Biomedical subjects

M Fein

Publications and source records attributed to M Fein.

42 records · Page 3Linked to original sources

PubMedDate not supplied

Duodenoesophageal reflux induces esophageal adenocarcinoma without exogenous carcinogen.

In the rat model, esophageal adenocarcinoma reproducibly develops following surgically induced duodenal reflux into the esophagus and administration of nitrosamine. In addition, decreasing gastric acid via partial or total gastrectomy increases the prevalence of adenocarcinoma in this model. We questioned whether carcinogen was necessary for cancer development in the gastrectomized model and whether esophageal acidification could reverse the effect of gastrectomy. Three groups of 26 rats each were randomized to a surgical procedure to produce one of the following reflux models: gastroduodenal reflux by esophagojejunostomy, duodenal reflux by total gastrectomy and esophagojejunostomy, or no reflux by Roux-en-Y reconstruction. In a second experiment, 42 rats were operated on to induce duodenal reflux. One week following surgery, they were randomized to receive acidified water (pH 1.8) or tap water. The animals were killed at 24 weeks of age, and the esophagus was evaluated histologically. All animals with reflux had severe esophagitis and 87% developed columnar lining of the distal esophagus. Nearly half (48%) developed adenocarcinoma at the anastomotic site 16 weeks postoperatively and without carcinogen administration. Cancer prevalence did not differ between animals with gastroduodenal or duodenal reflux but tended to be lower in animals receiving acidified water. Duodenoesophageal reflux is carcinogenic in the rat model. Exogenous carcinogen is not necessary for cancer development in gastrectomized rats.

Adenocarcinoma↗

PubMedDate not supplied

Gastroesophageal reflux disease and mucosal injury with emphasis on short-segment Barrett's esophagus and duodenogastroesophageal reflux.

Gastroeosphageal reflux disease has been associated with long segments of Barrett's esophagus </=3 cm), but little is known about its association with shorter segments. The aim of this study was to evaluate anatomic and physiologic alterations of the cardia and esophageal exposure to gastric and duodenal juice in patients with short and long segments of Barrett's esophagus. Furthermore, these patients were compared to each other and to patients with erosive esophagitis and those with no mucosal injury. Two hundred sixty-two consecutive patients with foregut symptoms were divided into the following four groups based on endoscopic and histologic findings: group 1, no mucosal injury; group 2, erosive esophagitis; group 3, short-segment Barrett's esophagus; and group 4, long-segment Barrett's esophagus. Esophageal exposure time to acid and bilirubin, lower esophageal sphincter characteristics, and endoscopic anatomy of the cardia were compared between the groups. Patients with short-segment Barrett's esophagus had elevated esophageal acid and bilirubin exposure, decreased lower esophageal sphincter pressure and length, and a high incidence of hiatal hernia. These abnormalities were similar to those in patients with esophagitis and in general less profound than those found in patients with long-segment Barrett's esophagus. The length of intestinal metaplasia was higher in patients with a defective lower esophageal sphincter. Short-segment Barrett's esophagus is a complication of severe gastroesophageal reflux disease and is associated with the reflux of both gastric and duodenal juice similar to that seen in patients with long-segment Barrett's esophagus.

Adult↗

PubMedDate not supplied

Variability in the composition of physiologic duodenogastric reflux.

Duodenogastric reflux has long been associated with various diseases of the foregut. Even though bile is often used as a marker, duodenogastric reflux consists of other components such as pancreatic juice and duodenal secretions. The aim of this study was to investigate the occurrence of duodenogastric reflux, its components, and the variability of its composition in normal subjects. Twenty healthy volunteers (7 men and 13 women) whose median age was 24 years underwent combined 24-hour bilirubin and gastric pH monitoring and intraluminal gastric aspiration. All probes were placed at 5 cm below the lower border of the lower esophageal sphincter. Aspiration was performed hourly and at any time when bilirubin and/or pH monitoring showed signs of duodenogastric reflux. Elastase and amylase were measured in the aspirate. All volunteers had episodes of physiologic duodenogastric reflux. A total of 70 episodes of duodenogastric reflux were registered with a median of three episodes (range 1 to 8) per subject. Most bile reflux occurred separately from pancreatic enzyme reflux. Pancreatic enzyme aspirate was significantly more often associated with a rise in pH in comparison to bile reflux (P <0.01). Duodenogastric reflux is a physiologic event with varying composition. Both bile and pancreatic enzyme reflux frequently occur separately. These findings could explain the disagreement regarding assessment and interpretation of duodenogastric reflux in the past. Thus monitoring of duodenogastric reflux requires more than the detection of just one component.

Adult↗

PubMedDate not supplied

Role of the lower esophageal sphincter and hiatal hernia in the pathogenesis of gastroesophageal reflux disease.

The relative importance of the lower esophageal sphincter (LES) and hiatal hernia in the pathogenesis of gastroesophageal reflux disease is controversial. To identify the role of hiatal hernia and LES in reflux disease, 375 consecutive patients with foregut symptoms and no previous foregut surgery were evaluated. All patients underwent upper endoscopy, stationary manometry, and 24-hour esophageal pH monitoring. Hiatal hernia was diagnosed endoscopically, when the distance between the crural impression and the gastroesophageal junction was >/=2 cm. The LES was considered structurally defective when the resting pressure was </=6 mm Hg, the overall length was less than 2 cm, and/or the abdominal length was less than 1 cm. Factors predicting abnormal esophageal acid exposure (composite score >14.7) were analyzed using multivariate analysis. The presence of a hiatal hernia and a defective LES were identified as independent predictors of abnormal esophageal acid exposure. LES pressure and abdominal length were reduced in patients with hiatal hernia by 4 mm Hg and 0.4 cm, irrespective of the presence of gastroesophageal reflux disease. It is concluded that both a structurally defective LES and hiatal hernia are important factors in the pathogenesis of reflux disease. It is hypothesized that in the presence of a structurally normal LES, the altered geometry of the cardia imposed by a hiatal hernia facilitates the ability of gastric wall tension to pull open the sphincter.

Adolescent↗

PubMedDate not supplied

Balancing act.

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Community-Institutional Relations↗

PubMedDate not supplied

The role of 24-hr gastric pH-monitoring in the interpretation of 24-hr gastric bile monitoring for duodenogastric reflux.

BACKGROUND/AIMS: Duodenogastric reflux is a physiologic phenomenon. For a number of years, alkalinization of the acidic intragastric pH environment, as assessed by 24-hour gastric pH-monitoring, was thought to be caused by duodenogastric reflux. The recent introduction of the fotooptic Bilitec system for intraluminal bilirubin measurement has created the possibility to directly quantify a component of duodenal juice. METHODOLOGY: In this study, 24-hour gastric pH-monitoring and 24-hour bilirubin monitoring were performed in healthy subjects. The upper limits for physiologic bile reflux are the percentage of total time of bile reflux of 28.2% and an average absorbance during a reflux episode of 0.62 (95th percentile with threshold 0.25). RESULTS: Comparing bile with pH-monitoring (absorbance > 0.25 and/or pH > 4), an increase of bilirubin was found most frequently with constant pH (43%) or an increase of pH with constant bilirubin (37%). CONCLUSIONS: The hypothesis was drawn that the composition of duodenogastric refluxate can vary. Bile and pancreatic juice may separately contribute to duodenogastric reflux.

Bile↗