Acid suppression therapies are the mainstay of pharmaceutical GERD treatment. Acid suppression therapy neutralizes stomach acid or reduces its secretion, minimizing the potential for damage during reflux episodes. Acid suppression therapies include antacids, Histamine-2 receptor blockers, and proton pump inhibitors.
Antacids. Antacids that neutralize stomach acid are the first medication(s) commonly used to provide quick relief for the reflux symptoms of GERD, and are often effective for mild symptoms. Typical antacids include aluminum hydroxide or magnesium hydroxide, calcium carbonate (Tums®), and sodium or potassium bicarbonate.
Histamine-2 receptor blockers (H2 blockers). H2 blockers prevent secretion of stomach acid by inhibiting the action of histamine, which is a stimulus for acid secretion. Examples of H2 blockers include cimetidine (Tagamet®), ranitidine (Zantac®), and famotidine (Pepcid®). H2 receptor blockers are effective for healing only mild esophagitis in 70-80% of patients with GERD and for providing maintenance therapy to prevent relapse. Tachyphylaxis has been observed, suggesting that pharmacologic tolerance can reduce the long-term efficacy of these drugs. Therefore, patients are more likely to develop resistance to the drug, limiting its long-term efficacy (Kim 2004). Still, for mild GERD symptoms, H2 blockers can be an effective treatment.
Proton pump inhibitors. Proton pump inhibitors (PPIs) (e.g., omeprazole, lansoprasole, rabeprazole, pantoprazole, esomeprazole) inhibit stomach acid by preventing the secretion of protons (acid) from acid-producing cells of the stomach. Proton pump inhibitors have been found especially useful when GERD is not well controlled by H2 blockers (Vanderhoff 2002). They are the drug of choice for conventional GERD management (Bruley 2010).
Acid suppression therapies can interfere with the absorption of nutrients that require stomach acid for proper digestion such as non-supplemental iron (Al-Quaiz 2001), vitamin B12 (Ruscin 2002; Dali-Youcef 2009), and dietary calcium (O'Connell 2005).
Acid-suppression-related nutrient deficiencies carry their own health risks. Based upon a study survey, the incidence of iron deficiency anemia secondary to chronic PPI usage has increased up to five-fold (Sarzynski 2011). Elevated homocysteine (a risk factor for cardiovascular disease) has been associated with vitamin B12 deficiency induced by PPIs (Ruscin 2002). Chronic high-dose PPI or H2 blocker usage can more than double risk of potentially deadly hip fracture (Corley 2010; Yang 2006) by impairing calcium absorption and bone metabolism. Impaired calcium absorption can also disrupt calcium balance and contribute to cardiac conduction problems. Individuals on long-term PPI therapy should monitor their iron and B12 status using convenient blood tests to identify possible drug-induced nutrient deficiencies. Homocysteine levels should be assessed as well. Long-term use of acid suppression therapy (drugs) may also be a risk factor for food allergies (Pali-Scholl 2011). In one study, more than 27% of GERD patients tested positive for food allergies; avoiding allergenic foods resulted in significant improvement of GERD symptoms (Pomiecinski 2010).
One of the roles of stomach acid is to provide defense against ingested pathogens. Therefore, reductions in stomach acid due to PPI usage can lower resistance 2-4 fold to intestinal infections from Salmonella, Campylobacter, and Clostridium difficile (Deshpande 2012; Bavishi 2011). Probiotics may prove a useful adjunct to PPI therapy. Saccharomyces boulardii (i.e., probiotic yeast) was effective in reducing side effects associated with PPI usage in one study (Song 2010). However, more investigation is needed, as a large 2012 study failed to link PPI therapy to small intestinal bacterial overgrowth (Ratuapli 2012).
Another major problem with PPI drugs is that they are often taken for much longer periods than recommended, which could compound their potential for causing side effects. PPI’s are approved for use for 14 day intervals, no more than three times yearly, but many patients take these drugs semi-permanently (Sheen 2011; FDA 2011). Use of PPI’s for not more than 14 days at a time and not more than 3 times yearly may reduce the negative side effects of these drugs.
Baclofen. A considerable proportion of GERD patients experience non-acid reflux not alleviated by medications that neutralize stomach acid or inhibit its secretion (van Herwaarden 2002). Treatments that reduce transient lower esophageal sphincter relaxations may be an effective strategy in these individuals.
Baclofen (Lioresal), a medication used to treat muscle spasms by activating gamma-aminobutyric acidB (GABAB) receptors (Mayo Clinic 2017), has now been found to reduce relaxations and increase after-meal pressure in the LES, thereby preventing reflux episodes (Scarpellini 2016; Curcic 2014). A meta-analysis of randomized controlled trials concluded that baclofen effectively reduces the frequency of LES relaxations and the number and duration of reflux episodes (Li 2014). Baclofen is generally used in patients who have an unsatisfactory response to standard treatment. This medication can cause a number of side effects, which has limited its usage in clinical medicine. These side effects include weakness, dizziness, sleepiness, and confusion (Li 2014; Fass 2017).
Surgery. The goal of anti-reflux surgery is the reconstruction of the LES mechanism. This is commonly performed by laparoscopic fundoplication, a minimally invasive technique in which a portion of the stomach (fundus) is wrapped (fully or partially) around the base of the esophagus and sutured into place. The lower portion of the esophagus passes through a small tunnel of stomach muscle (Rosemurgy 2011), thus reinforcing the closure of the LES. Additionally, as the stomach contracts, it constricts the lower esophagus (pinching it shut) instead of forcing acid into the esophagus. There are several surgical techniques for different applications. For example, patients prone to dysphagsia (difficulty swallowing) may benefit more from a laparoscopic fundoplication that only partially wraps the esophagus (Tan 2011). In some cases, these surgeries can be performed as an outpatient procedure (Mariette 2011).