Abstract
Over the past few decades, there was an encouraging breakthrough in bridging the gap between advancements in the evolution of diagnosis and treatment towards a better outcome in achalasia. The purpose of this review is to provide updated knowledge on how the current evidence has bridged the gap between advancements in the evolution of diagnosis and treatment of esophageal achalasia. The advent of high-resolution manometry and standardization based on the Chicago classification has increased early recognition of the disease. These 3 clinical subtypes of achalasia can predict the outcomes of patients, and the introduction of POEM has revolutionized the choice of treatment. Previous evidence has shown that laparoscopic Heller myotomy (LHM) and anterior fundoplication were considered the most durable treatments for achalasia. Based on the current evidence, POEM has been evolving as a promising strategy and is effective against all 3 types of achalasia, but the efficacy of POEM is based on short- and medium-term outcome studies from a limited number of centers. Types I and II achalasia respond well to POEM, LHM, and PD, while most studies have shown that type III achalasia responds better to POEM than to LHM and PD. In general, among the 3 subtypes of achalasia, type II achalasia has the most favorable outcomes after medical or surgical therapies. The long-term efficacy of POEM is still unknown. The novel ENDOFLIP measures the changes in intraoperative esophagogastric junction dispensability, which enables a quantitative assessment of luminal patency and sphincter distension; however, this technology is in its infancy with little data to date supporting its intraoperative use. In the future, identifying immunomodulatory drugs and the advent of stem cell therapeutic treatments, including theoretically transplanting neuronal stem cells, may achieve a functional cure. In summary, it is important to identify the clinical subtype of achalasia to initiate target therapy for these patients.
Highlights
Achalasia happens due to the absence of peristalsis and is a lower esophageal sphincter (LES) disorder that affects both sexes and all ethnicities [1, 2]
In patients with susceptible genetic backgrounds (HLA DQA1∗0103, HLA DQB1∗0603 alleles), virus-induced autoimmune-mediated ganglionitis has been proposed to trigger a cascade of events leading to the selective loss of inhibitory neurons of the myenteric plexus, in return inducing an imbalanced production of acetylcholine (Ach)/nitric oxide (NO) and unopposed excitation of the lower esophageal sphincter (LES) [3, 4]
We provide updated knowledge to bridge the gap between advancements in the evolution of diagnosis and treatment of esophageal achalasia to optimize treatment outcomes
Summary
Achalasia happens due to the absence of peristalsis and is a lower esophageal sphincter (LES) disorder that affects both sexes and all ethnicities [1, 2]. It is one of the rare primary motility dysfunctions of the esophagus that has no curative treatment. Common presentations of achalasia include gradual dysphagia to both liquid and solid foods, chest fullness, and heartburn. Food regurgitation due to dysphagia can cause pulmonary complications such as chronic cough, choking at night, and aspiration pneumonia. Chronic food regurgitation will lead to gradual weight loss
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