Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0031350 (pharyngitis)
2,405 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The combination of the two typical symptoms - heartburn and regurgitation - is almost proving gastrooesophageal reflux disease (GORD). Further - atypical - symptoms are dysphagia, odynophagia, pharyngitis, reflux-induced pulmonary symptoms or intermittent chest-pain. Endoscopic signs of GORD are patchy reddening of the mucosa, erosions, ulcers and stricture. Barretts oesophagus is characterized by columnar epithelial metaplasia. Consequence: Typical symptoms of GORD may be treated without further diagnostic procedure whereas in the case of atypical symptoms diagnosis of GORD has to be established by endoscopy.
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PMID:[Reflux esophagitis--diagnosis and differential diagnosis]. 897 50

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.
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PMID:Pathophysiology and pharmacological treatment of gastroesophageal reflux disease. 1106 Apr 72

Gastroesophageal reflux disease (GERD) is the most common esophageal disease. It typically presents with heartburn and regurgitation, but it may also cause atypical symptoms, either alone or in combination. About 20 to 60 percent of patients with GERD have ENT symptoms without any heartburn. The most common ENT symptom is a globus sensation, yet there are many possible clinical signs such as laryngitis, pharyngitis, sinusitis, laryngospasm, laryngeal edema and granuloma that may mislead the initial work-up. In this work the pathophysiology, symptomatology, diagnostic measurements and therapeutic options of GERD are discussed. It is suggested that GERD has to be included into differential diagnostic approaches especially when routine treatment of these ENT diseases failes.
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PMID:[Reflux-associated diseases of the otorhinolaryngology tract]. 1155 31

For a long time heartburn was not considered a symptom for serious illness. By now, however, it is accepted that the incidence of secondary carcinoma of the esophagus caused by chronic GERD has increased dramatically since the nineteen-seventies. Mechanisms leading to GERD are complex and its incidence is not necessarily pathological. However pathological reflux in the lower esophagus (pH lower than 4 in 6 % of 24 hours), caused by decreased sphinctertonus, impaired peristalsis and clearance of the esophagus, may lead to complications. Helicobacter pylori may play a key role in GERD. There is strong evidence for a protective effect of Hp-infection in the development of GERD. In pangastritis, caused by Hp-infection, gastric acid production is inhibited resulting in a reduction of stomach-acid-concentration. This may be caused by either the chronic infection itself and the resulting atrophy of the stomach-mucosa, by the ammonia-producing HP-bacteria, or an increase in acid re-absorbtion of gastric epithelium. Laryngopharyngeal reflux (LPR) often results in atypical manifestations with oral, pharyngeal, laryngeal, and pulmonary disorders. Laryngopharyngeal reflux is known to contribute to posterior acid laryngitis and laryngeal contact ulceration or granuloma formation, laryngeal cancer, chronic hoarseness, pharyngitis, asthma, pneumonia, nocturnal choking, and dental diseases. Today, PPI are the medication of choice in both acute and long-term (prophylactic) therapy of GERD. The so called "step-up-strategy" of medication is no longer recommended. Here, patients were first treated with antacids, then prokinetics followed by H2-blockers and finally low-dose PPI. Only in the case of persisting symptoms medication was further increased to high-dose PPI therapy. In the past this increase in medication lead to a prolonged healing process and consequently to higher medication costs. Studies have shown that a "step-down"-therapy, beginning with high dose PPI, is highly preferable, since it is much more effective. Depending on the degree of the symptoms, however, medication may also be applied "on-demand". The BfArM has approved this kind of medication application only for Esomeprazol (Nexium mups 20 mg).
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PMID:[Gastroesophageal reflux -- a common illness?]. 1262 41

Gastro-oesophageal reflux disease (GERD) covers a broad range of signs and symptoms arising from the orad movement of gastric contents into the oesophagus, oropharynx, larynx or airway. Most commonly, contact with and damage to the oesophageal epithelium by acidic refluxate causes micro or macroscopic defects leading to the symptom of heartburn. However, GERD can also give rise to extra-oesophageal manifestations such as pharyngitis, laryngitis, asthma and other disorders, identifiable as acid-mediated events by a favorable response to acid suppression. Only one-third of individuals with heartburn have endoscopic evidence of erosive oesophagitis; the remainder have endoscopy-negative or non-erosive reflux disease (NERD). Improved investigative technologies are increasing our understanding of the pathophysiology of NERD. For example, although a number of microscopic abnormalities have been identified, oesophageal damage in NERD has been shown to be characterized by the presence of 'dilated intercellular spaces' within oesophageal stratified squamous epithelium. Dilated intercellular spaces that reflect damage to the intercellular junctions enable levels of acidity that would be considered innocuous when present in the oesophageal lumen to initiate pathological responses within oesophageal nociceptors when present within the intercellular spaces. This effectively gives rise to the symptom of heartburn. Excessive acidity within the intercellular spaces in NERD also presages its evolution to erosive disease, the latter through inflammation-mediated disruption of the antireflux and luminal clearance mechanisms. Support for this scenario is evident by the ability of effective acid control with proton pump inhibitors both to control symptoms, and lead to resolution of dilated intercellular spaces in patients with both erosive and non-erosive disease. This article examines these concepts and how they shape our current understanding of GERD.
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PMID:Current understanding of the mechanisms of gastro-oesophageal reflux disease. 1686 42

The effect of proton pump inhibitor (PPI) therapy on extraesophageal or atypical manifestations of gastroesophageal reflux disease (GERD) remains unclear. This study aimed to evaluate the prevalence of atypical manifestations in patients with acid reflux disease and the effect of PPI treatment. Patients with symptoms and signs suggestive of reflux were enrolled. Erosive esophagitis was stratified using the Los Angeles classification. Demographic data and symptoms were assessed using a questionnaire and included typical symptoms (heartburn, regurgitation, dysphagia, odynophagia), and atypical symptoms (e.g., chest pain, sialorrhea, hoarseness, globus sensation, chronic coughing, episodic bronchospasm, hiccup, eructations, laryngitis, and pharyngitis). Symptoms were reassessed after a 3-month course of b.i.d. PPI therapy. A total of 266 patients with a first diagnosis of GERD (erosive, 166; non-erosive, 100) were entered in the study. Presentation with atypical symptoms was approximately equal in those with erosive GERD and with non-erosive GERD, 72% vs 79% (P = 0.18). None of the study variables showed a significant association with the body mass index. PPI therapy resulted in complete symptom resolution in 69% (162/237) of the participants, 12% (28) had improved symptoms, and 20% (47) had minimal or no improvement. We conclude that atypical symptoms are frequent in patients with GERD. A trial of PPI therapy should be considered prior to referring these patients to specialists.
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PMID:Effect of antisecretory therapy on atypical symptoms in gastroesophageal reflux disease. 1721 95