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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Esophageal intramural pseudodiverticulosis, which was first described by Mendl et al. in 1960, is characterized by multiple small flask-shaped outpouchings in the esophageal wall. The pseudodiverticula represent dilated excretory ducts of deep mucous glands in the esophagus. The etiology of this rare condition is unknown. Hiatal hernias, gastroesophageal reflux, esophageal strictures, candida esophagitis, herpes esophagitis, diabetes mellitus, and chronic alcoholism have been found associated with intramural pseudodiverticulosis. We report the second case of esophageal hypermotility in intramural pseudodiverticulosis.
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PMID:Diffuse esophageal intramural pseudodiverticulosis and nutcracker esophagus in a 54-year-old man. 210 56

An alcoholic man with known reflux esophagitis and Barrett's esophagus developed fever, epigastric pain, subcutaneous crepitus, and leukocytosis from an esophageal perforation at a Barrett's ulcer. Possible risk factors for perforation in this patient included alcoholism, severe gastroesophageal reflux, corticosteroid therapy, noncompliance with antacid and H2 blocker therapy, and the presence of acid-secreting parietal cells in the Barrett's epithelium. Five cases of this complication have previously been reported in a review of the literature, which included 536 cases of Barrett's esophagus or esophageal perforation. This entity may present with a clinical triad of a patient (a) in acute distress with fever and epigastric or noncardiac chest pain and without signs of peritonitis, (b) with symptoms of or known gastroesophageal reflux, and (c) with chest examination revealing subcutaneous crepitus, or chest roentgenogram revealing subcutaneous emphysema, pneumomediastinum, or hydropneumothorax.
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PMID:Esophageal perforation at a Barrett's ulcer. 258 67

In the gastroenterological diagnostic armamentarium, dysphagia is considered as an important symptom for diseases of the esophagus. Concerning the history of illness, symptoms such as retrosternal pain and heartburn are often associated with gastroesophageal reflux disease. Morphological changes of the mucosa can be diagnosed by flexible endoscopy and radiographic examinations. Investigation with 24-h pH monitoring, manometry, and pharmacological tests is necessary for the diagnosis of functional disorders. Additionally, dysphagia can be associated with multiple internal diseases, including muscular diseases such as dermatomyositis, progressive systemic sclerosis, as well as lupus erythematosus. Difficulties in swallowing associated with hypo- and hyperthyroidism can also be interpreted as muscular lesions. Metabolic disorders such as alcoholism, and diabetes mellitus can be the cause of dysphagia. Increasing importance in the differential diagnosis of dysphagia is attached to infections of the upper GI tract. Especially in immunocompromised patients, infections of Candida albicans, mycobacterias, herpes, varicella zoster, and cytomegaloviruses can produce dysphagia and odynophagia. The differential diagnosis of the "angina-like chest pain" has to differentiate between cardiac disease and a noncardiac genesis. Therefore, besides the cardiac diagnostic investigation, endoscopy, radiography, and manometry are often indicated.
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PMID:The gastroenterologist's approach to dysphagia. 846 28

The effects of ethanol upon the gastrointestinal tract (mouth, pharynx, esophagus, stomach, duodenum, Oddi's sphincter, small bowel, colon and rectum) were reviewed. Several studies showed that the incidence of cancer in the mouth and pharynx is increased in alcoholics as a consequence of ethanol effects and probably those of other compounds found in liquors. The gastroesophageal reflux disease may be induced by alcohol since it reduces the pressure in the lower and the upper esophageal sphincter, as well as the extent of primary peristalsis. Several studies showed a strong correlation between esophageal cancer and alcohol abuse. The risk for developing this kind of tumour is significantly increased when alcohol abuse and smoking coexist. Alcoholism predisposes patients to Mallory-Weiss syndrome as well as to bleeding of esophageal varices Ethanol may affect gastric secretion, motility, and permeability. Some drugs acting upon the gastric alcohol-dehydrogenase are able to affect gastric absorption of ethanol. Eradication of Helicobacter pylori increases the activity of alcohol-dehydrogenase in the pyloric antrum. The effects of alcohol upon the gastric mucosa include caustic damage, retrograde diffusion of H+, and cytoprotection. This agent may cause an acute gastritis but it is probably not involved in chronic gastritis. Whether alcohol is a risk factor for ulcer or not is unknown. Some studies found an increased incidence of gastric cancer associated with consumption of beer, wine and vodka. Some authors reported a decreased pressure in Oddi's sphincter while others found it increased in association with the consumption of ethanol. The acute and the chronic consumption of alcohol may affect the structure of small bowel as well as the absorption of nutrients. Several studies reported a significant correlation between colorectal cancer and the chronic consumption of ethanol.
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PMID:[Ethanol and the gastrointestinal tract]. 872 88

It is well known that acid regurgitated from the stomach into the mouth will erode teeth. Conditions such as anorexia and bulimia nervosa, chronic alcoholism and gastric disturbances cause palatal dental erosion. The common factor in these conditions is the role played by the stomach and oesophagus in the acid movement. Acid moving through the lower oesophageal sphincter into the oesophagus is described as gastro-oesophageal reflux (GOR). In some patients the acid movement becomes chronic, painful and requires treatment and is termed gastro-oesophageal reflux disease (GORD). It is felt by many gastroenterologists that GORD is a failure of the anti-reflux mechanism, which is predominantly controlled by the lower oesophageal sphincter (LOS). Regurgitation is the reflux of gastric juice through the upper oesophageal sphincter and into the oral cavity. Once the acid has reached the mouth the potential exists for damage to the teeth. This paper reviews the role of GOR, GORD and regurgitation in the aetiology of dental erosion.
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PMID:The relationship between gastro-oesophageal reflux disease and dental erosion. 873 40

Oesophageal motility disorders comprise various abnormal manometric patterns which usually present with dysphagia or chest pain. Some, such as achalasia, are diseases with a well defined pathology, characteristic manometric features, and good response to treatments directed at the pathophysiological abnormalities. Other disorders, such as diffuse oesophageal spasm and hypercontracting oesophagus, have no well defined pathology and could represent a range of motility changes associated with subtle neuropathic changes, gastro-oesophageal reflux, and anxiety states. Although manometric patterns have been defined for these disorders, the relation with symptoms is poorly defined and the response to medical or surgical therapy unpredictable. Hypocontracting oesophagus is generally caused by weak musculature commonly associated with gastro-oesophageal reflux disease. Secondary oesophageal motility disorders can be caused by collagen vascular diseases, diabetes, Chagas' disease, amyloidosis, alcoholism, myxo-oedema, multiple sclerosis, idiopathic pseudo-obstruction, or the ageing process.
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PMID:Oesophageal motility disorders. 1180 95

Diet analysis and advice for patients with tooth wear is potentially the most logical intervention to arrest attrition, erosion and abrasion. It is saliva that protects the teeth against corrosion by the acids which soften enamel and make it susceptible to wear. Thus the lifestyles and diet of patients at risk need to be analysed for sources of acid and reasons for lost salivary protection. Medical conditions which put patients at risk of tooth wear are principally: asthma, bulimia nervosa, caffeine addiction, diabetes mellitus, exercise dehydration, functional depression, gastroesophageal reflux in alcoholism, hypertension and syndromes with salivary hypofunction. The sources of acid are various, but loss of salivary protection is the common theme. In healthy young Australians, soft drinks are the main source of acid, and exercise dehydration the main reason for loss of salivary protection. In the medically compromised, diet acids and gastroesophageal reflux are the sources, but medications are the main reasons for lost salivary protection. Diet advice for patients with tooth wear must: promote a healthy lifestyle and diet strategy that conserves the teeth by natural means of salivary stimulation; and address the specific needs of the patients' oral and medical conditions. Individualised, patient-empowering erosion WATCH strategies; on Water, Acid, Taste, Calcium and Health, are urgently required to combat the emerging epidemic of tooth wear currently being experienced in westernised societies.
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PMID:Tooth wear: diet analysis and advice. 1588 Sep 60

Gastric juice entering the mouth causes dental erosion. Common causes for the migration of gastric juice through the lower and upper oesophageal sphincters are reflux disease, eating disorders, chronic alcoholism and pregnancy. Gastro-oesophageal reflux is a common condition affecting up to 65% of the western population at some point in their lifetime. A typical clinical sign of acidic gastric juice entering the mouth is palatal dental erosion. As the condition becomes more chronic it becomes more widespread. There have been relatively few randomised studies investigating the aetiology of acids causing erosion. Of the few that have reported their findings, it appears that gastric acids are equally likely to induce moderate-to- severe erosion as in dietary acids. This literature review reports the conditions associated with the movement of gastric juice and dental erosion using medical and dental sources.
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PMID:Intrinsic causes of erosion. 1668 91

Proton pump inhibitors (PPIs) are widely used drugs in the treatment or prophylaxis of peptic ulcer and gastro-oesophageal reflux disease. In addition to their well documented efficacy, these drugs are generally well tolerated with only rare serious adverse effects having been reported. Neutropenia and agranulocytosis are rare adverse events associated with PPI treatment. All previously published cases of isolated neutropenia have involved omeprazole, but leukopenia is labelled as a possible adverse effect in the summary of product characteristics of the other PPIs. In this report, we describe a case of omeprazole-induced neutropenia with further recurrence upon pantoprazole treatment. A 60-year-old man with chronic alcoholism and a medical history of pulmonary tuberculosis, untreated chronic C hepatitis, peripheral artery disease, chronic obstructive pulmonary disease and stable stage 3 chronic kidney disease was admitted with dehydration and malnutrition. Omeprazole 20 mg/day and sucralfate 3 g/day were started for diffuse gastritis on gastric endoscopy. While the patient's blood cell count had been within the normal range before this treatment, routine laboratory examination revealed moderate neutropenia (0.9 x 109/L) after 9 days of treatment. His blood cell count returned to the normal range after discontinuation of omeprazole and no further episodes of neutropenia were noted in the following months. One year later, oesophago-gastroscopy revealed a hiatal hernia with an extensive zone of Barrett's oesophagus. As the lesions did not improve with ranitidine and sucralfate therapy, the patient was started on pantoprazole 40 mg/day. His initial white blood cell count was normal, but moderate neutropenia (0.8 x 109/L) was again noted after only 2 days of pantoprazole treatment. Complete and further stable normalization was obtained within 3 days after replacement of pantoprazole with ranitidine. Toxic and immune-mediated mechanisms are the two commonly proposed mechanisms to explain the pathogenesis of drug-induced neutropenia. This report suggests that PPI-induced neutropenia is immune mediated and argues for a possible cross-reactivity between the two PPIs, as has already been described for PPI-induced hypersensitivity reactions. The report also indicates that patients with a history of neutropenia induced by one PPI may be at risk of recurrence of neutropenia if given another member of this drug class. In these patients, close haematological monitoring is proposed.
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PMID:Proton pump inhibitor-induced neutropenia: possible cross-reactivity between omeprazole and pantoprazole. 2058 18

Intramural pseudodiverticulosis of the esophagus is a rare benign disease of the eosphageal wall, with dilation of the submucosal glands, and the predominant symptom is dysphagia. This disorder may be associated with gastroesophageal reflux, motility disorders, candidiasis and alcoholism. Inflammation, resulting in periductal fibrosis and compression of the duct orifices, may be a causative factor. Good and long-lasting therapeutic success can be achieved by bouginage of the stenosis with concomitant treatment of the associated esophageal diseases. Esophageal intramural pseudodiverticulosis is a differential diagnosis in cases of dyspagia and/or esophageal strictures if no other causes are found.
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PMID:[Dysphagia and recurrent esophageal stenosis associated with intramural pseudodiverticulosis of the esophagus. A case report]. 2129 Aug 57


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