for colonoscopy is associated with reduced diagnostic yield, increased risk of perforation, and longer length of hospitalization. Prior studies have demonstrated inpatient status as a risk factor for poor bowel preparation. Research at our institution has identified risk factors that are associated with poor bowel preparation, but this study consisted primarily of an outpatient population. The aim of this study is to investigate the impact of known risk factors on bowel preparation quality in an inpatient population. METHODS: A retrospective chart review was performed for all patients undergoing inpatient colonoscopies from July 2017 - April 2019 at a single academic medical center. ICU patients were excluded. The indication for colonoscopy, amount of bowel preparation (4L vs >4L of polyethylene glycol), and documented quality of the bowel preparation (adequate vs poor) were reviewed. Previously identified risk factors for poor bowel preparation including gender, type 2 diabetes (T2DM) with end-organ damage, COPD, neurologic disease (stroke, dementia, Parkinson’s disease), TCA use, opioid use, and laxative use were recorded. Association of risk factors with poor bowel preparation was analyzed using chi-square tests. RESULTS: 306 patients underwent inpatient colonoscopy. 42 patients (13.7%) had poor bowel preparation. 31.7% (n = 13) of patients with at least 3 risk factors had poor bowel preparation while only 11.5% (n = 29) of patients with two or less risk factors had poor bowel preparation (P = 0.01). This statistically significant relationship was upheld when controlled for standard colonoscopy preparation (P = 0.03). Among the 42 patients with poor bowel preparation, 54.7% (n = 23) were male, 38% (n = 16) had active opioid use, 26% (n = 11) had T2DM with end-organ dysfunction, 26% (n = 11) had active laxative use, 14.2% (n = 6) had neurological disease, 11.9% (n = 5) had COPD, and 2.3% (n = 1) had active TCA use. CONCLUSION: To date, there is not a nationally accepted risk stratification system for identifying patients at high risk for poor bowel preparation in the inpatient setting. This study shows that patients with at least 3 risk factors were associated with a higher incidence of poor bowel preparation in hospitalized patients. Recognition of these risk factors and individualized bowel preparation could lead to a reduction in the incidence of poorly visualized colonoscopies in the inpatient setting.
INTRODUCTION: Combined checkpoint inhibitor immunotherapy with ipilimumab (anti-cytotoxic T-lymphocyte antigen 4 antibody) and nivolumab (anti-programmed cell death receptor 1 antibody) has greatly advanced the treatment of multiple malignancies but is associated with increased immune-related toxicities. Gastrointestinal toxicity is one of the most frequent adverse effects, and while lower GI tract toxicity, such as anti-CTLA-4-mediated colitis, is well known, severe toxicity of the upper GI tract is rare and not well described. We report a case of severe hemorrhagic gastritis in a patient after initiation of ipilimumab and nivolumab therapy for metastatic renal cell carcinoma. CASE DESCRIPTION/METHODS: A 70-year-old man with history of metastatic renal cell carcinoma and recent immune-related myocarditis initially presented with myasthenic weakness after receiving single doses of ipilimumab and nivolumab 5 weeks prior. His presentation was most consistent with seronegative, immune-mediated myasthenia gravis-like syndrome. He was treated with intravenous steroids and plasmapheresis. After 9 days of steroid therapy, he developed large volume melena requiring 4 units of blood despite twice-daily proton pump inhibitor therapy. Endoscopic evaluation revealed diffuse, severe inflammation with hemorrhage characterized by adherent blood and erythematous, friable gastric mucosa in the body, antrum, and prepyloric regions. Hemostatic spray was applied as a temporizing measure to control bleeding. Biopsy specimens demonstrated neutrophilic microabscesses with intraglandular apoptotic bodies, increased lymphocytes and scattered neutrophils in lamina propria, and reactive mucosal features. These findings were compatible with checkpoint inhibitor-induced acute gastritis. Immunohistochemical stains for H. pylori and cytomegalovirus were negative. Despite immunosuppressive therapy with high dose steroids, mycophenalate mofetil, and trial of infliximab, he continued to decline with ongoing anemia and progressive weakness. He was transitioned to comfort measures and died soon afterward. DISCUSSION: To our knowledge, this is the first reported case of severe hemorrhagic, non-infectious gastritis as a rare complication of immunotherapy with ipilimumab and nivolumab. Physicians should be aware that checkpoint inhibitor-induced toxicity of the upper GI tract can occur early after initiation of therapy and have a severe, refractory course. Management includes exclusion of infectious process and immunosuppressive therapy.
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