Therapeutic Areas

Erosive Esophagitis

When food enters the stomach during digestion, it is broken down by acid, enzymes and mechanical pressure. Pathology can occur when gastric acid flows back into the esophagus. Under healthy conditions, this type of back flow, known as reflux, is prevented by contraction of a muscular sphincter, which forms a physical barrier between the stomach and the esophagus. However, this normal functioning can be disrupted by several factors, including the excessive production of acid in the stomach, the distension of the stomach and a weakened gastroesophageal sphincter. Each of these can lead to reflux.

Gastroesophageal reflux disease (GERD) is a chronic disease that occurs when continued reflux causes symptoms such as heartburn and, in some patients, erosions of the tissue lining the esophagus (i.e., erosive esophagitis (EE)). When left untreated, GERD can lead to serious complications, including Barrett’s esophagus, a precancerous disease that has the potential to progress to esophageal cancer.

EE is a severe form of GERD caused by the inflammation, irritation and swelling of the lining of the esophagus, resulting in sores or erosions of the esophageal lining and, in some cases, GI bleeding. EE is classified by erosions in the gastric mucosa caused by acidic reflux of stomach contents into the esophagus.

EE is commonly graded by the Los Angeles classification system, or LA Scale, which characterizes the extent of erosions (mucosal breaks) in the esophagus and is graded on a scale of increasing severity from A to D, with D being the most severe. Approximately 25 percent of EE patients have severe LA grade C or D disease. Patients that have healed will have their mucosal breaks eliminated and will no longer meet the LA scoring criteria. The number and length of mucosal breaks determine the classification on the LA Scale.

Gastroparesis is a chronic, severe and debilitating disorder that may be associated with dysfunction in the enteric nervous system, causing the movement of food from the stomach to the small intestine to slow or stop, and preventing or disrupting normal digestion.

Gastroparesis is characterized by symptoms of nausea, vomiting, abdominal pain, early satiety and post-prandial fullness and is associated with a delay in stomach emptying. For most patients, the prevailing chronic symptom they experience is persistent nausea that intensifies after eating.

- Nausea may become so intense as to trigger vomiting after even a few sips of water. Some patients do not vomit but instead experience nausea all day, every day.

- Abdominal pain may be diffuse or associated with intestinal cramping or spasms in the upper portion of the stomach.

- In some patients, a poorly emptying stomach additionally predisposes patients to regurgitation of solid food, as well as GERD.

Patients with gastroparesis often limit their intake of food and liquids, leading to poor nutrition and dehydration, which in turn can ultimately require hospitalization. Even in patients who do not require hospitalization, the chronic symptoms generated by the stomach dysmotility greatly impair quality of life and disable about one in ten patients with the condition. The majority of patients with severe disease experience symptoms on a daily basis.

In gastroparesis, there are no physical blocks preventing the stomach from emptying, but rather a number of other factors that together prevent its normal function.

- About 29 percent of cases of gastroparesis are associated with diabetes. Diabetes can lead to damage to the nerves that control the muscles of the stomach and small intestine such that they do not work normally to move food through the digestive tract.

- Other patients develop gastroparesis due to Parkinson’s disease, complications from surgery or following a viral infection.

- In approximately 36 percent of cases of gastroparesis, classified as “idiopathic gastroparesis,” the underlying cause of disease is not known.