Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

After the skin, the gastrointestinal tract is the most frequently affected organ in systemic sclerosis. Gastrointestinal symptoms already may be present early in the course of the disease and do not necessarily correlate with objective findings. Esophageal dysmotility is not specific for systemic sclerosis but occurs in other connective tissue diseases as well. Peripheral macrovascular disease was shown to be increased in patients with limited cutaneous sclerosis; signs of autonomic dysfunction were found in patients with the CREST (calcinosis, Raynaud's phenomenon, esophageal dysfunction, sclerodactyly, and telangiectasia) variant. Pulmonary involvement was shown to be moderately or severely decreased in 40% of a large cohort of scleroderma patients. In one study, no support was found for the association between pulmonary involvement and gastroesophageal reflux. Peripheral nerve involvement is often subclinical and might be associated with anti-U1-RNP and anti-topoisomerase I antibodies. Internal organs are seldomly affected in localized scleroderma. When occurring in childhood and involving an extremity, localized scleroderma can cause growth failure, resulting in long-term functional disability.
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PMID:Clinical aspects of systemic and localized scleroderma. 857 77

Scleroderma or systemic sclerosis (Ssc) is a connective tissue disease which frequently involves the esophagus. Motility disorders, such as a low pressure level in the Lower Esophageal Sphincter (LES), and disturbed esophageal peristalsis cause a higher acid exposition and mucosal damage. We study twenty Ssc patients using computerized esophageal manometry, endoscopy and clinical interview looking for prevalence of symptoms, esophageal dysmotility and erosive esophagitis, and trying to find risk factors involved in esophageal damage. Esophagitis was found in 40% of patients. Clinical presentation (diffuse or limited), age and time since diagnosis wer'nt accurate predictors of esophageal involvement. Symptoms such as dysphagia and heartburn had not any significant difference in those with and without esophagitis, so 25% of patients with mucosal damage had no symptoms and 60% of healthy ones complained about them. LES values were not significantly different between the two groups, with a great degree of overlap with normal values. Disturbed motility pattern of aperistalsis was the only factor that identified high and low risk groups for esophagitis, with a high statistical significance (p > 0.02). Mucosal sensitivity in severe esophagitis and pharyngeal and upper esophageal functions were normal in all patients. Impaired peristalsis, with a delayed clearance of acid is the most important factor for mucosal damage in scleroderma. Symptoms of gastroesophageal reflux are not a reliable predictor of erosive esophagitis. Endoscopy should be the usual method of diagnosis, in order to make a proper use of therapeutic weapons.
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PMID:[Esophageal mucosal lesions and scleroderma: prevalence, symptoms and risk factors]. 866 79

High or pharyngo-oesophageal dysphagia (PD) is defined as difficulty in initiating the act of swallowing within 1s. It involves the mechanisms controlling the tongue, pharynx and upper oesophageal sphincter (UOS) and is associated with a wide variety of local, neurologic and muscular disorders, and can also occur after surgery in the area and in response to gastro-oesophageal reflux (GOR). Our study aims at defining the criteria for surgery in PD and to evaluate the clinical results of such treatment. Twenty-three patients who underwent surgery were evaluated with pharyngo-oesophageal motility and ambulatory 24-hr pH-metry. The following parameters were measured: 1) pharyngeal contraction amplitude, 2) duration, 3) repetitive pharyngeal contractions, 4) UOS tone, 5) percentage of UOS relaxation, 6) duration of relaxation, 7) UOS closing pressure, 8) UOS closing duration, 9) co-ordination of UOS closing pressure and upper oesophageal (UO) contractions. Preoperative manometry showed a variety of abnormalities in several of the parameters, such as prolonged pharyngeal contraction ("spasm"), unco-ordinated pharyngeal contractions and UOS relaxation, low amplitude pharyngeal contractions, unco-ordinated UOS closing tone and UO contractions and hypotonic UO. Surgery was directed at the specific abnormality in each patient taking into consideration the presence or absence of GOR. Seventeen patients (74%) had excellent results. Three other patients (13%), who had improved swallowing but who continued to have GOR complicated by some oesophageal dysmotility, oesophagitis and an oesophageal web, underwent subsequent anti-reflux surgery with relief of symptoms. In conclusion, pharyngo-oesophageal motility measurement is mandatory in PD, especially when a diverticulum is absent. Cricopharyngeal myotomy with or without diverticulectomy as indicated produces excellent results. Associated oesophageal problems have to be dealt with appropriately.
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PMID:Pharyngo-oesophageal dysphagia: surgery based on clinical and manometric data. 873 94

Although many factors are involved in the pathogenesis of gastroesophageal reflux disease (GERD), the antireflux barrier at the gastroesophageal junction is the final determinate of reflux. In the majority of cases, transient lower esophageal sphincter (LES) relaxations appear to be the necessary condition for reflux to occur. In severe cases of GERD, especially those with esophagitis, stricture, and Barrett's epithelium, diminished resting LES pressure plays a contributory role. Esophageal dysmotility may be an additive factor leading to increased esophageal acid contact time and predispose patients to developing erosive esophagitis. Also, delayed gastric emptying may further compromise the LES. Finally, the role of bile reflux across an incompetent gastroduodenal (pyloric) junction remains controversial.
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PMID:Contributing role of motility abnormalities in the pathogenesis of gastroesophageal reflux disease. 917 44

This study was undertaken to determine the prevalence of esophageal motor abnormalities, the incidence of gastroesophageal reflux, and the coexistence of gastroesophageal reflux with esophageal dysmotility in patients with intrinsic asthma. Based on clinical criteria, 34 consecutive asthmatics, 15 patients with gastroesophageal reflux, and 10 subjects with upper gastrointestinal symptoms with normal results of esophageal manometry and 24-hr esophageal pH test (controls) were studied. Esophageal motor disorders were noted in 23 of 34 asthmatics, and in 10 of 15 patients with acid reflux but in none of the subjects of the control group. A positive result of the prolonged esophageal pH study (pH in the distal esophagus less than 4 for more than 4.2% of the recording time) was obtained in 14 of 17 patients with asthma (only 17 of the original patients were tested because the others did not give informed consence for this test) and in all patients with gastroesophageal reflux. None of the members of the control group had positive test results. The findings of this study show that: (1) it is possible to identify a group of subjects with nonallergic asthma presenting with esophageal dysmotility, (2) the 24-hr esophageal pH study must be properly done in such patients; (3) esophageal motor abnormalities are often associated with positive pH results; and (4) more reflux was observed while in a supine position (especially during the night) than that observed either in control or reflux patients. Based on these results, patients with intrinsic asthma with reflux can benefit from both acid suppressive and prokinetic drugs with notable clinical implications regarding standard treatment for asthma, and those with prevalent supine compared to upright reflux could even benefit from surgery.
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PMID:Esophageal dysmotility and gastroesophageal reflux in intrinsic asthma. 920 Oct 82

Severe nonexertional (resting) chest pain may be due to myocardial ischemia, esophageal dysfunction, psychiatric disorder, or any combination thereof and frequently poses a difficult diagnostic challenge. Our aim was to investigate causes of chest pain in patients with coronary artery disease. Forty-five patients with angiographically proven obstructive coronary lesions and recurrent chest pain at rest were studied; 18 had refractory pain despite cardiac therapy (problem group), and 27 had documented myocardial ischemia (control group). Esophageal manometry, edrophonium provocation, 24-hr pH studies, and psychiatric interview were performed in all patients. The clinical evolution and the outcome of specific treatment during follow-up was used to establish the etiology of chest pain. Esophageal dysfunction was identified in all problem patients and in 52% of controls, and the esophagus was incriminated as the source of pain in 8 (44%) and 5 (18.5%), respectively. After a mean follow-up of 49 months (range 24-76 months), the cause of chest pain in the problem group was identified as panic disorder in 9 patients (50%), gastroesophageal reflux in 6 (33%), esophageal dysmotility in 2 (11%), and gallstone disease in 1 (6%). Of the control patients, 18 (67%) had ischemic pain alone, while 9 had concurrent causes: panic disorder in 5 (19%) and esophageal dysfunction in 4 (15%). Esophageal dysfunction and psychiatric disturbances are common in patients with coronary artery disease presenting with resting chest pain, and may contribute to patients' symptoms.
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PMID:Chest pain at rest in patients with coronary artery disease. Myocardial ischemia, esophageal dysfunction, or panic disorder? 924 27

A prospective study into the aetiology of acute food bolus obstruction (AFBO) was carried out on 17 consecutive patients who presented with this complaint. There were nine males and eight females. Twelve patients (71 per cent) had symptoms of oesophageal disease and 10 patients (59 per cent) had prior food bolus obstruction. Investigations included endoscopy, barium swallow, oesophageal pH and manometry studies. Evidence of oesophageal pathology was found in 12/14 (86 per cent) of patients investigated. No patients had malignancy and the most common abnormality, gastroesophageal reflux (GOR) was found in eight out of 14 (57 per cent) of cases. Oesophageal dysmotility was seen in five out of 12 (42 per cent) patients who had manometric studies. With such a high incidence of recurrence of AFBO, we suggest that patients with this condition be investigated to exclude malignancy and to identify benign oesophageal pathology using techniques such as oesophageal pH and manometry. Appropriate treatment of oesophageal disease may help prevent recurrence of this distressing condition.
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PMID:Acute food bolus impaction: aetiology and management. 950 6

Gastroesophageal reflux disease is believed to be uncommon in the East. This study aimed to determine if such a condition was a significant cause of noncardiac chest pain in Singapore. Eighty consecutive patients with recurrent chest pain, who had cardiac and other obvious causes excluded, underwent esophagogastroduodenoscopy, standard manometry, acid perfusion test, and prolonged ambulatory pH and pressure monitoring. Endoscopic esophagitis, positive acid perfusion tests, pathologic reflux, and positive chest pain-reflux correlation were detected in 7/80 (8.8%), 11/70 (15.7%), 14/61 (23.0%), and 12/25 (48.0%) patients, respectively. Among those with pathologic reflux, endoscopic esophagitis was present in only two (14.3%). Overall, 32 (40%) patients had gastroesophageal reflux disease. Esophageal motility disorder, alone or in association with gastroesophageal reflux disease, was demonstrated in only five (6.3%) patients. Our results confirmed western reports that gastroesophageal reflux disease was a common cause of noncardiac chest pain, whereas motility disorder was an infrequent cause of such pain.
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PMID:Gastroesophageal reflux disease is a common cause of noncardiac chest pain in a country with a low prevalence of reflux esophagitis. 975 64

Systemic sclerosis (SSc) is a heterogenous disease with a morbidity and mortality that varies widely. Nonetheless, the future clinical course of an individual patient can be estimated based on the severity of skin and internal organ involvement within the first several years of the disease. Patients with limited cutaneous SSc (ISSc) have skin thickening below the elbows or knees and may have face and neck involvement. Patients with this subtype of SSc have Raynaud's phenomenon, digital ulcers, and esophageal dysfunction. Significant morbidity and mortality arises in those patients with ISSc who develop interstitial lung disease or pulmonary artery hypertension. Patients with diffuse cutaneous SSc (dSSc) have skin thickening above the elbows and knees or on the trunk. These patients have a more abrupt onset of disease, often with constitutional symptoms and arthalgias. Severe heart, lung, gut, and renal involvement, if it occurs, tends to develop within the first 5 years of disease, especially within the first several years. Patients with significant internal organ involvement have a poorer prognosis than patients who do not. The goals of the initial history and physical and laboratory examinations are to classify the type of scleroderma as ISSc or dSSc, to estimate disease duration, and to define the extent and severity of organ involvement. Treatment of SSc is organ based. Treatment may reduce morbidity associated with Raynaud's phenomenon, digital ulcers, esophageal dysmotility, esophageal reflux, gut dysmotility, arthralgias, myositis, and pulmonary artery hypertension. Therapy may stabilize lung function in patients with interstitial lung disease with alveolitis and stabilize renal function in patients with renal crisis. The overall prognosis for patients with SSc appears to be improving. Patients with early dSSc should be considered for enrollment onto protocol testing of potential disease-modifying therapies.
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PMID:Clinical approach to scleroderma. 975 79

Dysphagia is related to the impairment of food passage from the mouth to the stomach. Globus pharyngis implies the frequent and often painful sensation of a lump in the throat that usually does not interfere with swallowing and may even be relieved by food intake. The diagnosis is based upon a careful history, clinical examination, endoscopy, dynamic imaging (videofluoroscopy, cinematography, videosonography) and electrophysiologic procedures (including pharyngoesophageal manometry, electromyography and pH determinations). Structural lesions of the cervical spine such as diffuse idiopathic skeletal hyperostosis are rare causes of dysphagia. Dysphagia following anterior cervical fusion as well as globus and dysphonia due to dysfunction of the vertebral joints are more likely. Symptoms with swallowing fluids indicate a neurogenic origin. Dyscoordinated swallowing, nasal reflux, dysphonia or general weakness may also occur. Chronic aspiration with respiratory compromize is the main consequence in a variety of neurological disorders as well as in cases of postsurgical dysphagia. Relaxation of the upper esophageal sphincter indicates coordinated muscle movement between the pharynx and esophagus. Dysfunction of the pharyngoesophageal segment may lead to cricopharyngeal achalasia. A dyskinetic sphincter commonly represents an extrapharyngeal cause: i.e., disease associated with gastroesophageal reflux. Disorders of the esophageal phase of deglutition can produce retrosternal pain, heartburn, regurgitation and vomiting, as well as laryngeal and respiratory signs. Esophageal motility disorders include lower achalasia, tumors, peptic strictures, inflammatory diseases, drug-induced ulcers, rings and webs. Motility disorders present with aperistaltic, spontaneous contractions, diffuse esophagospasm, or a hypermotile esophagus. Gastroesophageal reflux with esophagitis must always be excluded, especially in patients with a globus sensation. The multiple features of the appearance of the symptoms of dysphagia and globus makes multidisciplinary approach necessary in order to establish a diagnosis and begin effective treatment.
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PMID:[Deglutition disorders]. 977 28


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