A 37-year-old woman presents with complaints of severe heaburn with or without meals. She has a history of hypeension, which has been treated with captopril. She also has a history of Raynaud disease, multiple facial telangiectasias, and very taut skin on the dorsum of both hands. She has failed to obtain relief for her heaburn with large doses of antacids, or omeprazole. Esophageal manometry is ordered. Most likely results of this test is
This patient has the classic presentation of gastroesophageal reflux disease (GERD) in association with scleroderma. These patients have the deposition of collagen in the body of the esophagus, as well as the lower esophageal sphincter (LES). This results in the typical pattern of decreased esophageal peristalsis and the reduced ability of the LES to maintain its high pressures between swallowing. These patients are therefore at risk for severe GERD and subsequent complications of peptic stricture and Barrett&;s esophagus. Although there is no corrective therapy to improve esophageal motility or increase LES pressure, aggressive treatment is generally aimed at reducing acid production with the use of high doses of proton pump inhibitors. Neveheless, many of these patients develop the long-term consequences of GERD. Achalasia, in which impaired esophageal peristalsis is often accompanied by a lack of lower esophageal sphincter relaxation.
Decreased esophageal peristalsis and decreased LES pressure
Decreased esophageal peristalsis and increased LES pressure
Increased esophageal peristalsis and decreased LES pressure
Increased esophageal peristalsis and increased LES pressure
G.I.T