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)

We report the case of a 74-year-old woman who presented with a 2-year history of dysphagia, weight loss, nausea, and vomiting. She was diagnosed as having secondary achalasia due to external compression probably by a tumor of the lower part of the esophagus. At autopsy, however, no tumor was found at that site, whereas a pancreatic microcystic serous adenoma and multiple gastric leiomyomata--one of which occupied the pyloric sphincter area leading to gastric outlet obstruction--were noted. The esophagus displayed two fusiform dilatations located at the lower and midportions, the latter being associated with rupture and necrosis of the muscularis and adventitial wall layers. The lower dilatation showed only attenuation of the muscularis, without necrosis. The epithelium was intact in both dilatations. This was an unusual series of pathogenetic events, leading from gastric outlet obstruction to secondary achalasia and protracted vomiting, followed by spontaneous partial esophageal wall rupture (a variant of intramural hematoma) or atrophy of the muscularis, morphologically evident as fusiform dilatations.
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PMID:Fusiform dilatations of the esophagus secondary to protracted distention and emetogenic injury. 834 53

Secondary achalasia refers to the development of clinical, radiographic, and manometric findings of achalasia as a result of (i.e., secondary to) another underlying disorder. A variety of malignancies have been associated with secondary achalasia. Adenocarcinoma of the esophagogastric junction accounts for the majority of cases of malignancy-induced achalasia, however, noncontiguous tumors may also cause this disorder. Although rare, malignancy-induced achalasia will occasionally be encountered by gastroenterologists and gastrointestinal radiologists who see patients with dysphagia and/or achalasia. Since treatment is aimed at the underlying neoplasm, it is important to recognize this disorder. Three clinical features suggest the possibility of malignancy as a cause of achalasia: 1) short duration of dysphagia (< 1 year); 2) significant weight loss (> 15 pounds); and 3) age > 55 years. The presence of any of these should at least raise a suspicion of malignancy. Diagnosis may not be evident on routine esophagrams and endoscopy, and requires clinical suspicion for further evaluation with thoraco-abdominal CT scanning and endoscopic ultrasonography.
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PMID:Malignancy-induced secondary achalasia. 800 10

History taking is the first step in the evaluation of a patient. An analysis of the information obtained provides the basis for the choice and order of diagnostic tests. In addition, it provides the clinician with the necessary information to determine the relevance of "abnormal tests" to the patient's problem. Dysphagia is a reliable symptom that indicates an abnormality in the swallowing mechanism. The history should contain a detailed description of the symptoms associated with dysphagia from the onset. Especially relevant are questions to determine if dysphagia is experienced every day or intermittently, with solid food or liquids or both, as well as presence and timing of associated symptoms such as, choking, coughing and regurgitation, changes in speech, heartburn and chest pain. It is clinically useful to divide swallowing into three phases: oral, pharyngeal and esophageal. Oral dysphagia is usually due to a neurologic disorder, decreased salivary flow or painful oropharyngeal lesions. Pharyngeal dysphagia is most frequently caused by neuromuscular disorders and less frequently by a Zenker's diverticulum, neoplasm or a mucosal web. Esophageal dysphagia is caused by a structural narrowing, such as produced by a peptic stricture, neoplasm or a Schatzki's ring or by a primary motility abnormality, such as achalasia or diffuse esophageal spasm or by motility abnormalities produced by inflammation caused by gastroesophageal reflux, medication-induced esophageal ulceration or infectious esophagitis.
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PMID:Art and science of history taking in the patient with difficulty swallowing. 846 26

It was only the endoscopic ultrasonography that allowed the esophagus and posterior mediastinum to be accessible to ultrasonography. The esophageal wall may be presented in its different anatomic layers to a degree of precision unattained by any other imaging procedure. Being important in the esophagus, both the upper rim of the tumor and the infiltration depth can this way be prognosed correctly to about 85%. In consequence, this allows proceedings appropriate to the tumor stage within the bounds of a multimodal therapeutic concept of esophagus carcinomas. Impressions of the esophagus caused by mediastinal tumors are safely distinguished from intramural tumors. Multiple biopsies to get an examination specimen from a deeper layer should be performed under no other conditions than after endoscopic ultrasonographic examination and just for special questions. In the differential diagnosis of achalasia and peptic stenosis of the esophagus, endoscopic ultrasonography proved to be less efficient. As for bronchial carcinomas, conclusive hints may be drawn from transesophageal and intratracheal ultrasonography. However, due to limited possibilities of judgment caused by air-containing structures these methods are not firmly established in the preoperative staging.
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PMID:[Endosonography of the esophagus and mediastinum]. 858 80

Carcinosarcoma of the esophagus is a rare malignant neoplasm that consists of both carcinomatous and sarcomatous elements. The histogenesis of the sarcomatous component is generally considered to result from metaplasia of carcinomatous cells toward mesenchymal differentiation. True carcinosarcoma, characterized as a collision between a carcinoma and a sarcoma, is extremely rare. We describe a patient with primary achalasia who developed a true carcinosarcoma of the esophagus in which clonal differences between carcinomatous and sarcomatous elements were genetically and immunohistochemically demonstrated. A polypoid tumor located in the middle third of the esophagus developed in a 51-year-old man with longstanding achalasia. The tumor was predominantly composed of spindle-shaped sarcomatous cells. Squamous cell carcinoma in situ and islands of well-differentiated squamous cell carcinoma in the sarcomatous element were histologically observed. The sarcomatous element was immunoreactive for both mesenchymal and myoid markers. The carcinomatous component expressed type I and type II cytokeratins as well as epithelial membrane antigen. Analysis for chromosomal loss of heterozygosity performed in multiple microdissected samples of each sarcomatous and carcinomatous element revealed distinct genetic clonalities. These differences in immunohistochemical and genetic clonalities suggest that the tumor composed of squamous cell carcinoma and leiomyosarcoma originated separately from epithelial and mesenchymal precursors.
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PMID:Esophageal carcinosarcoma: a genetic analysis. 928 91

This was a retrospective analysis of 177 histologically confirmed cases of oesophageal carcinoma seen in the University College Hospital, Ibadan, Nigeria over a period of 30 years. Oesophageal carcinoma constituted 0.6 per cent of all malignant neoplasms and 1.4 cases per 1000 surgical biopsies during the study period. Dysphagia and weight loss were the most common clinical manifestations. Ninety three patients presented within one year of onset of clinical symptoms. The peak age incidence occurred in the seventh decade of life. Sex distribution was equal. The middle third of the oesophagus was the most common location of the neoplasm and the vast majority (94.5%) were squamous cell carcinomas. Achalasia of the cardia and Barrett's oesophagus were not associated with oesophageal carcinoma in this study. Regional lymph nodes and lungs were the most common sites of metastasis. Surgical complications included mediastinitis and bronchopneumonia, both occurring within seven days postoperatively. Late clinical presentation and high postoperative mortality are responsible for the persistently poor prognosis of oesophageal carcinoma despite significant advances in the diagnosis and management of these neoplasms.
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PMID:Carcinoma of the oesophagus in Ibadan. 933 9

Type 1 antineuronal nuclear autoantibody (ANNA-1, also known as "anti-Hu") is a marker of neurologic autoimmunity that is highly associated with small-cell lung carcinoma (SCLC). To determine the spectrum of symptoms and signs as well as the frequency of cancer in adult patients who are seropositive for ANNA-1, we reviewed 162 sequential patients (67% female) identified as ANNA-1-positive in a comprehensive immunofluorescence screening test. In 21% of these patients, the antibody test requested by the physician was not ANNA-1. By the end of the follow-up period, cancer had been found in 142 patients (88%). Ten of these lacked evidence of SCLC (4 had prostate carcinoma, 3 breast carcinoma, 1 both prostate carcinoma and melanoma, 1 lymphoma, and 1 squamous-cell lung carcinoma). Of the 132 patients (81%) with proven SCLC, 17 had one or more coexisting malignant neoplasms (6 had renal carcinoma, 4 another lung primary carcinoma, 3 prostate carcinoma, 3 breast carcinoma, and 4 assorted neoplasms). The diagnosis of SCLC in 128 patients (97%) followed the onset of paraneoplastic symptoms. SCLC was identified in 10 patients by chest MRI after an equivocal chest radiograph or CT; in 28 by bronchoscopy, mediastinoscopy, or thoracotomy; and in 7 at autopsy. Neurologic signs in decreasing frequency were neuropathy (sensory > mixed somatic > autonomic > cranial [especially cranial nerve VIII] > motor), cerebellar ataxia, limbic encephalitis, polyradiculopathy, associated Lambert-Eaton myasthenic syndrome, myopathy, myelopathy, opsoclonus/myoclonus, motor neuronopathy, brachial plexopathy, and aphasia. Nineteen patients had a solely gastrointestinal initial presentation, including gastroparesis, pseudo-obstruction, esophageal achalasia, or other dysmotility. We conclude that seropositivity for ANNA-1 can expedite the diagnosis and treatment of otherwise occult cancer in patients, especially tobacco abusers, with varied neurologic and gastroenterologic presentations. The search for SCLC should not end on discovering a different neoplasm.
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PMID:Paraneoplastic and oncologic profiles of patients seropositive for type 1 antineuronal nuclear autoantibodies. 952 Dec 51

Esophageal achalasia (EA) is a rare disease in man and animals and there are many discussions on its higher risk of esophageal cancer. N-Amyl-N-methylnitrosamine (AMN) which specifically induces esophageal tumors in mice and rats was given to three mutant mouse strains, i.e. 101/N, STX/Le and BXH-8, which develop a high incidence of EA. The incidence of EA in 101/N, STX/Le, BXH-8 and normal C57BL/6J mice was 38.5% (110/286), 30.1% (43/143), 91.8% (190/207) and 0% (0/167), respectively. The average numbers of AMN-induced esophageal tumors in EA(+) were significantly higher than those of EA(-) in all of the 101/N, STX/Le and BXH-8 mice. Furthermore, significantly larger size tumors and invasive squamous cell carcinomas were found in EA(+) mice than in EA(-) mice. These results indicate the higher sensitivity of EA for both tumor induction and promotion, possibly due to the longer retention of AMN. In fact, relaxation of the lower esophagus by a smooth muscle relaxing calcium-channel blocker, nicardipine hydrochloride, significantly prevented the induction of esophageal tumors.
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PMID:High incidence of esophageal cancer in esophageal achalasia by the oral administration of N-amyl-N-methylnitrosamine and its prevention by nicardipine hydrochloride in mice. 961 58

Using endosonography, esophageal wall thickening is commonly observed in patients with achalasia. Imaging artifacts with the endosonographic appearance of an esophageal tumor in some patients with achalasia suggest that endosonographic images must be interpreted with caution. The endosonographer must be aware of anatomical peculiarities (dilated, tortuous, or "sigmoid" esophagus) and imaging techniques (tangential imaging) that may lead to artifactual imaging, and thereby avoid misinterpretation of results. Failure to recognize such imaging artifacts may lead to an erroneous diagnosis of pseudoachalasia, thereby subjecting patients to unnecessary surgery. Future applications of endoscopic ultrasonography for patients with achalasia may include endosonographically guided therapy. Prospective analyses of EUS-guided therapy are anticipated.
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PMID:Endosonographic evaluation of the patient with achalasia. 976 84

Endoscopic ultrasound (EUS) of the esophagus has been used primarily in staging biopsy-proven cancers. Its use as a primary diagnostic modality for esophageal malignancy has not been previously described. We report our recent experience in four patients with dysphagia and endoscopic biopsies negative for malignancy, including one patient with clinical and manometric features suggestive of achalasia. In all cases, EUS revealed a large infiltrating tumor invading through the esophageal wall into the surrounding tissues, and in one case into the aorta. Computed tomography suggested the possibility of a tumor in only one of the cases. Two patients underwent esophagectomy and were found to have adenocarcinoma. Two patients underwent repeat biopsy with alternative aggressive biopsy techniques and were found to have squamous cell carcinoma. We conclude that EUS is useful in the diagnosis of esophageal cancer and should be performed in selected patients with esophageal strictures whose biopsies are negative for malignancy; i.e., those with suspicious endoscopic or radiographic appearance, atypical presentation (e.g., profound weight loss, short duration of symptoms, or advanced age), and failure to respond to treatment.
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PMID:Biopsy-negative malignant esophageal stricture: diagnosis by endoscopic ultrasound. 982 Apr 10


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