Disease relevance of Esophageal Achalasia

• We report here that loss of the Sprouty2 gene (also known as Spry2) in mice resulted in enteric nerve hyperplasia, which led to esophageal achalasia and intestinal pseudo-obstruction [1].
• The patients of group 1, who had megaesophagus without associated cardiomyopathy (n = 36), had a much higher rate of pulmonary tuberculosis (36.1 percent) than those with associated CCM (6.0 percent), and they also had the most severe forms of the pulmonary disease [2].
• A nasoesophageal tube was used to remove retained barium sulfate and saliva in a cat with megaesophagus and esophageal obstruction caused by gastroesophageal intussusception [3].
• One year later, there has been progressive weight gain, the megaesophagus and gastroesophageal reflux have lessened significantly, pneumonia has not recurred, and the tracheobronchitis and esophagitis have resolved [4].

High impact information on Esophageal Achalasia

• Clinical and manometric effects of nifedipine in patients with esophageal achalasia [5].
• IFN-gamma and MIG production was significantly higher in patients with megaesophagus compared to control [6].
• TP53 gene deletion was more frequent in mid-third (62.5%) than in distal-third megaesophagus cases (40%) [7].
• In chagasic megaesophagus, no amplification of the cyclin D1 gene (CCND1) was observed [7].
• DESIGN: An acute experimental protocol performed in control dogs and dogs with naturally acquired congenital idiopathic megaesophagus under pentobarbitone anesthesia [8].

Chemical compound and disease context of Esophageal Achalasia

• The megaesophagus, pharyngeal/laryngeal dysfunction, and anemia resolved with calcium EDTA treatment [9].
• Medical treatment of esophageal achalasia. Double-blind crossover study with oral nifedipine, verapamil, and placebo [10].
• Enhanced platelet release reaction and increased thromboxane generation in esophageal achalasia and selective in vitro inhibition of arachidonic acid induced platelet aggregation by vasoactive intestinal peptide [11].
• Comparison of the effects of sublingual isosorbide dinitrate and cardiomyotomy on esophageal emptying in patients with chagasic megaesophagus [12].
• Furthermore, the patients with megaesophagus needed a higher dose of pentagastrin to achieve the maximal contraction [13].

Anatomical context of Esophageal Achalasia

• This suggests that the gastroesophageal reflux and megaesophagus were due to an inadequate reservoir with a secondary gastric overflow as the esophagus dilated to enlarge the reservoir capacity of the upper gastrointestinal tract [4].
• In 12 patients with moderate chagasic megaesophagus the lower esophageal sphincter pressure was studied under basal conditions and after i. v. infusion of pentagastrin by open tips infused rapid pull through manometry [13].

Gene context of Esophageal Achalasia

• Effect of secretin on lower esophageal sphincter pressure in patients with esophageal achalasia [14].

References