No abstract

Background and Aim: The third leading preventable cause of death in the United States is excessive alcohol consumption. Our study sought to assess the impact of the coronavirus disease 2019 (COVID-19) on hospitalizations for alcohol-related hepatitis at a community hospital system. We hypothesized an increase in cases of alcohol-related hepatitis requiring inpatient management, mirroring the strain on economic and societal norms imposed by the COVID-19 pandemic.Approach/Results: We performed a retrospective chart review to study the incidence of alcohol-related hepatitis in patients presenting to 3 community hospitals in Fresno, California, before and during the COVID-19. Data including patient demographics, markers of disease severity, and clinical course were extracted from electronic medical records for 329 patients included in the study. There was a 51% increase in the overall incidence of alcohol-related hepatitis requiring hospitalization between 2019 and 2020 (P = 0.003) and 69% increase (P < 0.001) after implementation of the stay-at-home orders. In addition, 94% (P = 0.028) increase in rehospitalizations was noted in 2020 (P = 0.028), a 100% increase in patients under the age of 40 (P = 0.0028), as well as a trend towards a 125% increase (P = 0.06) of female patients admitted with this diagnosis during the COVID-19 pandemic.Conclusions: Our study revealed drastic increases in severe alcoholrelated hepatitis requiring inpatient management, specifically in patients under the age of 40 and in women during the COVID-19 pandemic. Given the high morbidity and mortality associated with severe alcohol-related hepatitis, these findings have far-reaching and lasting implications for our already strained health care system extending beyond the COVID-19 pandemic timeframe. Urgent public health interventions are needed to combat the rising misuse of alcohol and its consequences.

Eosinophilic gastroenteritis is a rare condition of unknown aetiology, first described by Kaijser in 1937. It is manifest by eosinophilic infiltration of the gastrointestinal tract and peripheral eosinophilia. Patients have various clinical presentations depending on the region of the gastrointestinal tract involved and the depth and extent of the bowel wall involvement. Whereas gastrointestinal obstruction associated with this condition is not uncommon, isolated biliary obstruction has only been reported twice. We present a case of eosinophilic gastroenteritis with involvement of the biliary tract causing ulceration, fibrosis and obstruction. Although a rare condition, we believe the diagnosis of eosinophilic gastroenteritis should be entertained in patients with gastrointestinal symptoms and a peripheral eosinophilia who have no evidence of parasitic infection, vasculitis or neoplasms.

Background and Aims We conducted a systematic review and meta-analysis evaluating the relapse rate after therapeutic de-escalation in inflammatory bowel disease [IBD] patients who achieved deep remission [DR]. Methods We searched MEDLINE, EMBASE, and major gastroenterology conferences up to July 2019 for studies reporting relapse in adult patients with DR who subsequently underwent therapeutic de-escalation. Eligible studies defined DR as at least a combination of clinical remission and mucosal healing/endoscopic remission. The primary outcome was cumulative 1-year and 2-year relapse rates after therapeutic de-escalation. Secondary outcomes were relapse rates in ulcerative colitis [UC] and Crohn’s disease [CD], relapse after anti-tumour necrosis factor-α [anti-TNFα] de-escalation, and the rate of disease response recapture following re-escalation. Results Thirteen studies encompassing 837 patients were identified. The cumulative relapse rate after therapeutic de-escalation was 28.7% within 1 year [12 studies], and 38.4% within 2 years [eight studies]. Relapse rates within 1 year and 2 years were comparable between UC [five studies; 25.4% and 37.4%] and CD [seven studies; 34.1% and 39.9%]. Ten studies reported de-escalation of anti-TNFα, of which 29.8% patients relapsed within 1 year and 41.4% within 2 years. Response recapture following re-escalation [eight studies] was 75.4%. Conclusions Despite achieving deep remission, therapeutic de-escalation in this patient population is associated with significant relapse risk within 1 year and 2 years. This risk is more pronounced in patients requiring anti-TNFα for management, likely because of more severe disease. Similar rates of relapse were reported among UC and CD within these time periods. These findings suggest that combined clinical and endoscopic remission should not be an impetus to consider therapeutic de-escalation.

The inflammatory bowel diseases (IBD) are a complex set of chronic gastrointestinal inflammatory conditions arising from the interplay of genetic and environmental factors. This study focuses on noncoding RNA transcripts as potential mediators of IBD pathophysiology. One particular gene, interferon γ-antisense 1 ( IFNG-AS1), has been consistently observed to be elevated in the intestinal mucosa of patients with actively inflamed IBD versus healthy controls. This study builds on these observations, demonstrating that the second splice variant is specifically altered, and this alteration even stratifies within inflamed patients. With the use of a CRISPR-based overexpression system, IFNG-AS1 was selectively overexpressed directly from its genomic loci in T cells. An unbiased mRNA array on these cells identified a large increase in many inflammatory cytokines and a decrease in anti-inflammatory cytokines after IFNG-AS1 overexpression. Media from T cells overexpressing IFNG-AS1 elicited an inflammatory signaling cascade in primary human peripheral blood mononuclear cells, suggesting the potential functional importance of IFNG-AS1 in IBD pathophysiology. The significance of these results is amplified by studies suggesting that a single-nucleotide polymorphism in IFNG-AS1, rs7134599, was associated with both subtypes of patients with IBD independently of race. NEW & NOTEWORTHY Long noncoding RNAs are an emerging field of inflammatory bowel disease (IBD) research. This study mechanistically analyzes the role of a commonly upregulated gene in IBD and shows IFNG-AS1 as a mediator of an inflammatory signaling cascade.