Medicinal Treatment and Drawbacks

Treatment for acid reflux (GERD) is essential to heal oesophagitis (inflammation of the esophagus), prevent recurrent of oesophagitis and other complications. The treatment includes lifestyle modification, medicinal treatments and surgical treatment. Medicinal treatments of GERD include:

1) Antacids

Antacids neutralise the acidity of gastric acid. These medications are usually taken after meal and at bedtime to control mild symptoms of GERD. Antacids with alginic acid contains a foaming agent that floats over the stomach contents. This may help to prevent gastric juice from entering the oesophagus; while antacids that contain simethicone may clear gas bubbles in the stomach to reduce burping which may otherwise push gastric acid into the oesophagus. In general, antacids are only a temporary solution to a long-term problem. Neutralising gastric acid by antacids does not heal the inflammation caused by GERD. Over time, the inflamed oesophagus will erode the oesophageal lining or develop into cancer.

Drawback of antacids:
Long-term use of antacids is associated with health problems such as poor digestion and poor absorption of nutrients such as vitamin C, iron, calcium, magnesium and zinc as well as increased risk of gastrointestinal infections. Antacids have also been associated with differing side effects which are dependent on the key ingredients of the antacid.

Antacid Neutralising power Undesirable side effects
Sodium bicarbonate Low Fluid retention, alkalosis (excessive blood alkalinity)
Magnesium hydroxide High Diarrhea, magnesium toxicity
Aluminium hydroxide Modest Constipation, drug or phosphate binding which inhibits absorption
Calcium carbonate Very high Acid rebound

2) H2 blockers

Histamine 2 blockers (H2 blockers) are the first-line medications for mild to moderate symptoms of GERD and mild oesophagitis. Effective only for mild oesophagitis, it provides a maintenance therapy to prevent relapse. Histamine is a compound that is involved in acid production in the stomach. H2 blockers prevent the histamine from binding to H2 receptors, thereby reducing acid production by the stomach. Commonly used H2 blockers are famotidine (Pepcid), cimetidine (Tagamet), nizatidine (Axid) and ranitidine (Zantac).

Drawback of H2 blockers:

Tachyphylaxis, a fast declining response to successive doses of H2 blockers has been observed, suggesting that pharmacologic tolerance can reduce the long-term effectiveness of these medications. In addition, H2 blockers are associated with an increased risk for pneumonia.

3) Proton pump inhibitors (PPIs)

Proton pump inhibitors (PPIs) are commonly prescribed to soothe and prevent GERD symptoms, treat oesophagitis (inflammation of the esophagus), hinder recurring of oesophagitis after recovery and avoid complications of GERD. Patient with Barrett’s oesophagus are treated with PPIs.

PPIs blocks an enzyme known as hydrogen/potassium adenosine triphosphatase (proton pump) in the parietal cells (cells lining the stomach), which are required for gastric acid production.  By blocking the action of the cells that produce acid, there will be little acid is left in the gastric juice. In case of a backflow into the oesophagus, the irritation will be reduced and this allows the oesophagus to heal. Examples of PPIs include esomeprazole (Nexium), lansoprazole (Prevacid), omeprazole (Prilosec), pantoprazole (Protonix) and rabeprazole (Aciphex).

Drawback of PPIs:

i) Less effective in treating GERD

Less than 5 out of 10 people had their GERD symptoms treated even after taking PPIs. In other words, more than 50% of the people taking PPIs still have some GERD symptoms.

ii) Impaired digestion and nutrient absorption

When PPIs reduce gastric acid in the stomach, food cannot be digested properly. Undigested or partially digested food that moves into the small intestine would not be properly absorbed into the body and the full benefit of the nutrients from the food would be compromised as well.

iii) Infection

Gastric acid is an essential defence against harmful bacteria in the stomach. PPI users whose gastric acid production is reduced by the drugs are vulnerable to infections such as Clostridium difficile.

In addition, PPIs also turn off the body’s proton pump (that makes hydrogen required for producing gastric acid) when the drug is administered. Upon completion of treatment and PPI withdrawn, most people could not initiate the making of hydrogen for up to 3 weeks. During this period when the level of gastric acid is low, users are exposed to an increased risk of being re-infected by H. pylori.

iv) Rebound acid hypersecretion and drug dependency

Withdrawal from PPI treatment is linked to a clinically significant increase in acid production to above pre-treatment levels, this is known as rebound acid hypersecretion. Rebound acid hypersecretion is speculated to be an excessive production of gastrin (a gastric acid-stimulating hormone) which is not apparent during PPI treatment but appears after the drug is stopped. This results in a return of symptoms for many patients after discontinuation of PPI treatment. Some people may have difficulty withdrawing from PPI treatment, and hence develop a long-term dependency on the medication. PPIs is unable to recognise and treat the underlying root cause of gastric symptoms.

v) Increased risk of dementia

A recent study has revealed a link between PPIs and an increased risk of dementia in older patients. 40% of subjects aged 75 years and older who did not have dementia at the start of the studies were diagnosed with dementia, with 59% of them diagnosed with at least two different types of dementia (Gomm W et al., 2016).

This data is also in line with animal testing in which the use of PPIs has increased the levels of amyloid β (the hallmark brain protein for dementia) in the brains of mice. Avoidance of PPIs drug may hinder the development of dementia.

vi) Increased risk of kidney disease

The use of PPIs has been associated to an increased risk of chronic kidney disease (CKD), CKD progression, and end-stage renal disease (ESRD). Analysis also revealed that the longer the duration of PPIs use, the greater the risk of renal outcomes (Xie Y et al., 2016). Another study also reported that those who took a PPI are associated with significant 35% increase in CKD risk, compared to those who have never taken PPIs.

vii) Increased risk of heart attack

Prolonged use of PPIs has been linked to a slight elevated risk of heart attack (Shah NH et al., 2015). Researchers found that PPI users were 16 – 21% more likely to experience a heart attack, compared to those with chronic acid reflux but were not taking the drugs. Another study suggests that PPIs can disrupt normal blood vessel function, which could elevate the risk of heart attacks.

viii) Increased risk of bone fracture

Long-term PPI treatment has been associated with an increased occurrence of bone fracture (Ito T & Jensen RT, 2010). Further investigations are required on the possible effects of chronic acid suppression by PPIs on absorption of key  vitamins and nutrients.

ix) Increased risk of pneumonia

PPIs have been associated with an increased risk of pneumonia (Herzig SJ et al. 2009).

Video on the action of PPIs on acid reflux