XXXX : a review.

@entity1318 @entity1 @entity662 @entity353 @entity384 @entity1208 @entity1282 @entity954 @entity356
Idiopathic @entity1318 is a primary @entity1208 characterized by loss of esophageal peristalsis and insufficient lower esophageal sphincter relaxation in response to deglutition. @entity1 with @entity1318 commonly complain of @entity1282 to solids and liquids, bland regurgitation often unresponsive to an adequate trial of proton pump inhibitor, and @entity662 . @entity353 is present in many, but not all @entity1 . Although the precise etiology is unknown, it is often thought to be either autoimmune, viral immune, or neurodegenerative. The diagnosis is based on history of the disease, barium esophagogram, and esophageal motility testing. Endoscopic assessment of the gastroesophageal junction and @entity356 is necessary to rule out malignancy. Newer diagnostic modalities such as high resolution manometry help in predicting treatment response in @entity1318 based on esophageal pressure topography patterns identifying three phenotypes of @entity1318 (I-III) and outcome studies suggest better treatment response with types I and II compared to type III. Although @entity1318 cannot be permanently cured, excellent outcomes are achieved in over 90 % of @entity1 . Current medical and surgical therapeutic options ( @entity384 , @entity954 , and pharmacologic agents) aim at reducing the LES pressure and facilitating esophageal emptying by gravity and hydrostatic pressure of retained food and liquids. Either graded pneumatic dilatation or laparoscopic surgical myotomy with a partial fundoplication are recommended as initial therapy guided by @entity1 age, gender, preference, and local institutional expertise. The prognosis in @entity1318 @entity1 is excellent. Most @entity1 who are appropriately treated have a normal life expectancy but the disease does recur and the @entity1 may need intermittent treatment.
