Effective Acid Reflux Relief

Treatment of Acid Reflux Disease is primarily medical, the mainstays being lifestyle modifications and drug therapy. The goals of treatment are to relieve symptoms and prevent relapse and complications. All patients should be advised about lifestyle modifications that help reduce symptoms and prevent relapse. Antacids or antacid-alginate combinations are recommended for safe, prompt, inexpensive relief of heartburn. The same agents, however, are poorly suited for regular use because of poor palatability and durability and side effects such as diarrhea, constipation, and possible magnesium or aluminum toxicity in renal patients. Protection against recurrence of heartburn is provided by acid-suppressing medications such as H2-receptor antagonists and PPIs. H2-receptor antagonists reduce gastric acid secretion moderately by inhibiting one of three acid-stimulating receptors on the basolateral membrane of the parietal cell. When prescribed twice a day, they can control symptoms in about 50% of Acid Reflux Disease patients and heal erosions in about 30%. PPIs irreversibly inhibit the H+, K+-ATPase or proton pump, the final common pathway for acid secretion on the apical membrane of the parietal cell. Consequently, PPIs markedly reduce gastric acidity with once-a-day dosing and provide relief of symptoms and healing of lesions in about 80 to 90% of Acid Reflux Disease patients. H2-receptor antagonists (+30 years) and PPIs (≈15 years) have excellent safety profiles. PPI safety beyond 15 years remains unclear because of uncertainty about the long-term risk for chronic gastric hypoacidity and hypergastrinemia. Although vitamin B12 levels can be reduced with chronic PPI use, clinically significant vitamin B12 deficiency has not been reported, so an increase in vitamin B12 intake is not currently recommended.

Early endoscopy is indicated for those with alarm symptoms. Endoscopy is also indicated for patients who fail once-a-day PPI therapy to confirm the diagnosis and assess severity, including the presence of Barrett's esophagus (see later). Testing for H. pylori is not recommended because the organism is not etiologic in Acid Reflux Disease and, when eradicated, may make treatment more difficult.

Failures with once-a-day PPI therapy are treated with twice-daily PPI therapy with or without H2-receptor antagonists at bedtime for 6 to 8 weeks, and patients who fail this regimen undergo esophageal pH monitoring during therapy to assess for control of esophageal acidity. If the acidity is controlled, the symptoms are not mediated by acid.

Effective therapy is often accompanied by relapse when medication ceases, especially in patients with erosive esophagitis, in whom maintenance therapy is indicated. Patients requiring maintenance therapy should undergo at least one endoscopy procedure to determine whether Barrett's esophagus is present. If endoscopy reveals NERD, no further endoscopy is necessary and treatment is guided by symptoms. If endoscopy reveals erosive esophagitis, treatment to healing should be documented by endoscopy so that Barrett's esophagus can be effectively established or excluded. Once Barrett's esophagus is excluded, endoscopy is unnecessary and treatment is guided by symptoms because subsequent relapse and treatment will rarely result in Barrett's esophagus.

Acid Reflux Relief : Combination Therapy

Most patients treated with PPIs in conventional dosages do not exhibit complete suppression of stomach acid secretion. Approximately 70% of individuals who take a PPI twice a day experience nocturnal stomach acid breakthrough (defined as a stomach pH lesser than 4 for more than 1 hour at night). Brief episodes of acid reflux occur frequently during these breakthrough periods in patients with GERD. For some patients taking a PPI twice daily, nocturnal acid breakthrough can be abolished by adding a histamine H2-receptor blocker at bedtime. It is not clear that this approach is desirable, however. Complete elimination of acid reflux usually is not necessary to effect the healing of reflux esophagitis. Indeed, most patients who are treated with a PPI in conventional dosage exhibit complete healing of their symptoms and signs of GERD. No clear clinical benefit yet has been demonstrated for the practice of adding a histamine H2-receptor blocker at bedtime to PPI therapy.

A few older investigations have explored the value of combination drug therapy for the healing of GERD. The great efficacy of the PPIs used as single agents in this condition has discouraged investigators from undertaking new studies on combination therapy. Drug combinations that have been studied have included an H2 blocker plus either sucralfate or a prokinetic agent. Cimetidine (1200 mg/d) combined with sucralfate (5 g/d) was found to be superior to cimetidine alone for relieving daytime heartburn and for improving the endoscopic signs of esophagitis. For patients unresponsive to treatment with cimetidine alone, the addition of metoclopramide resulted in symptomatic improvement significantly more often than the addition of placebo, but side effects of metoclopramide were frequent. A combination of ranitidine (300 mg/d) plus metoclopramide (40 mg/d) was not found to be as effective as omeprazole alone (20 mg/d) in healing the signs and symptoms of esophagitis. Some studies explored combination therapy with the prokinetic agent cisapride, but these studies are of historical interest only because cisapride has been withdrawn from general use due to serious side effects (lethal arryhythmias). For patients with moderately severe reflux esophagitis, the use of combination therapy may eliminate the need for treatment with a PPI. However, the addition of a second medication increases the cost of therapy and the potential for side effects. Furthermore, the long-term benefit of combination therapy has not been demonstrated. For patients who are refractory to single-agent therapy (with an H2 blocker, sucralfate, or a prokinetic), a change to a PPI generally is more likely to effect healing than the addition of a second drug.

Medications for Acid Reflux Relief

Medical Treatment of Gastroesophageal Reflux Disease
GERD is such a common condition that most sufferers with mild symptoms carry out self-medication. Sufferers when first seen with symptoms of heartburn without obvious complications can reasonably be placed on 8 to 12 weeks of simple antacids before extensive investigations are carried out. In many situations, this successfully aborts the attacks. Sufferers should be advised to elevate the head of the bed; avoid tight clothing; eat small, frequent meals; avoid eating their nighttime meal shortly before retiring; lose weight; and avoid alcohol, coffee, chocolate, and peppermints, which may aggravate the symptoms. Alginic acid, used in combination with simple antacids, may augment symptomatic relief by creating a physical barrier to reflux as well as by acid reduction. Alginic acid reacts with sodium bicarbonate in the presence of saliva to form a highly viscous solution that floats like a raft on the surface of the gastric contents. When reflux occurs, this protective layer is refluxed into the esophagus and acts as a protective barrier against the noxious gastric contents. Medications to promote gastric emptying, such as metoclopramide, domperidone, or cisapride, are beneficial in early disease but of little value in more severe disease. The mainstay of medical therapy is acid suppression. Sufferers with persistent symptoms should be given hydrogen potassium PPIs, such as omeprazole. In doses as high as 40 mg per day, they can effect an 80% to 90% reduction in gastric acidity. This usually heals mild esophagitis, but healing may occur in only three fourths of sufferers with severe esophagitis. It is important to realize that in sufferers who reflux a combination of gastric and duodenal juice, inadequate acid suppression therapy may give symptomatic improvement while still allowing mixed reflux to occur. This can result in an environment that allows persistent mucosal damage in an asymptomatic sufferer. Unfortunately, within 6 months of discontinuation of any form of medical therapy for GERD, 80% of sufferers have a recurrence of symptoms. In sufferers with reflux disease, esophageal acid exposure is reduced by up to 80% with H2-receptor antagonists and up to 95% with PPIs. Despite the superiority of the latter class of drug over the former, emerging evidence suggests that periods of acid breakthrough still occur. This occurs most commonly at nighttime and is some justification for a split rather than a single dosing regimen. Sufferers with breakthrough reflux symptoms were studied while on omeprazole 20 mg b.i.d. and found that many of them were still refluxing. Intragastric pH monitoring in 28 healthy volunteers and 17 sufferers with reflux disease revealed that nocturnal recovery of acid secretion (more than1 hour) occurred in 75% of the individuals. Recovery of acid secretion occurred within 12 hours of the oral evening dose of PPI, the median recovery time being 7.5 hours. This is particularly pertinent because it is during the nighttime and early morning that asthma symptoms are most pronounced and that peak expiratory flow rate is at its lowest. There have been also shown that ranitidine 300 mg at bedtime is superior to omeprazole 20 mg at bedtime in preventing acid breakthrough. it was speculated to be due to the abolition of histamine-mediated acid secretion in the fasting state. Sufferers presenting for the first time with symptoms suggestive of GE reflux may be given initial therapy with H2 blockers. In view of the availability of these as over-the-counter medication, many sufferers will have already self-medicated their symptoms. Failure of H2 blockers to control the symptoms or immediate return of symptoms after stopping treatment suggests that either the diagnosis is incorrect or the sufferers had relatively severe disease. Endoscopic examination at this stage of the sufferer's evaluation provides the opportunity for assessing the severity of mucosal damage and the presence of Barrett's esophagus. Both of these findings on initial endoscopy predict a high risk for medical failure. A measurement of the degree and pattern of esophageal exposure to gastric and duodenal juice, with 24-hour pH and bilirubin monitoring, should be obtained at this point. The status of the LES and the function of the esophageal body should also be measured. These studies identify features that predict a poor response to medical therapy, frequent relapses, and the development of complications and include supine reflux, poor esophageal contractility, erosive esophagitis or a columnar-lined esophagus at initial presentation, bile in the refluxate, and a structurally defective sphincter. Sufferers who have these risk factors should be given the option of surgery as a primary therapy with the expectation of long-term control of symptoms and complications.