Globally, GORD affects ~8818 per 100 000 population. In South Africa, an estimated 5661 per 100 000 population are affected. In 2017, GORD was responsible for more than six million years lived with disability, an increase of ~67% since 1990.¹

Definition of GORD

GORD is defined as a condition that develops when the reflux of stomach contents causes uncomfortable or troublesome symptoms, complications, or both. Apart from typical symptoms (eg heartburn and regurgitation), others include angina-mimicking chest pain and extra-oesophageal signs such as chronic cough and chronic laryngitis.¹

As mentioned, GORD increases the risk of oesophageal adenocarcinoma. Other complications include oesophageal inflammation, stricture, ulceration, perforation, and metaplasia (eg Barrett's oesophagus).¹

How is GORD diagnosed and treated?

There is no gold standard for the diagnosis of GORD. Generally, patients are classified into one of two categories:^2,3

1. Non-erosive reflux disease (NERD)
2. Erosive oesophagitis (EE).

The diagnosis of GORD is based on a combination of symptom presentation, endoscopic evaluation of oesophageal mucosa, reflux monitoring, and response to therapeutic intervention eg patients with NERD are less responsive to anti-reflux therapy.^2,3

Lifestyle changes to reduce reflux of stomach contents, such as weight loss and eating smaller meals, are commonly recommended. Often, however, effective control of symptoms requires the use of acid-suppressing medications, such as proton-pump inhibitors (PPIs).¹

The new ACG guideline recommends:²

• An eight-week trial of empiric PPIs once daily before a meal in patients with classic symptoms (heartburn and regurgitation), but no alarm symptoms
• Discontinuation of PPIs in patients whose classic symptoms respond to an eight-week empiric trial of PPIs
• Diagnostic endoscopy (ideally after PPIs are stopped for two to four weeks) in patients whose classic symptoms do not respond adequately to an eight-week empiric trial of PPIs, or whose symptoms return when PPIs are discontinued
• Objective testing for GORD (endoscopy and/or reflux monitoring) in patients who have chest pain without heartburn and who have had adequate evaluation to exclude heart disease
• Do not use a barium swallow solely as a diagnostic test for GORD
• Endoscopy as the first test for patients presenting with dysphagia or other alarm symptoms (weight loss and gastrointestinal bleeding), and for patients with multiple risk factors for Barrett’s oesophagus
• Reflux monitoring performed off therapy for patients with suspected GORD, but endoscopy shows no objective evidence of GORD
• Do not perform reflux monitoring off therapy solely as a diagnostic test for GORD in patients known to have endoscopic evidence of Los Angeles (LA) grade C or D reflux oesophagitis or in patients with long-segment Barrett’s oesophagus.

The ACG guideline recommends the following for symptom control:²

• Weight loss in overweight and obese patients
• Avoid meals within two- to three-hours of bedtime
• Avoid the use of tobacco products/smoking
• Avoid ‘trigger foods’
• Elevate the head of the bed for night-time symptoms.
• Treat with PPIs rather than H2 receptor antagonists (H2RAs) for healing EE
• PPI administration 30- to 60-minutes before a meal rather than at bedtime
• Try to discontinue PPIs in patients who do not have EE or Barrett’s oesophagus, and whose symptoms have resolved with PPI therapy
• PPIs should be administered in the lowest dose that effectively controls symptoms and maintains healing of reflux oesophagitis in patients who require maintenance therapy with PPIs
• Do not routinely add medical therapies in PPI non-responders
• Continue maintenance PPI therapy indefinitely or refer patients with LA grade C or D oesophagitis for anti-reflux surgery
• Do not use baclofen in the absence of objective evidence of GORD
• Do not treat patients with a prokinetic agent of any kind unless there is objective evidence of gastroparesis
• Do not use sucralfate for therapy except during pregnancy
• Recommend on-demand/or intermittent PPI therapy for heartburn symptom control in patients with NERD.

Extra-oesophageal GORD symptoms

• Evaluate for non-GORD causes in patients with possible extra-oesophageal manifestations before attributing symptoms to GORD
• Patients who have extra-oesophageal manifestations of GORD without typical symptoms should undergo reflux testing for evaluation before PPI therapy
• Considering a trial of twice-daily PPI therapy for eight to 12 week before additional testing in patients who have both extra-oesophageal and typical symptoms
• In patients treated for extra-oesophageal reflux disease, surgical or endoscopic anti-reflux procedures are only recommended if there is objective evidence of reflux.

Refractory GORD

• Optimisation of PPI therapy is the first step in the management of refractory GORD
• Perform oesophageal pH monitoring (Bravo [wireless pH testing], catheter-based, or combined impedance-pH monitoring) off PPIs if the diagnosis of GORD has not been established by a previous pH monitoring study or an endoscopy showing long-segment Barrett’s oesophagus or severe reflux oesophagitis
• Perform oesophageal impedance-pH monitoring on PPIs for patients with an established diagnosis whose symptoms have not responded adequately to twice-daily PPI therapy
• Consider anti-reflux surgery or transoral incisionless fundoplication (TIF) for patients who have regurgitation as their primary PPI-refractory symptom and who have had abnormal gastroesophageal reflux documented by objective testing.

Dexlansoprazole – a new generation PPI

Dexlansoprazole modified release (MR) is a new-generation PPI. Dexlansoprazole is indicated for the treatment of adults and adolescents (12- to 17-years), for the treatment of EE, maintenance of healed EE, and relief of heartburn for up to six months in adults, and up to four months in adolescents. Dexlansoprazole is also indicated for the short-term treatment of heartburn and acid regurgitation associated with symptomatic NERD.

The capsules contain dexlansoprazole in a mixture of two types of enteric-coated granules with different pH-dependent dissolution profiles. One type of granule is designed to release dexlansoprazole after the granules reach the proximal small intestine. The second type of granule is designed to release dexlansoprazole in the distal region of the small intestine, generally several hours later.⁶

Dexlansoprazole MR ensures the longest maintenance of drug concentration in the plasma of all known PPIs, and the longest proton pump inhibitory effect.⁴

The efficacy of dexlansoprazole have been shown in numerous studies. These  were some of the findings:^{7,8,9,10,11,12,13,14,15}

• Dexlansoprazole produced significantly greater gastric acid suppression compared to lansoprazole (mean 24-hour intragastric pH, 4.55 vs 4.13), and significantly higher 24-hour mean pH⁷
• Evaluation of the impact of food on dexlansoprazole found a lack of effect of food on the pharmacodynamic parameters and a lack of effect of timing of food intake relative to dosing⁷
• No clinically meaningful differences have been found when taking dexlansoprazole at different times of the day relative to food (fasted or fed conditions), indicating that it can be taken without regard to food or timing of meals⁹
• A comparison of single-dose dexlansoprazole 60mg with esomeprazole 40mg found that at 0–24 hours post-dose, the mean percentage of time with pH >4 was 58% and 48%, respectively, and the average mean pH values were 4.3 and 3.7, respectively¹⁰
• At >12–24 hours post-dose, dexlansoprazole resulted in greater mean percentage of time with pH >4 and average mean pH compared to esomeprazole (60% vs 42% and 4.5 vs 3.5, respectively)¹⁰
• Dexlansoprazole was significantly better than placebo in providing relief of nocturnal heartburn and GORD-related sleep disturbances (47.5% vs 19.6% and 69.7% vs 47.9%, respectively)¹¹
• Dexlansoprazole provided significantly more heartburn-free nights (80.8% and 76.9% for dexlansoprazole 30mg and 60mg, respectively, vs 51.7% for placebo) and reduced symptom severity. The median percentage of 24-hour heartburn-free days was 54.9% and 50%, respectively, vs 18.5% for placebo¹²
• Dexlansoprazole controlled heartburn (91%-96% for 24-hour heartburn-free days and 96%-99% for heartburn-free nights) and was superior to placebo for maintaining healed EE over six months at doses of 30mg and 60mg (life-table analysis: 74.9% and 82.5%, respectively, versus 27.2% for placebo¹³
• Dexlansoprazole was more effective in improving both heartburn and regurgitation in patients with NERD compared with placebo and in patients with EE compared with lansoprazole. These improvements were maintained for the duration of treatment (four weeks)¹⁴
• Dexlansoprazole 60mg and 90mg were superior to placebo for maintaining healed EE (86.6% and 82.1%, respectively, vs 25.7% for placebo. Both doses were superior to placebo for 24-hour heartburn-free days (95.8% and 94.4%, respectively, vs 19.2% and nocturnal heartburn (98.3% and 97.1%, respectively, vs 50%.¹⁵

REFERENCES AVAILABLE ON REQUEST.