Treatment of gastroesophageal reflux disease

Treatment of gastroesophageal reflux disease
A. Diet

• dietary restrictions: avoiding bulky meals, avoiding food that decreases LES pressure:coffee, chocolate, carbonated drinks, mint products, fatty foods, alcohol or foods that increase the acid secretion: orange juice, carbonated drinks, white vine, and acid food);
• avoiding smoking. It is said that smoking increases the acid secretion and lowers the LES pressure;
• avoiding lying recumbent immediately after eating;
• weight loss in the obese patients (reducing the abdominal pressure);
• avoiding medications that decrease the LES pressure: nifedipin (calcium channel blockers), nitrates, aminophylline, caffeine and anticholinergics. These are also studies suggesting that NSAIDS and aspirin are associated with esophageal lesions, being able to induce esophagitis and even esophageal strictures.

B. Medication – involves 2 types of drugs:

1. Antisecretory drugs. This treatment decreases the acid secretion:
Proton pump blockers are the most potent antisecretory drugs:

• Esomeprazole (Nexium) 40 mg/day.
• Omeprazole (Losec, Ultop, Antra) 20 mg bid;
• Pantoprazole (Controloc) 40 mg/day;
• Lanzoprazole (Lanzap) 30 mg/day;
• Rabeprazole 20 mg/day;

The duration of treatment is 4-8 weeks, or a few months in resistant cases.
H2 blocking agents:
Ranitidine 150 mg bid;
Famotidine 40 mg/day;
Nizatidine (Axid) 150 mg bid.
H2 blocking agents; they may be used 2-6 weeks or even more in resistant cases.

2. Prokinetic

• Metoclopramide, 10 mg tid, 30 bid minutes before meals. Its effect  is the increasing of LES tone; it also increases the esophageal clearance and hastens the gastric emptying.
• Domperidone (Motilium) is effective on the LES and gastrokietic; the effect on the reflux is lower than that of Metoclopramide.

3. Antiacids - medication with direct neutralizing effect: Maalox, Novalox, Rennie, Dicarbocalm, containing magnesium and aluminium salts; the patients se them when the symptoms appear, with a spectacular disappearance of symptoms. They effect is only symptomatic, the esophagitis lesions persisting. An interesting drug of this group is the sodium alginate (Gaviscon, Nicon), which forms a protective layer over the esogastric mucosa.
4. Mucosal protectives. Sucralfate is an aluminium polisulfatate sucrose, which links the billiary acids and pepsin and stimulates the gastric secretion of prostaglandins and epidermic growth factor, thus favoring the epithelium healing. It is sometimes indicated in esophagitis.
The strategy of treatment is to begin, generally, in case of acid reflux, with PPI, in case of failure, a prokinetic is added. If the patients complain of billiary reflux, the therapy will be prokinetic.
C. Endoscopic

• Esophageal structures. The most preffered treatment in peptic strictures is done endoscopically, by Savary probe dilators or pressure balloons.
• Superior digestive hemorrhage. The severe cases require endoscopic hemostasis by Adrenaline injections, Argon Beamer photocoagulation or hemoclips application.
• Barrett’s esophagus. The columnar epithelium patches with different degrees of dysplasia may be destroyed by Argon plasma photocoagulation.
• Endoscopic fondoplicature – represents a new noninvasive method, in which the gastric fundus is wrapped around the esophagus thus creating a very sharp His angle.

D. Surgical
  In rare cases with severe esophagitis without response to drug therapy, surgery may be needed.