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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Treatment of patients with an esophageal source of chest pain remains a challenging problem. Although a variety of measures--including nitrates, anticholinergics, sedatives, calcium channel antagonists, esophageal dilation, and psychological reassurance--are available for the management of esophageal chest pain, none has emerged as the treatment of choice. Studies of nitrate preparations for the treatment of painful motility disorders are limited by a small number of patients and the lack of randomized, placebo-controlled investigations. The efficacy of anticholinergic drugs in hypercontractile esophageal motility disorders has not been reported. In the only prospective placebo-controlled trial using an anti-depressant, trazodone was superior to placebo in relieving symptoms in patients with a variety of esophageal motility disorders. Conflicting results have been described in placebo-controlled trials of the calcium channel antagonists nifedipine and diltiazem in patients with "nutcracker esophagus" or diffuse spasm. Information about the efficacy of verapamil and hydralazine is limited. Esophageal dilation has been useful in selected patients. For many patients, esophageal chest pain may be associated with gastroesophageal reflux. Treatment of these patients with nitrates, calcium channel antagonists, or anticholinergics may aggravate their reflux. The mechanisms of esophageal chest pain remain unknown. Recent studies have suggested that abnormal motility may not be the only factor associated with chest pain. An important number of patients have behavioral abnormalities, increased nociception, impaired coronary vasodilatory reserve, or a diffuse abnormality of smooth muscle. Research into rational therapy for chest pain patients should take into account the contribution of these other factors.
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PMID:Current medical therapy for esophageal motility disorders. 159 73

When a patient presents with anginalike chest pain, the first objective is to rule out heart disease. Once cardiac problems have been ruled out, the second objective is to determine whether the history and/or symptoms suggest an esophageal abnormality. The diagnosis of gastroesophageal reflux-associated chest pain can occasionally be made from barium radiographic or endoscopic findings. A series of additional esophageal tests--motility studies, Bernstein test, edrophonium test, and balloon distention test--may be performed to help ascertain whether the pain stems from the esophagus. Reassurance should precede specific drug therapy. If any of the test results suggest gastroesophageal reflux, a trial of therapy for this indication, eg, a histamine2 receptor blocker, should be initiated. An esophageal motility disorder may be treated with an anticholinergic agent, nitro-glycerinlike product, or mild tranquilizer. If necessary, use of a calcium channel blocker may be appropriate.
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PMID:Chest pain associated with esophageal disease. 335 67

We evaluated the effect of the calcium channel blocking agent, nifedipine, on esophageal dysfunction in 15 patients with progressive systemic sclerosis, using a double-blind, randomized, crossover, placebo-controlled manometric study. Nifedipine significantly decreased lower esophageal sphincter pressure in these patients; this reduced lower esophageal sphincter pressure may cause gastroesophageal reflux. Thus, nifedipine may have detrimental effects on progressive systemic sclerosis patients.
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PMID:Nifedipine and esophageal dysfunction in progressive systemic sclerosis. A controlled manometric study. 389 Aug 64

Esophageal motor disorders may be clearly primary, as in achalasia or diffuse esophageal spasm (DES), or clearly secondary, as in scleroderma or intrathoracic malignancy. In patients with gastroesophageal reflux, abnormal motility of the esophageal body and stomach, and lower esophageal spasm (LES) appear to predispose patients to reflux. It is possible that esophagitis caused by refluxed gastric material then further impairs motility, propagating the injury. Therapeutically, appropriate use of recently available medications, such as calcium channel blockers and metoclopramide, and new applications of previously available agents, such as hydralazine and bethanechol, have improved our ability to relieve symptoms and at times restore more normal motility.
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PMID:Motor disorders of the esophagus: diagnosis and treatment. 646 93

New knowledge concerning the pathophysiology of gastroesophageal reflux gives an opportunity for updating measures of conservative antireflux treatment. There are only few controlled trials, and it is uncertain whether the requirement for pharmacological treatment may hereby be diminished. General advice such as eating small meals, reducing the fat intake, avoiding food intake for three hours before bedtime are recommended to all, while advice on more specific foods should be individualized according to actual food related symptoms. Patients with annoying symptoms of reflux are advised not to consume alcohol every day, while the consumption of tobacco seems to be of minor importance. Advising weight loss isn't well founded, but ought to be given to obese patients. Elevation of the head of the bed is suggested to patients with nocturnal symptoms of reflux, which usually coincide with the presence of a hiatal hernia. If possible, revision of other current pharmacotherapy should be done. Theophylline, calcium channel blockers, benzodiazepines and nonsteroidal antiinflammatory drugs, seem in particular to be able to provoke or aggravate reflux. Patient support groups with medical supervision might be useful and reduce the number of consultations. The non-pharmacological measures should still be the basis of treatment and it might be sufficient in mild cases. It is recommended that the advise be individualized to each patient in such a way that no unfounded changes of life style are recommended that impair the quality of life. Gastroesophageal reflux, nonpharmacological treatment, food advices, alcohol, tobacco, overweight, hiatal hernia, drugs, patient education.
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PMID:[Non-pharmacological therapeutic possibilities in gastroesophageal reflux dyspepsia]. 794 Oct 49

Achalasia is a primary esophageal motor disorder characterized by lack of esophageal peristalsis and poor lower esophageal sphincter (LES) relaxation. Clinically, achalasia manifests as progressive dysphagia to solids and liquids and mild weight loss. Predisposition to esophageal cancer is not prevalent, but certain tumors may mimic achalasia. The diagnosis of achalasia is relatively easy to make with a good history, radiography, and esophageal motility testing. The esophagogram reveals a typical bird-beak narrowing of the esophagogastric junction and esophageal dilation, the degree of which depends on the stage of the disease. Esophageal manometry reveals poor LES relaxation, aperistalsis, and often elevated intraesophageal pressure. Endoscopic examination is important to rule out malignancy as the cause of achalasia. The traditional treatment of achalasia is forceful dilation of the LES. Bougienage may be helpful in some cases. Pharmacological agents, such as nitroglycerin and calcium channel blockers, provide some relief by decreasing LES pressure. However, they are not a viable, long-term choice. Surgical myotomy offers slightly better results than pneumatic dilation, but it is accompanied by some increased gastroesophageal reflux. Laparoscopic and thoroscopic myotomy are in their infancy, and, if successful, they will make surgical treatment much more attractive. Intrasphincteric botulinum toxin injection is the newest form of therapy. Its safety and ease of administration are very encouraging, but long-term results are not available.
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PMID:Achalasia. 877 90

Achalasia is an esophageal motility disorder characterized by increased lower esophageal sphincter pressure and absence of peristalsis in the lower esophagus. Patients typically present with complaints of progressive difficulty swallowing over a period of several years. Diagnosis is confirmed by esophageal manometry. Complications of achalasia include esophagitis, aspiration and possibly an increased risk of esophageal carcinoma. Medical treatment options include pneumatic dilatation, esophageal bougienage, nitrates, calcium channel blockers and botulinum toxin injections. The primary method of surgical treatment is the Heller myotomy, in which longitudinal incisions are made in the muscle fibers of the lower esophageal sphincter to reduce sphincter pressure. Frequently, a fundoplication is performed in addition to the myotomy to decrease the likelihood of development of gastroesophageal reflux. In recent years, the Heller myotomy has been performed both thoracoscopically and laparoscopically. An additional development has been the placement of an endoscope in the esophagus to provide transillumination during surgery; intraoperative endoscopy allows improved assessment of the depth of myotomy incisions and reduces the risk of esophageal perforation. The case report below describes a 64-year-old-man with achalasia who presented with persistent dysphagia despite multiple attempts at medical treatment. A laparoscopic Heller myotomy with Toupet fundoplication was performed with subsequent eradication of symptoms. A discussion of the epidemiology, etiology, clinical presentation, diagnosis and treatment of achalasia follows the case report.
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PMID:Achalasia in a sixty-four-year-old man. 971 52

Incidence of adenocarcinomas of the esophagus and gastric cardia has risen dramatically over the past 2 decades in the U. S., for reasons that are not yet clear. A number of common medications (e.g., calcium channel blockers, tricyclic antidepressants, and certain asthma medications) promote gastroesophageal reflux by relaxing the lower esophageal sphincter (LES). Reflux is thought to increase cancer risk by promoting cellular proliferation, and by exposing the esophageal epithelium to potentially genotoxic gastric and intestinal contents. Recent studies have suggested that calcium channel blockers may also increase cancer risk by inhibiting apoptosis. Using personal interview data from a multicenter, population-based case-control study conducted between 1993 and 1995 in three areas of the U. S., we evaluated whether the use of LES-relaxing drugs was associated with increased risk of adenocarcinomas of the esophagus and gastric cardia. Cases of esophageal adenocarcinoma (n = 293) and gastric cardia adenocarcinoma (n = 261) were compared with general population controls (n = 695). Information on additional case groups of esophageal squamous cell carcinoma (n = 221) and noncardia gastric cancer (n = 368) were also available for comparison. Overall, 27.4% of controls had used one or more of these drugs for at least 6 months, compared with 30.2% of esophageal adenocarcinoma and 23.8% of gastric cardia adenocarcinoma cases. The adjusted odds ratios (ORs) for ever use were 1.0 [95% confidence interval (CI) = 0.7-1.5] and 0.8 (95% CI = 0.5-1.1), respectively. There was little evidence of increasing risk with increasing duration of use of all LES-relaxing drugs together. We found an increased risk of esophageal adenocarcinoma among persons reporting use of asthma drugs containing theophylline (OR = 2.5; 95% CI = 1.1-5.6) or beta agonists (OR = 1.7; 95% CI = 0.8-3.8). Risks were higher among long-term users (>5 years) of these drugs (OR = 3.1; 95% CI = 0.9-10.3 and OR = 2.3; 95% CI = 0.8-7.0, respectively). In contrast, there was no evidence that the use of calcium channel blockers or other specific groups of drugs increased the risk of any of the cancers studied. These results provide reassuring evidence that the increases in incidence of adenocarcinomas of the esophagus and gastric cardia are not likely to be related to the use of LES-relaxing drugs as a group, or calcium channel blockers in particular, but they do suggest that persons treated for long-standing asthma may be at increased risk of esophageal adenocarcinoma.
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PMID:Risk of esophageal and gastric adenocarcinomas in relation to use of calcium channel blockers, asthma drugs, and other medications that promote gastroesophageal reflux. 975 82

Hypertension is a significant and prevalent risk factor for the development of cardiovascular disease and target organ damage. The urgency of treatment of high blood pressure depends on the level of blood pressure elevation and the presence of coexistent risk factors for cardiovascular disease. Likewise, the level to which blood pressure is reduced is not restricted to the definition of high blood pressure but instead depends on the underlying disease. Diabetes and renal insufficiency, for example, require blood pressure goals below those that are traditionally defined. In the absence of contraindications, beta-blockers and diuretics are still recommended as first-line agents for treatment of uncomplicated hypertension. Calcium channel antagonists also may reduce mortality. In patients with diabetes, ACE inhibitors are effective first-line agents in type 1 and type 2 diabetic patients who are hypertensive or have microalbuminuria. ACE inhibitors may be beneficial in patients with nondiabetic renal insufficiency as well. Calcium channel antagonists may have some effect in retarding progression of diabetic nephropathy although a recent trial found a higher incidence of death as a secondary endpoint in hypertensive diabetic patients who were treated with calcium channel antagonists. Beta-blockers seem to be safe and well tolerated in patients with mild to moderate intermittent claudication, although patients with rest pain or limb ischemia have not been studied. Beta-blockers should not be used in patients with asthma. Dihydropyridine calcium channel antagonists are the preferred treatment of hypertension in patients with Raynaud's but should be avoided in patients with severe gastroesophageal reflux disease. NSAIDs, particularly piroxicam and indomethacin, raise mean blood pressure by approximately 5 mm Hg, enough to consider a change of either NSAID or antihypertensive to one that is not as affected by NSAIDs. Cyclosporine A can induce hypertension by its vasoconstrictive effects, particularly on the kidney. Calcium channel antagonists may antagonize this vasoconstriction while allowing the clinician to reduce the dose of cyclosporine A required to achieve its immunosuppressive effect.
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PMID:Evaluation and treatment of hypertension. 1046 27

We present 4 brothers with developmental delay, minor anomalies, and symptoms due to gastrointestinal dysmotility. There was some resemblance with FG syndrome, although none of the brothers had sufficient findings to make this diagnosis. The index case presented with at age 1 month with screaming episodes, mild gastro-esophageal reflux (GER), and severe constipation. Esophageal manometry studies were consistent with the diagnosis of "nutcracker esophagus." Symptomatic and manometric improvement followed treatment with oral calcium channel blockers. Two older and less severely affected brothers had similar manometric findings but did not require treatment. A fourth brother with symptoms in infancy now has normal esophageal manometry findings. These boys in all likelihood have an X-linked syndrome with manifestations of FG syndrome, in which treatment with calcium channel blockers, produces clinical and manometric improvement. The FG syndrome is an X-linked syndrome of multiple congenital anomalies/mental retardation with facultative manifestations of gastrointestinal dysmotility, including gastro-esophageal reflux, severe feeding difficulties, and constipation. Esophageal dysmotility, in particular "nutcracker esophagus," should be suspected in infants with the FG syndrome and screaming attacks.
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PMID:Esophageal dysmotility in brothers with an FG-like syndrome. 1075 39


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