Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0014848 (achalasia)
 2,804 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Esophageal disease has been reported in 70% to 90% of patients with scleroderma, of whom nearly 50% will have reflux esophagitis. The combined motility disorder of low LES pressure and aperistalsis of the esophageal body makes scleroderma patients especially susceptible to severe gastroesophageal reflux disease (GERD). Symptomatic GERD is a common problem in pregnancy, affecting 30% to 50% of women. Hormonal effects of estrogen and progesterone likely promote GERD by compromising LES function. Fortunately, the problem is usually relieved with delivery of the baby. Although difficult to quantitate, the reflux of both acid and especially alkaline material may be a common sequela of many types of gastric surgery. Medical therapy binding bile salts usually does not bring relief. The Rouxen-Y biliary diversion operation is the best solution for this problem. GERD complicates the treatment of achalasia after 10% of Heller myotomies and 2% of pneumatic dilatations. Nearly 50% of patients with the Zollinger-Ellison syndrome have esophagitis, which may be more difficult to treat than their ulcer disease.
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PMID:Medical and surgical conditions predisposing to gastroesophageal reflux disease. 222 65

The gastric emptying study using Tc-99m triethylene tetramine polystyrene resin with or without metoclopramide hydrochloride was used in six patients with different disease entities: achalasia, gastric lymphoma, primary amyloidosis, Zollinger-Ellison syndrome, duodenal diverticulum, and short bowel syndrome. All patients had abnormally prolonged gastric emptying times. The patient with gastric lymphoma and the patient with Zollinger-Ellison syndrome had virtually no effect from metoclopramide. The patient with a duodenal diverticulum and the patient with short bowel syndrome had partial and good response to metoclopramide, respectively. Endoscopic and/or autopsy examinations in patients with achalasia, Zollinger-Ellison syndrome, primary amyloidosis, and duodenal diverticulum proved the patency of the pyloric canal. The patient with gastric lymphoma had a mass associated with marked pyloric narrowing and lymphoma cell infiltration of the gastric wall, to explain the abnormal gastric emptying. The gastric emptying study with or without metoclopramide may be used noninvasively to measure gastric function, to determine the nature of gastric outlet obstruction, and to evaluate therapy with metoclopramide.
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PMID:Technetium-99m triethylene tetramine polystyrene resin gastric emptying studies in patients with various upper gastrointestinal diseases. 392 23

A review of 44 patients with 50 esophageal perforations from 1966 through 1980 is presented. The age span was 15 months to 94 years and the male to female ratio was 1 to 1. Each case was studied with regard to presentation, etiology, treatment and complications. Twenty-two cases of esophageal perforation followed instrumentation, including 6 secondary to Mosher bag dilatation for achalasia. Of the remainder, seven patients had spontaneous perforation, five had external trauma, five had intraoperative injury, two had caustic ingestion, and one each had foreign body ingestion, Zollinger-Ellison syndrome and an incarcerated paraesophageal hiatal hernia. Management was nonoperative in 12 patients, primary repair and drainage was performed in 23 patients, and 9 patients underwent drainage and diversion. This series plus 824 patients with esophageal perforation accumulated from a review of the literature emphasizes the importance of the influence of different methods of treatment and time lapse between occurrence and therapy. The type of perforation had no significance on this series. As a result of the experience gained from this series, a treatment protocol is proposed for the management of esophageal perforation.
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PMID:Esophageal perforations: a 15 year experience. 707 15

Refractory gastroesophageal reflux disease (GERD) is very common and may affect up to 40% of patients who use a proton pump inhibitor (PPI) once daily. Refractory GERD can present as incomplete or lack of response to PPI therapy. The disorder is clearly driven by patients, who present with a wide range of symptom severity and frequency while on PPI treatment. Poor compliance and improper timing of PPI consumption should always be excluded before further evaluation of this patient population. The putative mechanisms for refractory GERD include weakly acidic reflux, duodenogastroesophageal/bile reflux, visceral hypersensitivity, delayed gastric emptying, psychological comorbidity, and concomitant functional bowel disorders. Reduced PPI bioavailability, rapid PPI metabolism, PPI resistance, nocturnal reflux, and Helicobacter pylori infection status have very limited roles in refractory GERD. The contribution of eosinophilic esophagitis to refractory GERD is still unknown. Pill-induced esophagitis, Zollinger-Ellison syndrome, achalasia, and other disorders are rarely responsible for PPI failure and usually are not confused with GERD.
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PMID:Refractory GERD: what is it? 1862 35

Suspected reflux symptoms that are refractory to proton pump inhibitors (PPIs) are rapidly becoming the most common presentation of gastroesophageal reflux disease (GERD) in patients seen in gastroenterology clinics. These patients are a heterogeneous group, differing in symptom frequency and severity, PPI dosing regimens, and responses to therapy (from partial to absent). Before testing, the physician needs to question the patient carefully about PPI compliance and the timing of drug intake in relation to meals. Switching PPIs or doubling the dose is the next step, but only 20% to 25% of the group refractory to PPIs will respond. The first diagnostic test should be upper gastrointestinal endoscopy. In more than 90% of cases, the results will be normal, but persistent esophagitis may suggest pill esophagitis, eosinophilic esophagitis, or rarer diseases, such as lichen planus, Zollinger-Ellison syndrome, or genotype variants of PPI metabolism. If the endoscopy results are normal, esophageal manometry and especially reflux testing should follow. Whether patients should be tested on or off PPI therapy is controversial. Most physicians prefer to test patients off PPIs to identify whether abnormal acid reflux is even present; if it is not, PPIs can be stopped and other diagnoses sought. Testing patients on PPI therapy allows nonacid reflux to be identified, but more than 50% of patients have a normal test result, leaving the clinician with a conundrum-whether to stop PPIs or continue them because the GERD is being treated adequately. Alternative diagnoses in patients with refractory GERD and normal reflux testing include achalasia, eosinophilic esophagitis, gastroparesis, rumination, and aerophagia. However, more than 50% will be given the diagnosis of functional heartburn, a visceral hypersensitivity syndrome. Treating patients with PPI-refractory GERD-like symptoms can be difficult and frustrating. Any of the following may help: a histamine-2 receptor antagonist at night, baclofen to decrease transient lower esophageal sphincter relaxations, pain modulators, acupuncture, or hypnotherapy. At this time, antireflux surgery should be limited to patients with abnormal acid reflux defined by pH testing and a good correlation of symptoms with acid reflux.
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PMID:Current Diagnosis and Management of Suspected Reflux Symptoms Refractory to Proton Pump Inhibitor Therapy. 2755 Dec 49