Clinical evaluation of a real-time artificial intelligence-based polyp detection system: a US multi-center pilot study.

Artificial intelligence (AI) has increasingly been employed in multiple fields, and there has been significant interest in its use within gastrointestinal endoscopy. Computer-aided detection (CAD) can potentially improve polyp detection rates and decrease miss rates in colonoscopy. However, few clinical studies have evaluated real-time CAD during colonoscopy. In this study, we analyze the efficacy of a novel real-time CAD system during colonoscopy. This was a single-arm prospective study of patients undergoing colonoscopy with a real-time CAD system. This AI-based system had previously been trained using manually labeled colonoscopy videos to help detect neoplastic polyps (adenomas and serrated polyps). In this pilot study, 300 patients at two centers underwent elective colonoscopy with the CAD system. These results were compared to 300 historical controls consisting of consecutive colonoscopies performed by the participating endoscopists within 12 months prior to onset of the study without the aid of CAD. The primary outcome was the mean number of adenomas per colonoscopy. Use of real-time CAD trended towards increased adenoma detection (1.35 vs 1.07, p = 0.099) per colonoscopy though this did not achieve statistical significance. Compared to historical controls, use of CAD demonstrated a trend towards increased identification of serrated polyps (0.15 vs 0.07) and all neoplastic (adenomatous and serrated) polyps (1.50 vs 1.14) per procedure. There were significantly more non-neoplastic polyps detected with CAD (1.08 vs 0.57, p < 0.0001). There was no difference in ≥ 10 mm polyps identified between the two groups. A real-time CAD system can increase detection of adenomas and serrated polyps during colonoscopy in comparison to historical controls without CAD, though this was not statistically significant. As this pilot study is underpowered, given the findings we recommend pursuing a larger randomized controlled trial to further evaluate the benefits of CAD.

A prospective study of gastric acid analysis and esophageal acid exposure in patients with gastroesophageal reflux refractory to medical therapy.

A number of factors have been proposed to account for the lack of response to medical therapy in patients with gastroesophageal reflux; however, no controlled studies are available in the literature. The goal of this study was to determine possible causes of medical refractoriness in patients with gastroesophageal reflux. Gastric acid output and esophageal acid exposure were measured in patients who continue to have reflux symptoms despite aggressive antisecretory therapy. In addition, an upper endoscopy was also performed in each patient. Patients with a drug-controlled acid output < 1 mEq/hr and a supine total esophageal pH < 4 for less than 1.7% of the time measured were considered responsive to therapy; on the other hand, those with a drug-controlled gastric acid output > 1 mEq/hr and a supine esophageal pH < 4 for more than 1.7% of the time measured were considered resistant to therapy. Twenty-four patients met the inclusion criteria (13 male and 11 female; mean age, 52). Drug-controlled gastric acid output was more than 1 mEq/hr in 25% of patients and less than 1 mEq/hr in the remainder. Of those patients with a gastric acid output of less than 1 mEq/hr (18 patients), 8(44%) had a supine esophageal pH < 4 for more than 1.7% of the time, suggesting that factors other than gastroesophageal reflux likely contributed to their reflux-like symptoms. Acid suppression appears adequate in the majority of patients with gastroesophageal reflux refractory to medical therapy. The exact cause of persistent reflux-like symptoms in patients who fail medical treatment is uncertain but may be related to non-acid-related factors such as esophageal hypersensitivity to physiologic reflux, increased intake of air resulting in aerophagia, or other factors such as bile reflux.

Drug- and chemical-induced cholestasis.

Cholestasis caused by medicinal and chemical agents is an increasingly well-recognized cause of liver disease. Clinical drug-induced cholestatic syndromes producing jaundice and bile duct injury can mimic extrahepatic biliary obstruction, primary biliary cirrhosis, and sclerosing cholangitis, among others. This article updates the various forms of drug-induced cholestasis, focusing on the clinicopathologic features of this form of hepatic injury and on the known or putative mechanisms by which drugs and chemicals lead to cholestasis.