Does Smoking Cannabis Increase the Risk of Barrett's Esophagus?

Millions of Americans smoke cannabis every day. With the recent legalization of cannabis in many states, the number of Americans who smoke cannabis is expected to climb even higher. This case report presents a chronic cannabis smoker who developed severe Barrett's esophagus at a young age. A 41-year-old African American male presented with an exacerbation of nausea and vomiting. The patient reported that he smoked cannabis two to three times daily for the past 20 years. Upper endoscopy and subsequent histology analysis displayed long-segment Barrett's esophagus indefinite for dysplasia. The patient was encouraged to cease cannabis use and have a follow-up endoscopy in 3-6 months. Barrett's esophagus is rare in African Americans; however, with the increase in the prevalence of cannabis smoking, endoscopic surveillance guidelines may need to be modified to include younger African Americans who chronically smoke cannabis.

Overexpression of CCN1 in Het1A cells attenuates bile-induced esophageal metaplasia through suppressing non-canonical NFκB activation.

GERD is the most common gastrointestinal diagnosis given during office visit. People who suffer from a long history of GERD eventually develop Barrett's esophagus, a premalignant intestinal metaplasia due to NFκB activation. Previous studies focused on the contribution of TNF-triggered canonical NFκB pathway to this event. In this study, we demonstrated in vitro that it was LTA, rather than TNF, initiated canonical NFκB activation at the beginning of acid/bile attacks, but later it switched to CD40-activated non-canonical pathway, which played a bigger part in esophageal metaplasia. CCN1 attenuated this cellular transformation by suppressing CD40 and its associated proteins involved in non-canonical signaling.

Chronic Gingivostomatitis with Esophagitis in Cats.

BACKGROUND: Chronic gingivostomatitis in cats (FCG) is a debilitating disease with potentially deleterious effects on overall health. HYPOTHESIS/OBJECTIVES: Little is known about the pathophysiology and overall impact of FCG. The aims of our study were to investigate whether gingivostomatitis occurs concurrently with esophagitis, if FCG treatment contributes to esophagitis and if esophagitis exacerbates signs of FCG. ANIMALS: Fifty-eight cats with clinical signs of FCG and 12 healthy control cats exhibiting no signs of oral disease, all client-owned. METHODS: Prospective study. Physical, oral and endoscopic examinations were performed on all cats. Measurements of salivary and esophageal lumen pH were obtained from both groups. Biopsies were acquired from sites of esophageal inflammation in cats with FCG and from normal-appearing esophageal mucosa in control cats. RESULTS: The majority of cats with clinical signs of FCG exhibited some degree of esophagitis especially in the proximal (44/58) and distal (53/58) parts (P < 0.001) with or without columnar metaplasia, compared to controls. All cats lacked signs related to gastrointestinal disease. Salivary and esophageal lumen pH were not statistically different compared to controls. CONCLUSIONS AND CLINICAL IMPORTANCE: Feline chronic gingivostomatitis seems to occur concurrently with esophagitis. Esophagitis also should be managed in cats with chronic gingivostomatitis because it may aggravate the existing condition.

A substantial incidence of silent short segment endoscopically suspected esophageal metaplasia in an adult Japanese primary care practice.

AIM: To determine the incidence and characteristics of endoscopically suspected esophageal metaplasia (ESEM) in a primary adult care institution. METHODS: Eight hundred and thirty two consecutive individuals (mean age, 67.6 years) undergoing upper gastrointestinal endoscopy between January 2009 and December 2010 were included in this study. The diagnosis of ESEM was based on the criteria proposed by the Japan Esophageal Society, and was classified as long segment ESEM (3 cm or more) or short segment ESEM (< 3cm). Short segment ESEM was further divided into circumferential and partial types. Age, gender, hiatus hernia, esophagitis, gastroesophageal reflux disease (GERD)-suggested symptoms, and antacid medications were recorded as background factors. Esophagitis was graded according to the Los Angeles classification. Hiatus hernia was divided into absent and at least partially present. RESULTS: Long and short segment ESEM were found in 0 and 184 (22.1%) patients, respectively (mean age of short segment ESEM patients, 68.3 years). Male gender and hiatus hernia were shown to be significant factors affecting short segment ESEM by both univariate (P = 0.03 and P = 9.9x10(-18)) and multivariate [Odds ratio (OR) = 1.45; P = 0.04, and OR = 43.3; P = 1.5x10(-7))] analyses. Two thirds of patients with short segment ESEM did not have GERD-suggested symptoms. There was no correlation between short segment ESEM and GERD-suggested symptoms. CONCLUSION: The incidence of short segment ESEM in our community practice seems higher than assumed in Asian countries. As GERD-suggested symptoms are a poor predictor of ESEM, endoscopists should bear in mind that silent short segment ESEM does exist and, in fact, was found in the majority of our patients.