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

Anorexia nervosa (AN) and bulimia nervosa (BN) are potentially fatal eating disorders which primarily affect adolescent females. Differentiating eating disorders from primary gastrointestinal (GI) disease may be difficult. GI disorders are common in eating disorder patients, symptomatic complaints being seen in over half. Moreover, many GI diseases sometimes resemble eating disorders. Inflammatory bowel disease, acid peptic diseases, and intestinal motility disorders such as achalasia may mimic eating disorders. However, it is usually possible to distinguish these by applying the diagnostic criteria for eating disorders and by obtaining common biochemical tests. The primary features of AN are profound weight loss due to self starvation and body image distortion; BN is characterized by binge eating and self purging of ingested food by vomiting or laxative abuse. GI complications in eating disorders are common. Recurrent emesis in BN is associated with dental abnormalities, parotid enlargement, and electrolyte disturbances including metabolic alkalosis. Hyperamylasemia of salivary origin is regularly seen, but may lead do an erroneous diagnosis of pancreatitis. Despite the weight loss often seen in eating disorders, serum albumin, cholesterol, and carotene are usually normal. However, serum levels of trace metals such as zinc and copper often are depressed, and hypophosphatemia can occur during refeeding. Patients with eating disorders frequently have gastric emptying abnormalities, causing bloating, postprandial fullness, and vomiting. This usually improves with refeeding, but sometimes treatment with pro-motility agents such as metoclopromide is necessary. Knowledge of the GI manifestations of eating disorders, and a high index of suspicion for one condition masquerading as the other, are required for the correct diagnosis and management of these patients.
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PMID:Gastrointestinal and nutritional aspects of eating disorders. 840 9

A careful history can localize gastrointestinal motility disorders and suggest appropriate diagnostic tests. Dysphagia, odynophagia, heartburn and reflux have esophageal origins. The same symptoms occur in achalasia, a classic motor disorder of the lower esophageal sphincter, which can be diagnosed by barium swallow, endoscopy and esophageal motility studies. Nausea, vomiting, anorexia, bloating and abdominal pain are symptoms of motor disorders of the stomach and small intestine. When these symptoms are accompanied by unexplained right upper quadrant pain, elevated liver enzyme levels and unexplained recurrent pancreatitis, the diagnosis of impaired biliary motility is suggested. Colorectal motility disorders may present as abdominal pain, diarrhea, constipation and/or fecal incontinence. If symptoms do not resolve with dietary changes and appropriate medications and the anatomy is normal on lower gastrointestinal studies, colorectal motility studies may be indicated.
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PMID:Gastrointestinal motility disorders. 859 65

Achalasia is a motility disorder of the esophagus characterized by absence of normal peristalsis and failure of relaxation of the lower esophageal sphincter. Among the most common clinical findings are vomiting and weight loss. Roentgenographically, a narrowed gastroesophageal junction and dilated esophagus are observed. This condition is uncommon in children. Here a seven-year old female patient with achalasia is reported.
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PMID:Childhood achalasia. 882 12

Dysphagia and vomiting are frequently present in untreated Addison's disease. These non-specific symptoms may be due either to the metabolic disorder and myopathy or to disorders associated with Addison's disease. We describe a patient with autoimmune adrenal failure as a feature of autoimmune polyglandular syndrome (APS) type II. This patient was referred initially because of megaoesophagus. The association of megaoesophagus with Addison's disease or any of the three types of APS has not previously been described in humans. The association of megaoesophagus and adrenal failure, however, is known to occur in Allgrove's syndrome, a disease with primary manifestation in childhood characterized by adrenal failure, achalasia and alacrimia. Moreover, there are several reports on the association of megaoesophagus with adrenocortical insufficiency and other autoimmune endocrine diseases in dogs. Vomiting and dysphagia usually resolve with hormone substitution in patients with isolated Addison's disease. In our patient these symptoms disappeared in spite of the radiological persistence of megaoesophagus, which might have been overlooked if the diagnosis of Addison's disease had been made earlier. The occurrence of megaoesophagus might be more common than previously suspected and we suggest a systematic search for similar findings in other patients with autoimmune Addison's disease, even when minor dysphagia is present.
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PMID:Megaoesophagus in a patient with autoimmune polyglandular syndrome type II. 895 91

From 1974 to 1995, 19 children with achalasia of the esophagus have been treated at our institution. Presenting symptoms included vomiting (n = 14), dysphagia (n = 13), failure to thrive (n = 6), and odynophagia (n = 1). Diagnosis was established by a barium swallow in 19, with eight also undergoing esophageal manometry. Six boys and 13 girls with an average age of 10 years (range, 1.3 to 17.6) underwent a transthoracic, modified anterior Heller esophagomyotomy (HM). Five underwent a concomitant, modified, Belsey fundoplication (BF). Follow-up ranging from 6 months to 21 years (mean, 9 years) was accomplished in all 19 patients by both office visits and telephone interviews. Early postoperative follow-up showed initial swallowing difficulty in two (14%) patients with a HM alone and in four out of five (80%) patients treated with a HM and BF. All patients (n = 5) with a HM and BF and one with a HM alone required one esophageal dilation during the first postoperative year. These initial swallowing difficulties resolved in all six patients during this first postoperative year. Late postoperative follow-up, however, indicates occasional, mild dysphagia in two out of five with an HM and BF resulting in complete relief of presenting symptoms in 17 of the 19 patients (90%). All patients rated their overall result as either excellent (68%) or good (32%) with none rating it as fair or poor. None of the 19 patients had clinical evidence of gastroesophageal reflux, although five patients had evidence of nonpathologic reflux noted during upper gastrointestinal x-ray. Recurrent vomiting, asthma, wheezing, or esophagitis symptoms have not been reported by any patients. No patients required reoperation, and there were no deaths or postoperative complications. Modified Heller esophagomyotomy is safe (0% mortality) and effective (90% relief of symptoms) in children with achalasia. A concurrent modified Belsey fundoplication results in early and late mild postoperative dysphagia that was responsive to esophageal dilation. The transthoracic, modified Heller esophagomyotomy without a fundoplication is currently our treatment of choice for achalasia in children.
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PMID:Efficacy of the transthoracic modified Heller myotomy in children with achalasia--a 21-year experience. 904 49

Seven children with achalasia cardia, six of them infants, were seen over a 10-year period. In infantile achalasia, respiratory symptoms predominate and vomiting may easily be mistaken for gastroesophageal reflux (GER). Vomiting of uncurdled milk is characteristic of achalasia. Six children underwent esophagocardiomyotomy with good results in five. The procedure was transthoracic in two and transabdominal combined with an anterior fundoplication in the others. There was one post-operative death. Achalasia and alacrima were associated in two infants. One baby with this association also had a neurogenic bladder.
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PMID:Achalasia cardia in infancy and childhood: an Indian experience. 962 34

The purpose of this study was to retrospectively evaluate the radiologic findings in young adults with dysphagia undergoing barium swallow and to compare these with the final clinical diagnosis. Clinical history, barium swallow, endoscopy (21 patients), manometry (18 patients), 24 h pH monitoring (4 patients), and outcome of treatments were studied and compared in 43 patients aged 14-30 years (mean 24 years). There were 26 men and 17 women. Duration of symptoms varied between 2 weeks and 22 years and included globus (n = 22), obstruction (n = 31), water brash (n = 6), classic reflux symptoms (n = 10), atypical reflux symptoms (n = 9), slow eating (n = 6), and vomiting (n = 11). The final diagnosis was achalasia (n = 2), arteria lusoria (n = 1), esophagitis (n = 1), esophageal dysfunction (n = 11), esophageal stricture (n = 5), gastroesophageal reflux disease (n = 8), and pharyngeal dysfunction (n = 2). Thirteen patients were assessed to be normal. The result of the barium swallow was in agreement with the final diagnosis in all but 3 patients who were assessed as normal, and the final diagnosis was esophagitis (n = 1), dysmotility (n = 1), and reflux disease (n = 1). Anatomic and functional abnormalities are common in young adults with dysphagia. Barium swallow reveals the explanation of the symptoms in 70% of such patients. Radiology therefore should be the method of choice for the investigation of dysphagic young adults.
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PMID:Clinical and radiologic evaluation reveals high prevalence of abnormalities in young adults with dysphagia. 971 50

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

Surgical treatment of cardiac achalasia in children is still the main line of treatment with a success rate of 70-80%. Balloon dilatation is less widely used due to inappropriate size of balloons. The authors report on their experience in 11 children with cardiac achalasia over the last 7 years using balloon dilatation as the treatment of choice, 8 boys and 3 girls with ages ranging from 1.5-14 years (average 7.5 years) were investigated. One family (brother and sister) presented with no glucocorticoid deficiency or other anomalies, one patient had mental retardation, the rest had no associated anomalies. All patients presented with vomiting, 7 with dysphagia, 6 with loss of weight, 5 with recurrent chest infection and 2 with retrosternal pain. Radiological diagnosis was accurate in all patients, endoscopy with biopsy were done to confirm diagnosis and exclude other pathology, manometry yielded positive results in 4 patients. Dilatation was done under general anesthesia with fluoroscopic control, balloons were used over a guide wire (balloon sizes were 18-35 mm). Seven patients had 2 sessions and 4 had 3 sessions with radiological follow-up after the second dilatation. Follow-up ranged from 2-7 years: excellent results were achieved in 8 patients (72.7%) with disappearance of symptoms and marked radiologic improvement, 2 still have mild symptoms with overall success (90.9%), one had mild gastroesophageal reflux, controlled medically, and one had mild dysphagia but his status was improved compared to that before dilatation. One patient had recurrent dysphagia necessitating cardiomyotomy (9.1%). Results were not related to age or sex. The authors recommend balloon dilatation in children with cardiac achalasia as the treatment of choice or even as the only feasible treatment.
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PMID:Cardiac achalasia in children. Dilatation or surgery? 1058 88

Anorexia nervosa and psychogen vomiting are psychiatric eating disorders characterized by unexplained weight loss and induced vomiting. These diagnoses require absence of somatic disease. Achalasia is a primary disorder of the esophagus that can be responsible for the same symptoms. This may occult the real diagnosis, especially as dysphagia is not constant and variable in time. We report four cases of achalasia mistakenly diagnosed and treated as anorexia nervosa or psychogen vomiting. Achalasia was unrecognized because specific symptoms, such as dysphagia, were overlooked or misinterpreted by the patients' physicians and psychiatrists, or by the patients themselves. In patients with such eating disorders considered to be psychiatric, physicians should inquire about signs suggestive of achalasia. The diagnosis of achalasia is suspected by imaging and endoscopy, and confirmed or ruled out by manometry.
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PMID:[Achalasia mimicking psychiatric eating disorders]. 1139 78


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