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Gastroesophageal Reflux Disease

Gastroesophageal Reflux Disease (GERD; or GORD when spelling œsophageal, the BrE form) is defined as chronic symptoms or mucosal damage produced by the abnormal reflux of gastric contents into the esophagus.

This is commonly due to transient or permanent changes in the barrier between the esophagus and the stomach. This can be due to incompetence of the lower esophageal sphincter (LES), transient LES relaxation, impaired expulsion of gastric reflux from the esophagus, or a hiatal hernia.

Current Research

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Symptoms

Adults

Heartburn is the major symptom of acid in the esophagus, characterized by burning discomfort behind the breastbone (sternum). Findings in GERD include esophagitis (reflux esophagitis) — inflammatory changes in the esophageal lining (mucosa) — strictures, difficulty swallowing (dysphagia), and chronic chest pain. Patients may have only one of those findings. Typical GERD symptoms include cough, hoarseness, voice changes, chronic ear ache, burning chest pains, nausea or sinusitis. GERD complicatons include stricture formation, Barrett's esophagus, esophageal ulcers, and possibly even lead to esophageal cancer, especially in adults over 60 years old.

Occasional heartburn is common but does not necessarily mean one has GERD. Patients with heartburn symptoms more than once a week are at risk of developing GERD. A hiatal hernia is usually asymptomatic, but the presence of a hiatal hernia is a risk factor for developing GERD.

Children

GERD may be difficult to detect in infants and children. Symptoms may vary from typical adult symptoms. GERD in children may cause repeated vomiting, effortless spitting up, coughing, and other respiratory problems. Inconsolable crying, failure to gain adequate weight, refusing food, bad breath, and belching or burping are also common. Children may have one symptom or many — no single symptom is universal in all children with GERD.

It is estimated that of the approximately 8 million babies born in the U.S. each year, up to 35% of them may have difficulties with reflux in the first few months of their life. Most of t hose children will outgrow their reflux by their first birthday. However, a small but significant number of them will not outgrow the condition.

Babies' immature digestive systems are usually the cause, and most infants stop having acid reflux by the time they reach their first birthday. Some children do not outgrow acid reflux, however, and continue to have it into their teen years. Children that have had heartburn that does not seem to go away, or any other GERD symptoms for a while, should talk to their parents and visit their doctor.

Diagnosis

A detailed history taking is vital to the diagnosis. Useful investigations may include barium swallow X-rays, esophageal manometry, 24 hour esophageal pH monitoring and Esophagogastroduodenoscopy (EGD). In general, an EGD is done when the patient does not respond well to treatment, or has alarm symptoms including: dysphagia, anemia, blood in the stool (detected chemically), wheezing, weight loss, or voice changes. Some physicians advocate once-in-a-lifetime endoscopy for patients with longstanding GERD, to evaluate the possible presence of Barrett's esophagus, a precursor lesion for esophageal adenocarcinoma.

Esophagogastroduodenoscopy (EGD) (a form of endoscopy) involves insertion of a thin scope through the mouth and throat into the esophagus and stomach (often while the patient is sedated) in order to assess the internal surfaces of the esophagus, stomach, and duodenum.

Biopsies can be performed during gastroscopy and these may show:

Edema and basal hyperplasia (non-specific inflammatory changes)
Lymphocytic inflammation (non-specific)
Neutrophilic inflammation (usually due to reflux or Helicobacter gastritis)
Eosinophilic inflammation (usually due to reflux)
Goblet cell intestinal metaplasia or Barretts esophagus.
Elongation of the papillae
Thinning of the squamous cell layer
Dysplasia or pre-cancer.
Carcinoma.

Pathophysiology

GERD is caused by a failure of the Anti-Reflux Barrier (ARB) and its primary component, the GastroEsophageal valve (GEV). The understanding of the GEV has continued to progress in recent years, and more focus is currently being placed on the GEV, rather than the Lower Esophageal Sphincter (LES), as the largest contributor to the ARB. Researchers have shown the GEV's robust nature and have shown that the intact GEV alone is highly competent to stop reflux. For example, in cadavers, where no muscle tone or LES pressure is present, the stomach ruptures when filled with water before reflux can occur. This shows the GEV's power to stop reflux even in the absence of any LES pressure.

In healthy patients, the "Angle of His," the angle at which the esophagus enters the stomach, is intact creating a valve that prevents duodenal bile, enzymes, and stomach acid from traveling back into the esophagus where it can cause burning and inflammation of sensitive esophageal tissue.

Another paradoxical cause of GERD-like symptoms is not enough stomach acid (hypochlorhydria). The valve that empties the stomach into the intestines is triggered by acidity. If there is not enough acid, this valve does not open and the stomach contents are churned up into the esophagus. However, there is still enough acidity to irritate the esophagus.

Factors that can contribute to GERD are:

Hiatus hernia, which increases the likelihood of GERD due to mechanical and motility factors
Zollinger-Ellison syndrome, which can be present with increased gastric acidity due to gastrin production
Hypercalcemia, which can increase gastrin production, leading to increased acidity
Scleroderma and systemic sclerosis, which can feature esophageal dysmotility
Gallstones which can impede the flow of bile into the Duodenum which can affect the ability to neutralize gastric acid

GERD has been linked to laryngitis, chronic cough, pulmonary fibrosis, earache, and asthma, even when not clinically apparent, as well as to laryngopharyngeal reflux and ulcers of the vocal cords.

Treatment

The rubric "lifestyle modifications" is the term physicians use when recommending non-drug GERD treatments. A 2006 review suggested that evidence for most dietary interventions is anecdotal; only weight loss and elevating the head of the bed were supported by evidence.

Foods

Certain foods and lifestyle are considered to promote gastroesophageal reflux:

Coffee, alcohol, and excessive amounts of Vitamin C supplements stimulate gastric acid secretion. Taking these before bedtime especially can cause evening reflux. Calcium containing antacids are in this group. (Although a study published in 2006 by Stanford University researchers disputes the effect of coffee, acidic, spicy foods etc. as a myth.)
Foods high in fats and smoking reduce lower esophageal sphincter competence, so avoiding these tends to help. Fat also delays stomach emptying.
Having more but smaller meals also reduces GERD risk, as it means there is less food in the stomach at any one time.
Eating shortly before bedtime (For clinical purposes, this usually means 2-3 hours before going to bed).
Large meals
Chocolate and peppermint
Spicy foods
Acidic foods like oranges and tomatoes (However, they are okay when fresh.)
Cruciferous vegetables: onions, cabbage, cauliflower, broccoli, spinach, brussel sprouts
Milk and milk-based products contain calcium and fat, so should be avoided before bedtime.

However, directly following this list of foods is not 100% accurate for some have a more serious GERD case than others. Thus, it is up to each individual to decide which foods bother them and which ones do not. But practical advice offered by many sources is to avoid food for at least two (2) hours before bedtime and, also, not lying down after meals.

Positional Therapy

Sleeping on one's left side has been shown to drastically reduce nighttime reflux episodes in patients.

Elevation to the head of the bed is the next easiest to do. When combining drug therapy, food avoidance before bedtime, and elevation of the head of the bed, over 95% of patients will have complete relief[citation needed]. Additional conservative measures may be considered if there is incomplete relief. Another approach is to apply all conservative measures for maximum response. A meta-analysis suggested that elevating the head of bed is an effective therapy, although this conclusion was only supported by nonrandomized studies.

Elevating the head of the bed can be done by using various items: plastic or wooden bed risers that support bed posts or legs, a bed wedge pillow, or a wedge or an inflatable mattress lifter that fits in between mattress and box spring. The height of the elevation is critical and must be at least 6 to 8 inches (15 to 20 cm) in order to be at least minimally effective to prevent the backflow of gastric fluids. It should be noted that some innerspring mattresses do not work well when inclined and tend to cause back pain, thus foam based mattresses are to be preferred. Moreover, some use higher degrees of incline than provided by the commonly suggested 6 to 8 inches (15 to 20 cm) and claim greater success.

Drug Treatment

A number of drugs are registered for GERD treatment, and they are among the most-often-prescribed forms of medication in most Western countries. They can be used in combination with other drugs, although some antacids can interfere with the function of other drugs:

Proton pump inhibitors are the most effective in reducing gastric acid secretion. These drugs stop acid secretion at the source of acid production, i.e., the proton pump.
Antacids before meals or symptomatically after symptoms begin can reduce gastric acidity (increase pH).
Alginic acid (Gaviscon) may coat the mucosa as well as increase pH and decrease reflux. A meta-analysis of randomized controlled trials suggests alginic acid may be the most effective of non-prescription treatments with a number needed to treat of 4.
Gastric H2 receptor blockers such as ranitidine or famotidine can reduce gastric secretion of acid. These drugs are technically antihistamines. They relieve complaints in about 50% of all GERD patients. Compared to placebo (which also is associated with symptom improvement), they have a number needed to treat of eight (8).
Prokinetics strengthen the LES and speed up gastric emptying. Cisapride, a member of this class, was withdrawn from the market for causing Long QT syndrome.
Sucralfate (Carafate®) is also useful as an adjunct in helping to heal and prevent esophageal damage caused by GERD, however it must be taken several times daily and at least two (2) hours apart from meals and medications.

Posture and GERD

In adults, a slouched posture is an important factor contributing to GERD. With a slouched posture there is no straight path between the stomach and esophagus; muscles around the esophagus go into a spasm. Gas and acidity get blocked in the spasm, causing coughing and other asthma-like symptoms. A meta-analysis suggested that elevating the head of bed is an effective therapy, although this conclusion was only supported by nonrandomized studies.

Surgical Treatment

The standard surgical treatment, sometimes preferred over longtime use of medication, is the Nissen fundoplication. The upper part of the stomach is wrapped around the LES to strengthen the sphincter and prevent acid reflux and to repair a hiatal hernia. The procedure is often done laparoscopically.

An obsolete treatment is vagotomy ("highly selective vagotomy"), the surgical removal of vagus nerve branches that innervate the stomach lining. This treatment has been largely replaced by medication.

Endoluminal Fundoplication

In June 2006 EndoGastric Solutions introduced EsophyX ELF in the Europe Union as an alternative to surgical and pharmaceutical approaches for GERD treatment. EsophyX ELF is intended to deliver similar benefits as the time-proven laparoscopic fundoplication procedures, by reducing hiatal hernia, recreating the Angle of His, and creating a GastroEsophageal Valve (GEV). The key differences are that EsophyX ELF is an endoscopic non-invasive procedure that is performed transorally (through the mouth), does not require incisions, and does not dissect any part of the natural anatomy.

Previous endoluminal treatments focused predominantly on the LES. However, failure to effectively treat reflux long-term with endoluminal therapies that focused only on the Lower Esophageal Sphincter (LES) combined with the fact that surgical approaches like Nissen fundoplication recreate the GEV and have excellent long-term efficacy, has led to an awareness that the GEV is probably the most powerful component of the Anti-Reflux Barrier. The device has been designed to deploy multiple tissue fasteners to create a robust and durable valve and is intended to restore the geometry of the GastroEsophageal Junction and recreate the natural, unidirectional valve mechanism necessary to prevent GERD. EsophyX ELF has not been cleared by the US FDA and is not yet available in the U.S.

Other Treatments

In 2000 , the U.S. Food and Drug Administration (FDA) approved two endoscopic devices to treat chronic heartburn. One system, Endocinch, puts stitches in the LES to create little pleats that help strengthen the muscle. Another, the Stretta Procedure, uses electrodes to apply radio frequency energy to the LES. The long term outcomes of both procedures compared to a Nissen fundoplication are still being determined.

Subsequently the NDO Surgical Plicator was FDA cleared for the endoscopic GERD treatment. The Plicator creates a plication, or fold, of tissue near the gastroesophageal junction, and fixates the plication with a suture-based implant. The Plicator is currently marketed by NDO Surgical, Inc.

Another treatment that involved injection of a solution during endoscopy into the lower esophageal wall was available for about one year ending in late 2005. It was marketed under the name Enteryx. It was removed from the market due to several reports of complications from misplaced injections.

Barrett's Esophagus

Barrett's esophagus, a type of dysplasia, is a precursor high-grade dysplasia, which is in turn a precursor condition for carcinoma. The risk of progression from Barrett's to dysplasia is uncertain but is estimated to include 0.1% to 0.5% of cases, and has probably been exaggerated in the past. Due to the risk of chronic heartburn progressing to Barrett's, EGD every 5 years is recommended for patients with chronic heartburn, or who take drugs for chronic GERD.

(adapted from Wikipedia, the free encyclopedia http://en.wikipedia.org/wiki/Gerd)

Findings From Current Research

The Association Between Gastroesophageal Reflux Disease and Asthma: A Systematic Review

Authors: Havemann B, Henderson CA, El-Serag HB.

Baylor College of Medicine/Houston VAMC, United States.

BACKGROUND AND AIMS: Gastroesophageal reflux disease (GERD) has been linked to a number of extra-esophageal symptoms and disorders, primarily in the respiratory tract. This systematic review aimed to provide an estimate of the strength and direction of the association between GERD and asthma. METHODS: Studies that assessed the prevalence or incidence of GERD in individuals with asthma, or of asthma in individuals with GERD, were identified in Medline and EMBASE via a systematic search strategy. RESULTS: Twenty-eight studies met our selection criteria. The sample-size weighted average prevalence of GERD symptoms in asthma patients was 59.2%, while in controls it was 38.1%. In patients with asthma, the average prevalence of abnormal esophageal pH, esophagitis and hiatal hernia was 50.9%, 37.3% and 51.2%, respectively. The average prevalence of asthma in individuals with GERD was 4.6%, while in controls it was 3.9%. Pooling the odds ratios gave an overall ratio of 5.5 (95% CI: 1.9-15.8) for studies reporting the prevalence of GERD symptoms in individuals with asthma and 2.3 (95% CI: 1.8-2.8), for those studies measuring the prevalence of asthma in GERD. One longitudinal study showed a significant association between a diagnosis of asthma and subsequent diagnosis of GERD (RR: 1.5; 95% CI: 1.2-1.8), while the two studies that assessed whether GERD precedes asthma gave inconsistent results. The severity-response relationship was examined in only nine studies, with inconsistent findings. CONCLUSIONS: This systematic review indicates that there is a significant association between GERD and asthma, but a paucity of data on the direction of causality.

Journal: Gut. 2007 Aug 6
Adapted from PubMed; click here to access full journal article.

A Feasibility Trial of Narrow Band Imaging Endoscopy in Patients with Gastroesophageal Reflux Disease

Authors: Sharma P, Wani S, Bansal A, Hall S, Puli S, Mathur S, Rastogi A.

Division of Gastroenterology and Hepatology, University of Kansas School of Medicine, Kansas City, Missouri 64128-2295, USA. psharma@kumc.edu

BACKGROUND AND AIMS: Narrow band imaging (NBI) endoscopy system enhances visualization of microvasculature and mucosal patterns. This study assessed the utility of NBI in patients with gastroesophageal reflux disease (GERD) symptoms. METHODS: Patients with and without GERD symptoms completed 2 validated GERD questionnaires prior to enrollment. The distal esophagus was examined by standard white light endoscopy followed by NBI. The features seen only by NBI were compared between GERD patients and controls. RESULTS: Overall, 80 patients (50 GERD, 30 controls) were eligible for final analysis (mean age, 58.4 years; males, 93.7%; white, 82.5%). A significantly higher proportion of patients with GERD had increased number (OR, 12.6; 95% CI: 3.7-42; P < .0001), dilatation (OR, 20; 95% CI: 6.1-65.3; P < .0001), tortuosity of intrapapillary capillary loops (IPCLs) (OR, 6.9; 95% CI: 2.5-19; P < .0001), presence of microerosions (P < .0001), and increased vascularity at the squamocolumnar junction (OR, 9.3; 95% CI: 1.9-43.6; P = .001) compared with controls. On multivariate analysis, increased number (OR, 5.5; 95% CI: 1.4-21.6) and dilatation (OR, 11.3; 95% CI: 3.2-39.9) of IPCLs were the best predictors for diagnosing GERD. The maximum, minimum, and average number of IPCLs/field were significantly greater in the GERD group compared with controls (P < .0001). Although the interobserver agreement for the various NBI findings was very good, the intraobserver agreement was modest. CONCLUSIONS: NBI endoscopy may represent a significant improvement over standard endoscopy for the diagnosis of GERD. These preliminary findings including inter- and intraobserver agreement need to be evaluated in future prospective, controlled, and blinded GERD trials.

Journal: Gastroenterology. 2007 Aug;133(2):454-64; quiz 674. Epub 2007 Jun 8
Adapted from PubMed; click here to access full journal article.

Gastric Fluid Bile Concentrations and Risk of Barrett's Esophagus

Authors: Nason KS, Farrow DC, Haigh G, Lee SP, Bronner MP, Rosen SN, Vaughan TL.

Department of Surgery, University of Washington, Seattle, WA, USA. ks.nason@hosp.wisc.edu

Patients with Barrett's esophagus are at high risk of progression to adenocarcinoma. A growing, but conflicting body of evidence implicates bile reflux as a contributor to Barrett's esophagus. To investigate whether duodenogastric reflux was associated with an increased risk of Barrett's esophagus, a case-control study of incident Barrett's esophagus was performed. Cases (n=72) were identified by new histologically-confirmed diagnosis of specialized intestinal metaplasia (indicative of Barrett's esophagus) following upper endoscopy for refractory gastroesophageal reflux between October 1997 and September 2000. Cases were compared to gastroesophageal reflux patients without specialized intestinal metaplasia (controls; n=72). There was no difference in total bile acid concentrations between cases and controls. Risk of Barrett's esophagus did not significantly vary with increasing concentrations of total or free bile acids, respectively (OR 0.35 (95% CI 0.12, 1.02) and 0.60 (95% CI 0.22, 1.66)). Low gastric fluid pH (toxic range 3-5), was associated with a non-significant increase in the risk of Barrett's esophagus. In conclusion, no significant association between Barrett's esophagus and total or free bile acids in gastric refluxate was found. Patients with low gastric fluid pH (3-5) may represent a subset of patients at high risk of developing Barrett's esophagus.

Journal: Interact Cardiovasc Thorac Surg. 2007 Jun;6(3):304-7. Epub 2007 Feb 8.
Adapted from PubMed; click here to access full journal article.

Endotherapy and Surgery for GERD

Authors: Triadafilopoulos G.

Division of Gastroenterology and Hepatology, Stanford University School of Medicine, Stanford, CA 94305-5187, USA. vagt@stanford.edu

Today, there are several modalities to treat gastroesophageal reflux disease (GERD) (medications, endoscopic therapies, surgery) and such therapies can be used either singly, or in tandem, or in combination with the others, aiming at "normalization" of the patient's GERD-related quality of life and, if possible, esophageal acid exposure. Several intermediate end points or clinically significant outcomes have not been reached by some therapeutic modalities and no single modality is or can be perfect. Statistically significant improvements in these intermediate end points have been shown in "some" but not all studies. Although healing of esophagitis can be accomplished with either medical or surgical therapy, there is inadequate data with endotherapies, because most patients treated with endotherapies have had prior trials of proton pump inhibitors (PPIs) and hence healed their esophagitis. Effective prevention of complications, such as esophageal adenocarcinoma, remains challenging for all modalities. Patients who have not normalized their GERD-related quality of life with once or twice daily PPI therapy should undergo functional esophageal evaluation with pH testing and esophageal motility study and they should be evaluated by both an endoscopist and a surgeon. The decision on how to proceed should be made on the basis of the criteria for endotherapy and surgery, availability of local endoscopic and surgical expertise and patients' preference. Such multimodality therapy model is in many ways similar to the long-term management of coronary artery disease where pharmacotherapy, angioplasty, and bypass surgery are frequently used in tandem or in combination. Multimodality therapy aiming at normalization of GERD-related quality of life is an option today, and should be available to all patients in need of therapy. The target population for GERD endotherapy currently consists of PPI-dependent GERD patients, who have a small (<2-cm-long) or no sliding hiatal hernia, and without severe esophagitis or Barrett esophagus. Thus far, only Stretta and the NDO plicator have been studied in sham-controlled trials. Registries of complications suggest that these techniques are relatively safe, but serious morbidity, including rare mortality have been reported (for a continuous update on complications related to endoscopic therapies see: http://www.fda.gov/cdrh/maude.html). All can be performed on an outpatient basis, under intravenous sedation and local pharyngeal anesthesia. Future comparative studies with predetermined clinically significant end points, validated outcome measures, prolonged follow-up, and complete complication registries will eventually determine the precise role of endoscopic procedures for the patients with GERD.

Journal: J Clin Gastroenterol. 2007 Jul;41(6 Suppl 2):S87-96.
Adapted from PubMed; click here to access full journal article.

Gastroesophageal Reflux Disease: Beyond Mucosal Injury

Authors: Shaker R.

Division of Gastroenterology and Hepatology, Department of Medicine, MCW Digestive Disease Center, Medical College of Wisconsin, Milwaukee, WI 53223, USA. rshaker@mcw.edu

Emerging information on physiology and pathophysiology of gastroesophageal reflux disease raises the question of whether our thought process should go beyond mucosal injury and consider 2 parallel tracks that may cross each other at some time, but at other times they may indeed remain parallel, that is, neurally mediated effects of reflux events beyond the esophageal wall and inflammation mediated effect of reflux within the esophageal wall. In this process, intraesophageal events with and without causing mucosal injury may induce changes in the neural function on a temporary or long-term basis resulting in symptoms at different organs and various levels not completely in lock-step with esophageal mucosal injury. Emerging data also suggest the influence of liminal and subliminal esophageal acid exposure on cerebral cortical networks involved in motor function such as swallowing in addition to its effect on sensory centers. These observations suggest the existence of a more extensive influence of esophageal sensory input to the cerebral cortical processing mechanisms than previously thought and may provide new avenues for research in pathophysiology of reflux disease.

Journal: J Clin Gastroenterol. 2007 Jul;41(6 Suppl 2):S160-2.
Adapted from PubMed; click here to access full journal article.

Gastrooesophageal Reflux Disease

Authors: Richter JE.

Department of Medicine, Temple University School of Medicine, 3401 North Broad Street, 801 Parkinson Pavilion, Philadelphia, PA 19140, USA.

Gastrooesophageal reflux disease, GERD, is a common problem which is expensive to diagnose and treat. The disease is increasing in prevalence in the Western world with important risk factors being obesity and the eradication of Helicobacter pylori. Increasing research points to transient LES relaxation and spatial separation of the diaphragm and LES (hiatal hernia in chest) being the critical mechanisms of acid reflux. Heartburn and acid regurgitation are classic symptoms of GERD, but their sensitivity is poor. Ambulatory oesophageal pH testing is the most sensitive test for GERD, while endoscopy is the most specific test. Medical treatment with PPIs has revolutionized the treatment of GERD and its complications, but long-term side effects do exist. Laparoscopic antireflux surgery and PPIs have similar efficacy in the few available long-term trials. Currently, endoscopic treatments for GERD should not be a clinical alternative outside of research trials. New drug therapies should be directed at modulating transient LES relaxation.

Journal: Best Pract Res Clin Gastroenterol. 2007;21(4):609-31.
Adapted from PubMed; click here to access full journal article.

Significant Enhancement of Esophageal Pre-Epithelial Defense by Tegaserod: Implications for an Esophagoprotective Effect

Authors: Majewski M, Jaworski T, Sarosiek I, Sostarich S, Roeser K, Edlavitch SA, Kralstein J, Wallner G, McCallum RW, Sarosiek J.

Kansas University Medical Center, Department of Internal Medicine, Division of Gastroenterology & Hepatology, The Center for GI Nerve & Muscle Function, Gastroenterology Research Laboratory, Kansas City, Kansas 66160, USA.

BACKGROUND & AIMS: Tegaserod, a serotonin 5-hydroxytryptamine (5-HT)4 receptor agonist, is thought to stimulate intestinal secretions. The aim of the current study was to assess the effect of tegaserod vs placebo on salivary and esophageal protective factors in patients with gastroesophageal reflux disease (GERD). METHODS: This study was a randomized, double-blind, placebo-controlled, cross-over trial in 38 GERD patients treated with tegaserod 6 mg twice a day vs placebo. Salivary samples were collected basally and during mastication. In addition, in 32 GERD patients, salivary and esophageal secretions also were collected during infusion of NaCl, HCl/pepsin, and NaCl in a consecutive fashion using a specially designed esophageal catheter. Saliva and esophageal perfusates were assessed for the pH, volume, content of buffers, protein, mucin, epidermal growth factor (EGF), transforming growth factor alpha (TGFalpha), and prostaglandin E (PGE)2 and analyzed statistically. RESULTS: Salivary flow rates during administration of tegaserod increased over corresponding values during both basal conditions (P < .01) and mastication (P < .001). The rate of secretion of salivary bicarbonate and nonbicarbonate buffers also increased in basal conditions (P < .001 and P < .01, respectively) and during mastication (P < .05 and P = .05). Salivary EGF increased during mastication (P < .05), whereas PGE2 and TGF alpha increased in basal conditions (P < .05 and P < .01). Esophageal perfusate volumes increased during administration of tegaserod in basal conditions (P < .05), whereas esophageal EGF secretion increased after mucosal exposure to HCl/pepsin and subsequent final perfusion with NaCl (P < .05). CONCLUSIONS: Significant stimulatory impact of 5-HT4 agonist on several salivary protective factors as well as esophageal EGF secretion may have esophagoprotective implications in patients with GERD and may help to address new therapies in the future.

Journal: Clin Gastroenterol Hepatol. 2007 Apr;5(4):430-8.
Adapted from PubMed; click here to access full journal article.

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