Gastroesophageal reflux in cirrhotic patients with esophageal varices without endoscopic treatment

Abstract

-Background -Portal hypertension in patients with liver cirrhosis causes manifestations such as esophageal varices, ascites and edema. Some studies have been conducted about the role of esophageal varices in the development of esophageal motor disorders and abnormal gastroesophageal reflux in these patients. Ascites could be a factor promoting gastroesophageal reflux and it has been questioned whether reflux would favor the rupture of varices. However there are a few studies using ambulatory esophageal pH recording in the evaluation of these patients. Aims -Evaluate gastroesophageal reflux by pH recording in cirrhotic patients with esophageal varices and possible predictors. Methods -Fifty one patients (28 men, 23 women, mean age of 54 years) with liver cirrhosis, diagnosed by clinical, laboratorial, image and histological findings were prospectively evaluated. All patients had esophageal varices confirmed by endoscopy and were submitted to a questionnaire about typical gastroesophageal reflux disease symptoms (heartburn and or acid regurgitation). pH recording was performed with the probe placed 5 cm above the superior lower esophageal sphincter limit, as determined by manometry. Abnormal reflux (% total time with pH <4 >4.5%) was related to the size of varices, congestive gastropathy, ascites, severity of cirrhosis and typical gastroesophageal reflux disease symptoms. Results -The caliber of the varices was considered to be small in 30 patients (59%), medium in 17 (33%) and large in 4 (8%), 21 (41%) congestive gastropathy. Ascites was observed in 17 (33%), 32 patients (63%) were classified as Child-Pugh A, 17 (33%) Child-Pugh B and 2 (4%) Child-Pugh C. Twenty seven patients (53%) presented with typical gastroesophageal reflux disease symptoms. Abnormal reflux at pH recording was found in 19 patients (37%). One of them presented with erosive esophagitis at endoscopy. There was no relation between ascites, variceal size, congestive gastropathy and Child-Pugh score and abnormal reflux. There was a correlation between typical gastroesophageal reflux disease symptoms and abnormal reflux. Conclusions -Abnormal gastroesophageal reflux was found in 37% of the patients with hepatic cirrhosis and esophageal varices. Only typical gastroesophageal reflux disease symptoms predicted these findings.

Risk factors associated with oral manifestations and oral health impact of gastro-oesophageal reflux disease: a multicentre, cross-sectional study in Pakistan

“…This result is consistent with our finding that GI conditions and their oral manifestations have a considerable adverse impact on oral health 16. Notably, in this study, 43.3% of the study population had GORD alone, and the rest had additional upper GI conditions, including gastritis, portal gastropathy, PUD, GORD-related oesophagitis and hiatal hernia, which are believed to be factors that initiate and/or lead to progression of GORD 16 50–52. However, a significant proportion of patients were habitual towards unhealthy dietary pattern (45%), experienced frequent nausea/vomiting (83%) and also self-medicated themselves with NSAIDs for pain relief (46%), which are risk factors that further aggravate upper-GI illness (particularly GORD) 22 27 50…”

High prevalence of reflux esophagitis among upper endoscopies in Chinese patients with chronic liver diseases

“…In the last few decades, as variceal bleeding continued to be a severe complication, new risk factors for rupture have been evaluated [19,20]. GERD was again studied and the prevalence among cirrhotic patients with EV has been studied [9,10]. Therefore, in cirrhotic patients, increased contact time between dyspepsia and EV could lead to the eventual erosion of the mucosa and EV bleeding.…”

“…Some studies have been conducted regarding the role of esophageal varices in the development of esophageal motor disorders and abnormal gastroesophageal reflux in these patients [7,8]. Ascites could be a factor promoting gastroesophageal reflux and it has been questioned whether or not reflux would favor the rupture of varices [9,10]. However, there are few studies on the prevalence of RE and factors related to RE in patients with chronic liver disease.…”

Asymmetrical circumferential distribution of esophagogastric junctional lesions: anatomical and physiological considerations

“…However, the triggering factor for variceal rupture has not been clarified, although an abrupt increase in intraabdominal pressure with increased blood flow into the varices has been hypothesized. Another hypothesis states that refluxes of gastric acidic contents erode the esophageal squamous epithelium and digest the walls of superficially located varices, thus triggering their rupture [25]. Although this hypothesis is attractive, the lack of drugs potent enough to inhibit gastric acid secretion prevent its proof.…”