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 44-year-old woman who suffered from biliary-type pain after cholecystectomy, dysphagia, and weight loss. Examinations revealed sphincter of Oddi dysfunction (SOD) and achalasia. Complete relief of symptoms was achieved by endoscopic sphincterotomy and pneumatic dilation of the distal esophagus. This case report demonstrates for the first time the concomitant manifestation of two motility disorders of the upper gastrointestinal tract, i.e. achalasia and SOD. At present, any causal relationship seems speculative; however, both diseases were successfully treated using endoscopic procedures.
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PMID:Concomitant manifestation of achalasia and sphincter of Oddi dysfunction. 1127 21

Esophageal Heller myotomy and a partial antireflux procedure for achalasia are the ideal procedures to benefit from the advances in minimally invasive surgery. The magnified view of the operative field provided by the laparoscope allows precise division of the esophageal muscle fibers with excellent results. Laparoscopic Heller myotomy results in reduced postoperative pain, less morbidity, shorter hospitalization, better resolution of dysphagia, and less postoperative heartburn when compared with the open abdominal and even the thoracoscopic approach. A longer myotomy especially at the distal end, and a loose, well-formed partial fundoplication are the keys to a successful outcome. Superior long-term results after surgical myotomy when compared with nonsurgical interventions argue strongly in favor of surgery in any patient who is fit enough to undergo general anesthesia.
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PMID:Laparoscopic myotomy: technique and efficacy in treating achalasia. 1131 66

Non-cardiac-chest-pain is frequently associated with esophageal diseases. Gastroesophageal reflux disease (GERD) is present in 60%, esophageal motility disorder in 40-50%, tumours in 5-10% and achalasia in 5% of such cases. Diagnosis is based on endoscopy and in patients with no endoscopy findings on 24-h esophageal pH-monitoring. GERD can present with various symptoms and can best be managed with proton pump inhibitors (PPI). Considering increased mortality and morbidity operation should only be performed in special situations. Esophageal motility disorders most frequently produce retrosternal pain. Pain in achalasia may not respond to standard therapy. Motility disorders and achalasia are diagnosed by perfusion manometry and videofluoroscopy. If a tumour is suspected diagnosis is made by endoscopy (biopsy, endosonography) and radiology.
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PMID:[Thoracic pain from the viewpoint of the gastroenterologist: diagnosis and therapy]. 1145 75

Disorders of the oesophagus present a diagnostic and therapeutic challenge. The presenting symptoms of dysphagia, reflux, pain and vomiting are almost universal, irrespective of the underlying pathology. A combination of endoscopy, barium studies, pH studies and manometry are often required to determine the exact diagnosis and to plan the most effective treatment. Paraoesophageal hiatal hernia is an uncommon condition, present in 14% of all hiatal hernias, which requires urgent correction to prevent life-threatening complications. It is unusual for other oesophageal disorders to coexist. We present a case where achalasia and a paraoesophageal hiatal hernia probably coexisted.
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PMID:Coexisting achalasia and paraoesophageal hiatal hernia. 1178 83

The past decade has seen major advances in the pharmacological understanding of the nervous system of the gastrointestinal tract, the enteric nervous system, and its importance for gut functions in several states of disease. Indeed, the enteric nervous system has become a promising target in the treatment of many gastrointestinal symptoms and disorders. Some of these new therapeutic concepts, such as botulinum toxin for achalasia and serotonergic drugs for functional bowel diseases, are already in clinical use. This paper is part 3 of three Minireviews in Pharmacology & Toxicology, and presents the neurogastrointestinal pharmacological therapeutic options in gastrointestinal pain, functional gastrointestinal disorders, inflammatory bowel diseases, cancer and related conditions with focus on future drug targets. The diagnosis of gastrointestinal neuropathy, the role of serotonin and related neuroendocrine transmitters, serotonergic drugs, and neurotrophic factors in neurogastrointestinal pharmacology will be addressed in this context.
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PMID:The enteric nervous system III: a target for pharmacological treatment. 1282 68

Noncardiac chest pain is a heterogeneous condition for which diagnosis and treatment are challenging. Research is needed to streamline evaluation to minimize unnecessary invasive testing and costs. Chest pain clinics to assess chest pain patients are popular in the United States and may be of value in reassuring patients and reducing presentation to hospital; however, recently this has been contended [111]. Options for the effective treatment of NCCP are dependent on the risk of an adverse outcome and the cost-effectiveness of the management algorithm that is followed. Most (64%) of those presenting to the emergency department with chest pain are classified as having NCCP [112,113]. GERD is probably the most important cause and application of a test of acid suppression with a high-dose PPI for 1 to 2 weeks seems to be a useful diagnostic tool. In those patients with GERD-related NCCP, short-term and potentially long-term therapy with a PPI (commonly higher than standard dose) is required to alleviate symptoms. Esophageal dysmotility is relatively uncommon in patients with NCCP and evaluation by esophageal manometry might be limited to rule out achalasia. Chest wall syndromes are common but probably often missed. Many patients with NCCP have psychologic or psychiatric abnormalities, as either the cause or an effect of the chest pain, but diagnosis here depends on techniques not applied easily in the acute situation. Pain modulators seem to offer significant improvement in chest pain symptoms for non-GERD-related NCCP. Finally, trials of management strategies to deal with this problem are required urgently, because the earlier discharge of patients with NCCP may exacerbate the problem. Fig. 2 provides a flow chart for diagnosis and treatment of NCCP.
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PMID:Noncardiac chest pain: evaluation and treatment. 1285 5

The pathogenesis of achalasia involves the degeneration of enteric and autonomic nervous systems with resultant effects on esophageal motility. The neural degeneration could affect visceral sensation in achalasia. The aim of this study was to examine mechanosensitivity and chemosensitivity in patients with achalasia. Perceptual responses to esophageal distension and acid perfusion were assessed in nine achalasia patients and nine healthy subjects. Mechanosensitivity was evaluated using a barostat with a double-random staircase distension protocol. Responses were graded as follows: 0, no sensation; 1, initial sensation; 2, mild discomfort; 3, moderate discomfort; and 4, pain. Chemosensitivity was graded along a visual analog scale after perfusion of saline and 0.1 N HCl. Barostat pressure-volume relationships were used to report esophageal body compliance. Barostat pressures for initial sensation and mild discomfort were not significantly different for patients and controls. The pressures for moderate discomfort (37.9 +/- 3.5 vs. 25.7 +/- 2.4 mmHg; P < 0.05) and pain (47.8 +/- 2.3 vs. 32.2 +/- 3.5 mmHg; P = 0.002) were significantly higher in achalasics than controls. Seven of the eight achalasia patients never reached pain thresholds at the maximum distension pressure (50 mmHg). Sensation to acid perfusion was significantly lower in achalasics compared with controls (2.2 +/- 1.2 vs. 6.7 +/- 1.7 cm; P < 0.05). Compliance was significantly increased in patients with achalasia compared with controls. We conclude that both mechanosensitivity and chemosensitivity are significantly diminished in achalasia patients compared with controls. Also, initial sensation and pain sensation are differentially affected in achalasics. These findings suggest that neuropathic defects in achalasia may manifest themselves in visceral sensory and motor dysfunction.
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PMID:Diminished mechanosensitivity and chemosensitivity in patients with achalasia. 1461 20

Hypertensive lower esophageal sphincter (LES) is an uncommon manometric abnormality found in patients with dysphagia and chest pain, and is sometimes associated with gastroesophageal reflux disease (GERD). Preventing reflux by performing a fundoplication raises concerns about inducing or increasing dysphagia. The role of myotomy in isolated hypertensive LES is also unclear. The aim of this study was to determine the outcome of surgical therapy for isolated hypertensive LES and for hypertensive LES associated with GERD. Sixteen patients (5 males and 11 females), ranging in age from 39 to 89 years, with hypertensive LES (>26 mm Hg; i.e., >95th percentile of our control population) who had surgical therapy between 1996 and 1999 were reviewed. Patients with a diagnosis of achalasia and diffuse esophageal spasm were excluded. All patients had dysphagia or chest pain. Eight of 16 patients had symptoms of GERD, four had a type III hiatal hernia, and four had isolated hypertensive LES pain. Patients with hypertensive LES and GERD or type III hiatal hernia had a Nissen fundoplication, and those with isolated hypertensive LES had a myotomy of the LES with partial fundoplication. Outcome was assessed as follows: excellent if the patient was asymptomatic; good if symptoms were present but no treatment was required; fair if symptoms were present and required treatment; and poor if symptoms were unimproved or worsened. All patients were contacted by telephone for symptom assessment at a median of 3.6 years (range 3 to 6.1 years) after surgery. Patients with hypertensive LES and GERD or type III hiatal hernia had significantly lower LES pressure than those with isolated hypertensive LES (29.9 vs. 47.4 mm Hg; P=0.013). Dysphagia and chest pain were relieved in all patients at long-term follow up. Outcome was excellent in 10 of 16, good in 3 of 16, and fair in 3 of 16. All patients but one were satisfied with their outcome. Patients with hypertensive LES are a heterogeneous group in regard to symptoms and etiology. Treatment of patients with hypertensive LES should be individualized. A Nissen fundoplication for hypertensive LES with GERD or type III hiatal hernia relieves dysphagia and chest pain suggesting reflux as an etiology. A myotomy with partial fundoplication for isolated hypertensive LES relieves dysphagia and chest pain suggesting a primary sphincter dysfunction.
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PMID:Surgical management of hypertensive lower esophageal sphincter with dysphagia or chest pain. 1467 8

FROM AN ETIOLOGICAL POINT OF VIEW: Thoracic pain is a frequent symptom. Before confirming the oesophageal origin of the pain, a coronary disease must be excluded. Two principle causes are source of thoracic pain of oesophageal origin: gastro-oesophageal reflux disease and oesophageal motility abnormalities. THE DIAGNOSTIC APPROACH: This must include the questioning of the patient and the usual paraclinical examinations. To confirm the diagnosis, these examinations must establish a chronological relationship between the symptoms and the abnormalities. For economic reasons, following a normal gastroscopy, there is a tendency to propose an empirical proton pump inhibitor (PPI) test rather than a 24 hour pH-metry antireflux as first line. The improvement or even the disappearance of the symptoms confirms the diagnosis; long-term treatment with a double dose of PPI should therefore be envisaged. The pH-metry with search for results should be proposed to the non-responders and to patients with atypical reflux manifestations. Dysphagia and odynophagia suggest an oesophageal motility disorder that basal manometry should confirm. A chronological relationship is rarely revealed, but the sensitivity of the pH-meter can be enhanced by provocation tests. REGARDING TREATMENT: Other than achalasia, treatment of the other spastic-like motor disorders is not well codified. Diltiazem is efficient. Some patients exhibit a hyperalgic oesophagus. The physiopathological mechanisms are still theoretical. Low dose tricyclic antidepressors and psychological management are useful.
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PMID:[Thoracic pain of oesophageal origin. Diagnostic management and treatment]. 1471 71

Since its introduction in the late 1970s for the treatment of strabismus and blepharospasm, botulinum toxin (BoNT) has been increasingly used in the interventional treatment of several other disorders characterized by excessive or inappropriate muscle contractions. The use of this pluripotential agent has extended to a plethora of conditions including: focal dystonia; spasticity; inappropriate contraction in most sphincters of the body such as those associated with spasmodic dysphonia, esophageal achalasia, chronic anal fissure, and vaginismus; eye movement disorders; other hyperkinetic disorders including tics and tremors; autonomic disorders such as hyperhidrosis; genitourinary disorders such as overactive and neurogenic bladder, non-bacterial prostatitis and benign prostatic hyperplasia; and aesthetically undesirable hyperfunctional facial lines. In addition, BoNT is being investigated for the control of the pain, and for the management of tension or migraine headaches and myofascial pain syndrome. BoNT injections have several advantages over drugs and surgical therapies in the management of intractable or chronic disease. Systemic pharmacologic effects are rare; permanent destruction of tissue does not occur. Graded degrees of relaxation may be achieved by varying the dose injected; most adverse effects are transient. Finally, patient acceptance is high. In this paper, clinical experience over the last years with BoNT in urological impaired patients will be illustrated. Moreover, this paper presents current data on the use of BoNT to treat pelvic floor disorders.
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PMID:Management of bladder, prostatic and pelvic floor disorders with botulinum neurotoxin. 1572 17


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