1 comments Wednesday, December 16, 2009

Gastroesophageal reflux disease (GERD) is defined as the pathological retrograde movement of gastric contents into the esophagus. Various esophageal motility disturbances which may be important in reflux are observed in patients with GERD. The main esophageal motility disorder in these patients is ineffective esophageal motility (IEM). Increased acid clearance time and IEM have been shown to be strongly associated with isolated proximal reflux. However, there are no data that conclusively link motility disorders with isolated distal reflux (IDR).

A research team, led by Dr. Yasemin Ozin from Turkey Yuksek Ihtisas Training and Research Hospital investigated manometric measurements in patients with IDR and compare the findings in individuals with and without erosive esophagitis.

Their study was published in the World Journal of Gastroenterology. In their study, patients with symptoms of GERD were evaluated with esophageal manometry, 24-h ambulatory pH monitoring, and upper gastrointestinal endoscopy. Among patients with isolated distal reflux, the manometric findings of patients who had erosive disease and non-erosive disease were compared. There were no significant differences between the isolated distal reflux group and control group with respect to age, body mass index, and esophageal body contraction amplitude. Mean lower esophageal sphincter pressure was significantly higher in the control group. There were no differences between the erosive reflux disease and non-erosive reflux disease subgroups with respect to mean esophageal body contraction amplitude (EBCA), lower esophageal sphincter pressure, or DeMeester score. However, IEM was observed only in patients with erosive reflux disease.

The authors provided more insight into the pathophysiology of reflux disease. The finding of very low EBCA being observed only in patients with erosive disease might be helpful in identifying these patients.

Reference: Ozin Y, Dagli U, Kuran S, Sahin B. Manometric findings in patients with isolated distal gastroesophageal reflux. World J Gastroenterol 2009; 15(43): 5461-5464 http://www.wjgnet.com/1007-9327/15/5461.asp

Source: Ye-Ru Wang
World Journal of Gastroenterology

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Gastroesophageal reflux (GER) is a common problem in mechanically ventilated patients and contributes to the development of esophageal mucosal injury and even erosive esophagitis. The relationship between percutaneous endoscopic gastrostomy (PEG) and subsequent development of GER is complex and not well understood.

A research article published in the World Journal of Gastroenterology addresses this question. The research team from Greece explored the factors that interfere with failure of PEG to reduce GER in critically ill, mechanically ventilated patients.

A cohort of 29 consecutive mechanically ventilated patients undergoing PEG was prospectively evaluated. The patients were divided into 2 groups based on whether GER decreased to less than 4% (responders, RESP group) or remained unchanged or worsened (non-responders, N-RESP group) after PEG placement. Reflux esophagitis and the gastroesophageal flap valve (GEFV) grading differed significantly between the two groups.

The researchers drew a conclusion that gastroesophageal reflux is not a contraindication for PEG tube placement. By identifying the factors that predict failure of PEG to decrease GER, their study may represent a reference in deciding which patients are likely to benefit from PEG tube placement and thus protect them from the development of esophagitis and even ventilator-associated pneumonia.

Reference: Douzinas EE, Andrianakis I, Livaditi O, Bakos D, Flevari K, Goutas N, Vlachodimitropoulos D, Tasoulis MK, Betrosian AP. Reasons of PEG failure to eliminate gastroesophageal reflux in mechanically ventilated patients. World J Gastroenterol 2009; 15(43): 5455-5460 http://www.wjgnet.com/1007-9327/15/5455.asp

Source: Ye-Ru Wang
World Journal of Gastroenterology

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Stomach acid may only be part of the problem when it comes to esophagus injury related to gastroesophageal reflux disease (GERD). A new study suggests that an immune system response may be the real culprit behind reflux esophagitis.

Researchers say it's been assumed that reflux esophagitis develops when cells in the lining of the esophagus become burned and damaged by stomach acid backing up into the esophagus.

But in a rat model of GERD, researchers found that this acid reflux didn't directly damage the lining of the esophagus. Instead, the acid triggered the release of chemicals called cytokines that attract inflammatory immune cells to the area, which were responsible for the real damage.

If further studies in humans confirm these results, researchers say new GERD treatments that target this immune response may be needed to effectively manage the disease.

"Currently, we treat GERD by giving medications to prevent the stomach from making acid," says Rhonda Souza, MD, associate professor of internal medicine at the University of Texas Southwestern Medical Center, in a news release. She says "maybe we should create medications that would prevent these cytokines from attracting inflammatory cells to the esophagus and starting the injury in the first place."

In the study, published in Gastroenterology, researchers created GERD in rats by performing an operation to connect the duodenum (first section of the small intestine) to the esophagus, allowing stomach acid and bile to enter the esophagus.

The results showed damage to the lining of the esophagus did not occur immediately after exposure to the stomach acids. It happened weeks later.

"That doesn't make sense if GERD is really the result of an acid burn," says researcher Stuart Spechler, MD, professor of internal medicine at UT Southwestern, in the news release. "Chemical injuries develop immediately. If you spill battery acid on your hand, you don't have to wait a month to see the damage."

Within three days after the operation, researchers found no damage to the cells on the surface layer of the esophagus, but they found inflammatory cells in the deeper layers. Those inflammatory cells rose to the surface three weeks later after the initial stomach acid exposure.

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