Aside from heartburn, there are several other symptoms associated with GERD that reduce quality of life. These include nausea, hypersalivation (increased saliva production), globus (the sensation of a constant lump in the throat), trouble swallowing, bad breath, and dental erosion (Stanghellini 2004). Sleep disturbances and nocturnal choking are also possible (Kamal 2010). Because of the close proximity of the larynx (the opening of the windpipe) and esophagus, GERD can manifest respiratory symptoms (e.g., including chronic hoarseness, cough, and laryngitis) as well. GERD can be associated with inflammation of lung tissue (pneumonitis), sinusitis, asthma, and middle ear inflection (otitis media) (Amarasiri 2010; Bresci 2010). Recent evidence suggests that GERD may also be associated with idiopathic pulmonary fibrosis (IPF), an incurable lung disease resulting from the deposit of fibrous tissue on the lung surface. The incidence of GERD is high in IPF patients, which places them at risk for aspiration (reflux) of material into the lungs and the subsequent damage as a result (Lee 2010; Fahim 2011).
Prolonged exposure of the esophagus to gastric reflux can result in dramatic alterations to its function. Serious complications of GERD include:
Peptic Stricture. In people with long-term GERD, healing of ulcerations can lead to the deposit of fibrous scar tissue as well as a stricture (i.e., narrowing) of the esophagus (Rosemurgy 2011). Segments of the esophagus with stricture are usually thickened, stiff, and may be shortened. As the esophagus shortens, it can pull the stomach up through the esophageal hiatus, resulting in hiatal hernia (Horvath 2000). The prevalence of peptic stricture among patients with GERD is about 10 to 25% (Hoang 2005). Treatment of severe peptic stricture involves the mechanical dilation of the narrowed region by a stent or balloon combined with acid suppression therapy (Kamal 2010).
Barrett’s Esophagus. Barrett’s esophagus is a change in the cellular makeup of the mucous membrane of the esophagus. A normal esophagus is lined with a layer of flattened cells (squamous epithelial cells). In Barrett’s esophagus, these cells are replaced by a layer of thicker, taller cells (columnar epithelial cells) similar to those found on the inner surface of the stomach or intestines (Chen 2011). This reversible replacement of one differentiated cell type with another mature differentiated cell type is called metaplasia, and is distinct from the cellular transformation that occurs during cancer progression. The main cause of Barrett’s esophagus is thought to be an adaptation to chronic acid exposure from reflux esophagitis (Gerson 2002; Toruner 2004). Barrett’s esophagus can increase the risk of esophageal cancer. Although endoscopic examination of the esophagus can identify potential tissue changes that are indicative of Barrett’s esophagus, a confirmed diagnosis requires a biopsy of the esophageal mucous membrane (Lekakos 2011).
Esophageal Cancer. The two major types of esophageal cancer are esophageal squamous cell carcinoma and esophageal adenocarcinoma. Esophageal adenocarcinoma EAC arises from metaplasia of tissue in the lower part of the esophagus, and is thought to develop as a result of long-term GERD and Barrett’s esophagus (Siersema 2007). Two large studies of Barrett’s esophagus patients estimate the risk of progression to esophageal adenocarcinoma at approximately 0.27% to 0.4% per person per year (de Jonge 2010; Wani 2011). The risk is highest in men and increases with age, aspirin/NSAID use, smoking, and incidence of hiatal hernia or esophageal dysplasia (de Jonge 2010).