Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0011168 (dysphagia)
 15,644 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lichen planus (LP) is an inflammatory papulosquamous disease which may affect the squamous epithelium of the esophagus. We reviewed six patients with esophageal lichen planus (ELP) seen at Mayo Clinic Rochester between 1984 and 1998. The presenting symptoms were dysphagia (in all six patients) and odynophagia (two patients). Cervical esophageal strictures were seen in four patients; average number of esophageal dilatations required was 15 (range, 10-18). Esophageal biopsies demonstrated the classical histologic findings of ELP in two patients, and a lymphocytic infiltrate in the other four. Concomitant lichen planus (LP) was seen at other sites in five patients: all five had oral LP preceeded by ELP symptoms in all five; three had genital LP preceeded by ELP symptoms in all three; two had dermal LP, preceeded by ELP symptoms in one. Proton pump inhibitors were tried unsuccessfully in all patients. Four patients were started on systemic steroid medication; three had resolution of symptoms within 1 month.
 ...
PMID:Esophageal lichen planus: the Mayo Clinic experience. 1077 Mar 69

The introduction of proton pump inhibitors (PPI) and laparoscopic fundoplication in the treatment of gastroesophageal reflux disease offered an opportunity for definitive healing. The indication for surgery is the failure of medical treatment, recurrence of symptoms following conservative treatment, severe side effects of the medication, and the patient's wish to stop taking drugs. The laparoscopic treatment has a low rate of complications. Apart from temporary dysphagia (30%), rapid satiety, increased flatulence and suppressed eructation are possible undesirable sequelae. Intra-operative bleeding and organ perforation (1%) are major feared occurrences. The rate of conversion to open surgery is 5.8%, and the mortality rate is 0.1%. Persistent dysphagia in 3.4% may be caused by a slipped cuff. A revision procedure is necessary in 0.7% of the patients. Patient satisfaction with the results of the operation ranges between 87 and 100%.
 ...
PMID:[A retaining dam against reflux. Laparoscopic fundoplication helps even in stubborn cases]. 1087 18

Gastroesophageal reflux is a very common disorder. Typical symptoms are heartburn, regurgitation and chest pain. Recently, it has been demonstrated that gastroesophageal reflux may generate or worse extraesophageal symptoms such as asthma, chronic bronchitis, posterior laryngitis, and chronic cough. The diagnosis of gastroesophageal reflux is suggested by typical symptoms which improve under a therapy with proton pump inhibitors. pH-monitoring over 24 hours is able to establish directly the diagnosis by measuring acid reflux into the esophagus. Manometry detects the two most common causes of gastroesophageal reflux: insufficiency of the lower esophageal sphincter or esophageal motility abnormalities. Gastroesophageal reflux can lead to reflux esophagitis, which is diagnosed endoscopically. An endoscopy should routinely be performed in case of dysphagia, anemia, or loss of weight. A long-term sequela of gastroesophageal reflux is the development of Barrett's-esophagus, a condition which has to be verified by endoscopy and biopsy. This premalignant lesion is defined by a metaplastic change from the normal squamous mucosa to a specialized intestinal epithelium characterized by goblet cells. Because dysplasia in these metaplastic areas can lead to esophageal adenocarcinoma, regular endoscopic surveillance with biopsies is recommended. Gastroesophageal reflux can significantly impair the quality of life and can cause complications that include the neoplastic progression from Barrett's esophagus to carcinoma. Therefore, appropriate diagnostic procedures and adequate therapy are required. This article summarizes the diagnostic approach to patients with gastroesophageal reflux, reflux esophagitis and Barrett's-esophagus. The impact of endoscopy, pH-monitoring, esophageal manometry, radiology and scintigraphy are reviewed.
 ...
PMID:[Diagnosis of gastroesophageal reflux and Barrett esophagus]. 1092 25

Management of gastro-oesophageal reflux disease (GORD) patients must consider two issues: (i) how to optimize the treatment of a presenting symptom complex, and (ii) how to manage risk of adenocarcinoma associated with GORD. In most cases the need for, and potency of, pharmacological therapy used is decided by symptom assessment. Considering cost effectiveness, the three increments of pharmacological therapy are: (i) generic histamine(2)receptor antagonists, (ii) standard dose proton pump inhibitors, and (iii) higher dose proton pump inhibitors. Endoscopy is warranted if there is doubt regarding the diagnosis of GORD or if the patient relays alarm symptoms suggesting more ominous diagnoses (dysphagia, bleeding, weight loss, odynophagia). The other major indication for endoscopy is to screen for adenocarcinoma or Barrett's metaplasia in the patient with chronic symptoms. In most patients, the need for maintenance medical therapy is determined by the rapidity of symptom recurrence during a trial period off the medication.
 ...
PMID:Strategies for medical management of reflux disease. 1100 9

Gastroesophageal reflux disease (GERD) is one of the most common diagnoses in a gastroenterologist's practice. Gastroesophageal reflux describes the retrograde movement of gastric contents through the lower esophageal sphincter (LES) to the esophagus. It is a common, normal phenomenon which may occur with or without accompanying symptoms. Symptoms associated with GERD include heartburn, acid regurgitation, noncardiac chest pain, dysphagia, globus pharyngitis, chronic cough, asthma, hoarseness, laryngitis, chronic sinusitis and dental erosions. The introduction of fiberoptic instruments and ambulatory devices for continuous monitoring of esophageal pH (24-hour pH monitoring) has led to great improvement in the ability to diagnose reflux disease and reflux-associated complications. The development of pathological reflux and GERD can be attributed to many factors. Pathophysiology of GERD includes incompetent LES because of a decreased LES pressure, transient lower esophageal sphincter relaxations (TLESRs) and deficient or delayed esophageal acid clearance. Uncomplicated GER may be treated by modification of life style and eating habits in an early stage of GERD. The various agents currently used for treatment of GERD include mucoprotective substances, antacids, H(2) blockers, prokinetics and proton pump inhibitors. Although these drugs are effective, they do not necessarily influence the underlying causes of the disease by improving the esophageal clearance, increasing the LESP or reducing the frequency of TLESRs. The following article gives an overview regarding current concepts of the pathophysiology and pharmacological treatment of GERD.
 ...
PMID:Pathophysiology and pharmacological treatment of gastroesophageal reflux disease. 1106 Apr 72

Gastroesophageal reflux disease poses special diagnostic and therapeutic challenges in the elderly. These patients may not report the classic symptoms of dysphagia, chest pain, and heartburn, and they are more likely to develop severe disease and complications such as esophageal ulceration and bleeding. Therapeutic options include lifestyle changes, medication, and surgery. Polypharmacy and changes in renal, hepatic, and gastrointestinal function can complicate treatment. Proton pump inhibitors can help optimize disease management. The most common primary presenting symptoms of GERD in the elderly are regurgitation, dysphagia, dyspepsia, vomiting, and noncardiac chest pain, rather than heartburn. Because the elderly commonly take multiple drugs for various comorbidities, drug interactions and treatment responses must be carefully assessed in this patient population. Nonpharmacologic measures may be helpful but often do not relieve nighttime GERD symptoms.
 ...
PMID:Diagnosis and treatment of gastroesophageal reflux disease in the elderly. 1106 Sep 61

There are no reliable means of quantifying the edema that results from acid exposure to the posterior larynx in patients with laryngopharyngeal reflux (LPR). However, it is possible to quantify laryngopharyngeal sensitivity in these patients by endoscopic administration of air pulses to the laryngeal mucosa in order to elicit the laryngeal adductor reflex. The purpose of this study was to determine whether patients with LPR have sensory deficits in the laryngopharynx, and whether treatment of these patients with a proton pump inhibitor (PPI) results in resolution of sensory deficits. Flexible endoscopic evaluation of swallowing with sensory testing was prospectively performed in 54 patients with dysphagia without neurologic disease and in 25 healthy controls. The laryngopharyngeal sensory level, posterior laryngeal edema, and LPR were assessed. We defined LPR as passage of food material from the esophageal inlet retrograde into the hypopharynx. Patients with LPR were placed on 3 months of omeprazole or lansoprazole and then retested. Patients without LPR were placed on H2 blockers for 3 months and then retested. In the dysphagia group, 48 of 54 patients (89%) had edema of the posterior larynx, and 42 of 54 (78%) had laryngopharyngeal sensory deficits. We noted LPR in 38 of 54 (70%). In the control group, 1 of 25 subjects (4%) had edema, sensory deficits, and LPR. The differences in incidence of edema, sensory deficits, and LPR between the dysphagia group and the control group were significant (p < .001, chi2 test). Twenty-three patients with LPR placed on a PPI returned for follow-up, with improvement in laryngeal edema in 14 of the 21 (67%) who had pretreatment edema and resolution of sensory deficits in 15 of the 19 (79%) who had pretreatment deficits. In the non-LPR, non-PPI group, 11 of 16 patients returned for follow-up, with improvement in laryngeal edema in none of the 11 and improvement in sensory deficits in 1 of the 11 (9.1%). The differences in improvement in laryngeal edema and sensory deficits between the LPR, PPI group, and the non-LPR, non-PPI group were significant (p < .01, Fisher's exact test). We conclude that patients with dysphagia and edema of the posterior larynx as a result of LPR have sensory deficits in the laryngopharynx. Treatment of these patients with a PPI appears to result in resolution of laryngopharyngeal edema and improvement of sensory deficits, both subjectively and objectively.
 ...
PMID:Laryngopharyngeal sensory deficits in patients with laryngopharyngeal reflux and dysphagia. 1108 89

Cardiac and musculoskeletal disease should be excluded before considering an esophageal etiology for chest pain. Acid reflux is a common cause of chest pain and should be identified and treated. A therapeutic trial should consist of a proton pump inhibitor (omeprazole 20 mg or lanzoprazole 30 mg) given one or two times per day for at least 6 to 8 weeks. An alternative is to use an ambulatory pH study to confirm reflux. Also, if the patient fails the initial treatment, reflux should be confirmed with pH testing before increasing the dose of proton pump inhibitor or considering combination or surgical therapy. Esophageal manometry should be considered in patients with chest pain and dysphagia. It is also reasonable to perform manometry before a pH study since manometric localization of the lower esophageal sphincter (LES) is needed to ensure accurate pH probe placement. Only after manometric confirmation of a spastic esophageal motility disorder should patients be treated for esophageal spasm. In these patients, it is reasonable to try a long-acting formulation of a calcium-channel blocker or nitrate. Patients with chest pain who have a negative cardiac evaluation and who do not have reflux may have an abnormality in esophageal or cardiac sensation. These patients should be treated with a trial of an antidepressant and considered for referral to a mental health practitioner. All medication trials should continue at least 6 to 8 weeks to avoid a placebo effect and to allow adequate time for a therapeutic response.
 ...
PMID:Noncardiac Chest Pain of Esophageal Origin. 1109 64

Cardiomyotomy is now usually performed using a minimally invasive approach. A consecutive series of 18 patients with an intention to treat thoracoscopically were followed by the same number of patients treated laparoscopically. Both groups have been followed prospectively for a minimum of 2 years. The groups were well matched for age, symptom duration, preoperative lower esophageal sphincter pressure, and number having undergone balloon dilatation. There was one conversion from a thoracoscopic to a laparoscopic approach so that, for the purpose of analysis, there are 17 in the thoracoscopic group and 19 in the laparoscopic group. There was no difference in the average operating time, rate of conversion to open operation, mucosal breaches, or length of hospitalization. Nor was there any difference in dysphagia symptoms, with 14/17 having a satisfactory result after thoracoscopic myotomy and 18/19 after laparoscopic myotomy. Frequency of reflux symptoms was similar and, although mild reflux was common, only two patients required treatment with a proton pump blocker. In the treatment of achalasia, thoracoscopic and laparoscopic myotomy without fundoplication are equally effective in relieving dysphagia and have a similar safety profile.
 ...
PMID:Heller's myotomy: thoracoscopic or laparoscopic? 1128 74

Apart from gastroesophageal reflux disease, achalasia, non-cardiac chest pain and functional dysphagia are the most important manifestations of disturbed esophageal motility. Achalasia is characterized by esophageal aperistalsis and impaired deglutitive relaxation of the lower esophageal sphincter. The morphological correlate is a degeneration of nitrergic neurons in the myenteric plexus. Diagnosis is based on barium esophagram or esophageal manometry with the latter setting the gold standard. Endoscopic exclusion of a tumor at the gastroesophageal junction is mandatory. Appropriate therapeutic interventions are pneumatic dilatation or (laparoscopic myotomy) of lower esophageal sphincter. In patients unfit for these procedures endoscopic injection of botulinum toxin into the lower esophageal sphincter is appropriate. Non-cardiac chest pain may be of esophageal origin. Gastroesophageal reflux, spastic motility disorders and visceral hypersensitivity are arguable underlying mechanisms. The most important diagnostic procedure is 24 h esophageal pH metry correlating symptoms and reflux episodes. Proton pump inhibitors and tricyclic antidepressants serving as visceral analgesics are appropriate therapeutic approaches. Functional dysphagia defines the sensation of impaired passage without mechanical obstruction or a neuromuscular disease with known pathology, e.g. scleroderma. Impaired transit is proven by esophageal scintigraphy or radiogram both using solid boluses. Manometry assesses the underlying mechanisms.
 ...
PMID:[Diagnosis and treatment of esophageal motility disorders]. 1130 49


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>