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)

In order to test the hypothesis that esophageal achalasia may be due to neurotropic viral damage to the esophageal myenteric plexus, esophageal tissue with or without achalasia was analyzed by polymerase chain reaction for the presence of human herpes virus DNA or measles virus RNA. The DNA and RNA were extracted from the esophageal muscle of 12 patients with achalasia and six patients with upper esophageal carcinoma. Peripheral blood mononuclear cells from eight adult volunteers and two samples of umbilical blood mononuclear cells were also used as controls. PCR amplification with a pair of primers specific for herpes simplex type 1 and 2 viruses identified 92-bp fragments in nearly all specimens, including those without achalasia. Each 92-bp fragment was confirmed to be identical to a single herpes simplex virus sequence by automated DNA sequence analysis. No amplification for five other herpes viruses or measles virus was detected. Therefore, a specific viral etiology for achalasia was not identified in this study.
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PMID:Are human herpes viruses or measles virus associated with esophageal achalasia? 772 Apr 82

In a search for past or present infection with herpes viruses, serum antibody titres to herpes simplex type 1 virus, cytomegalovirus, and varicella-zoster virus were measured by complement fixation test in 58 patients with achalasia. Serum was also taken from 40 age and sex matched patients without oesophageal symptoms who formed a control group. All titres were low, and those for herpes simplex type 1 virus and cytomegalovirus did not differ in the achalasia patients and the controls. However, the incidence of varicella-zoster virus antibodies was significantly greater in the achalasia than in the control group (p < 0.05). Using oesophageal tissue containing myenteric plexus removed at the time of cardiomyotomy in nine patients with achalasia, in situ DNA hybridisation showed evidence of varicella-zoster virus in three, but all were negative for the other two viruses. No positive results were obtained for herpes simplex type 1 virus, cytomegalovirus, or varicella-zoster virus in oesophageal tissue from 20 patients undergoing oesophageal resection for diseases other than achalasia. The incidence of positivity for varicella-zoster virus was significantly increased in the achalasia group compared with the controls (p < 0.02). The findings indicate that varicella-zoster virus DNA may persist in the oesophageal myenteric plexus in some patients with achalasia and raise the possibility that this virus is of aetiological importance in achalasia.
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PMID:Varicella-zoster virus DNA in the oesophageal myenteric plexus in achalasia. 838 30

Achalasia is an esophageal motility disorder of unknown etiology. Several studies suggest possible herpes or measles virus etiology, but results are inconclusive. The aim of this study was to test whether herpesvirus (HV), measles (MV), or human papilloma virus (HPV) sequences could be detected in myotomy specimens from a wide spectrum of achalasia patients, using the polymerase chain reaction (PCR) technique. Myotomy specimens from 13 achalasia patients, esophagectomy specimens from nine esophageal cancer patients, and autopsy specimens from six fetuses were studied with the PCR technique. Paired oligonucleotide primers of HV (HSV-1 and 2, CMV, EBV, VZV, and HHV-6), MV and HPV sequences and exon 3 of the HPRT gene were used for the PCR DNA amplification. Amplified products were resolved on agarose gels and stained with ethidium bromide. All specimens yielded the appropriate-sized products for exon 3 of the HPRT and viral controls. No amplified products were seen in the achalasia specimens or controls corresponding to any of the virus sequences tested. The absence of HV, MV, and HPV sequences suggests that these viruses are not associated with achalasia but does not exclude the possibility of a previously unidentified virus as a causal agent. Further studies aimed at identifying an unknown viral agent as a cause for achalasia are warranted.
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PMID:Achalasia is not associated with measles or known herpes and human papilloma viruses. 905 10

Achalasia, a motor disorder of the esophagus, is characterized by myenteric plexitis leading to neuronal loss. Cytotoxic T cells, isolated from the lower esophageal sphincter of achalasia patients, respond to human herpes virus-1 (HSV-1) with gamma-IFN (and to a lesser extent IL-2) production and clonal proliferation. In addition, HSV-1 DNA was demonstrated in the vast majority of patients, but also in controls. These exciting data suggest that achalasia is an immune-mediated inflammatory disease in which a (latent) infection with HSV-1 leads to persistent immune activation and self-destruction of esophageal neurons, most likely in genetic susceptible subjects only.
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PMID:Achalasia: virus-induced euthanasia of neurons? 1855 6

Idiopathic achalasia is an archetype esophageal motor disorder, causing significant impairment of eating ability and reducing quality of life. The pathophysiological underpinnings of this condition are loss of esophageal peristalsis and insufficient relaxation of the lower esophageal sphincter (LES). The clinical manifestations include dysphagia for both solids and liquids, regurgitation of esophageal contents, retrosternal chest pain, cough, aspiration, weight loss and heartburn. Even though idiopathic achalasia was first described more than 300 years ago, researchers are only now beginning to unravel its complex etiology and molecular pathology. The most recent findings indicate an autoimmune component, as suggested by the presence of circulating anti-myenteric plexus autoantibodies, and a genetic predisposition, as suggested by observed correlations with other well-defined genetic syndromes such as Allgrove syndrome and multiple endocrine neoplasia type 2 B syndrome. Viral agents (herpes, varicella zoster) have also been proposed as causative and promoting factors. Unfortunately, the therapeutic approaches available today do not resolve the causes of the disease, and only target the consequential changes to the involved tissues, such as destruction of the LES, rather than restoring or modifying the underlying pathology. New therapies should aim to stop the disease at early stages, thereby preventing the consequential changes from developing and inhibiting permanent damage. This review focuses on the known characteristics of idiopathic achalasia that will help promote understanding its pathogenesis and improve therapeutic management to positively impact the patient's quality of life.
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PMID:New insights into the pathophysiology of achalasia and implications for future treatment. 2767 86