Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0017168 (gastroesophageal reflux disease)
 11,783 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

"It is not the death of GERD that I seek, but that it turns from its evil ways and follows the path of righteousness." The reflux world is fully aware of what GERD is and what GERD does. What the world does not know, however, is the answer to the most important yet least asked question surrounding GERD's raison-d'etre: Why is GERD here and why do we have it? What GERD is: abnormal gastric reflux into the esophagus that causes any type of mischief. What GERD does: causes discomfort and/or pain with or without destroying the mucosa; causes stricture or stenosis, preventing food from being swallowed; sets the stage for the development of esophageal adenocarcinoma; invades the surrounding lands to harass the peaceful oropharyngeal, laryngeal and broncho-pulmonary territories; reminds us that we are not only human, but that we are dust and ashes. Why GERD is here: We propose three separate and distinct etiologies of GERD, and we offer the following three hypotheses to explain why, after 1.5 million years of standing erect, we have evolved into a species (specifically Homosapiens sapiens) that is destined to live with the scourge of GERD. Hypothesis 1: congenital. The antireflux barrier, comprising the smooth-muscled lower esophageal sphincter, the skeletal-muscled right crural diaphragm and the phreno-esophageal ligament does not completely develop due to a developmental anomaly or incomplete gestation. Hypothesis 2: acute trauma: The antireflux barrier in adults suffering acute traumatic injury to the abdomen or chest is permanently disrupted by unexpected forces, such as motor vehicle accidents (with steering wheel crush impact), blows to the abdomen (from activities such as boxing, etc.), heavy lifting or moving (e.g., pianos, refrigerators) or stress positions (e.g., hand stands on parallel gym bars). The trauma creates a hiatal hernia that renders the antireflux mechanism useless and incapable of preventing GERD. Hypothesis 3: chronic trauma: The antireflux barrier in children and adults is gradually weakened over time as a result of chronic straining to defecate and straining in an unphysiologic position, both of which stem from our modern day habits of eating a low-fiber diet and living on the high-seated toilet. We suggest that the chronic traumatic hiatal hernia is (a) the cause of more than 90 percent of the GERD that stalks the Western world; (b) is a direct result of abandoning the popular and worldwide practice of squatting to socialize, eat and defecate; and (c) is our just reward for adopting the "civilized" high sitting position on chairs and modern toilets.
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PMID:Defining GERD. 1078 May 68

Vocal cord dysfunction (VCD) is a condition of paradoxical adduction of the vocal cords during the inspiratory phase of the respiratory cycle. VCD often presents as stridorous breathing, which may be misdiagnosed as asthma. The mismanagement of this disorder may result in unnecessary treatment and iatrogenic morbidity. An association with psychogenic factors has been reported, and a higher incidence of anxiety-related illness has been demonstrated in patients with VCD. Definitive diagnosis of VCD is made by visualization of adducted cords during an acute episode using nasopharyngeal fiber-optic laryngoscopy. Diagnosis can be problematic, because it may be difficult to reproduce an attack in a controlled setting. To maximize diagnostic yield during laryngoscopy, provocation of symptoms using methacholine, histamine, or exercise challenges have been used. We report a case of an 11-year-old boy, wherein hypnotic suggestion was used as an alternative method to achieve a diagnosis of VCD. The patient was admitted to the pediatric intensive care unit for elective fiber-optic laryngoscopy to confirm a diagnosis of VCD. The patient had a 4-year history of refractory asthma, severe gastroesophageal reflux disease (GERD) for which he had undergone a Nissen fundoplication, and suspected VCD. At 9 years of age the patient began manifesting monthly respiratory distress episodes of a severe character different from those that had been attributed to his asthma. Typically, he awoke from sleep with shortness of breath and difficulty with inhalation. He described a "neck attack" during which he felt as if the walls of his throat were "beating together." The patient was at times noted by his mother to exhibit a "suckling" behavior before onset of his respiratory distress episodes. On 4 occasions the patient became unconscious during an attack and then spontaneously regained consciousness after a few minutes. On these occasions, he was transported by ambulance to the hospital and the severe difficulty with inhalation resolved within a few minutes on treatment with oxygen and bronchodilators. Sometimes he was noted to manifest wheezing for several hours, which was responsive to bronchodilator therapy. Given the severity of the patient's disease, it was imperative to determine whether VCD was a complicating factor. It was proposed that an attempt be made to induce VCD by hypnotic suggestion while the patient underwent a fiberscopic laryngoscopy to establish a definitive diagnosis. The patient and his mother gave written consent for this procedure. He was admitted for observation to the pediatric intensive care unit for the induction attempt. The patient requested that no local anesthesia be applied in his nose before passage of the laryngoscope because he wanted to eat right after the procedure. Therefore, the nasopharyngeal laryngoscope was inserted while he used self-hypnosis as the sole form of anesthesia. He demonstrated no discomfort during its passing. Once the vocal cords were visualized, the patient was instructed to develop an episode of respiratory distress while in a state of hypnosis by recalling a recent "neck attack." His vocal cords then were observed to adduct anteriorly with each inspiration. The patient then was asked to relax his neck. When he did, the vocal cords immediately abducted with inspiration, and he breathed easily. After removal of the laryngoscope, the patient alerted from hypnosis and said he felt well. He reported no recollection of the procedure, thus demonstrating spontaneous amnesia that sometimes is associated with hypnosis. Because the diagnosis of VCD was confirmed, the patient was encouraged to use self-hypnosis and speech therapy techniques to control his symptoms. He also was referred for counseling. To our knowledge this is the first description in the medical literature of the use of hypnotic suggestion for making a diagnosis of VCD. (ABSTRACT TRUNCATED)
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PMID:Hypnosis as a diagnostic modality for vocal cord dysfunction. 1109 24

The hypertensive lower oesophageal sphincter (HLOS) is a distinct clinical entity defined by a lower oesophageal sphincter (LOS) pressure > or = 30mmHg and normal LOS relaxation and oesophageal peristalsis. The clinical, physiological, and radiological details of 27 patients with HLOS diagnosed in a 3-year period were reviewed. The reasons for referral included: gastro-oesophageal reflux disease (GORD) (33%), dysphagia (18.5%), epigastric discomfort (11%), non-cardiac chest pain (15%), globus (7.5%) and other (15%). All patients had manometric evidence of HLOS (Median LOS pressure 30 mmHg, range 25-50 mmHg) and 6 patients (20.7%) had abnormal pH studies. Less than 22% of contrast studies demonstrated an abnormality. There was no change in manometric findings following pharmacological treatment. Two patients underwent oesophagomyotomy and had normal manometry on follow up. We conclude that HLOS mimics a variety of upper gastrointestinal disorders and oesophageal manometry is the gold standard of diagnosis. There was an unexpectedly high incidence of GORD (22%) in this group. The significance and treatment of HLOS is discussed.
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PMID:The isolated hypertensive lower oesophageal sphincter: audit in a specialist unit. 1113 54

Enteric coating of peppermint oil/caraway oil capsules avoids subjective discomfort to the patient caused by gastroesophageal reflux. In order to confirm bioequivalence of an enteric coated formulation containing peppermint oil and caraway oil (CAS 277309-55-4, Enteroplant) and an immediate release formulation of both oils, the pharmacokinetics of menthol and carvone after oral administration of the two formulations were studied in a randomized, two-period cross-over study in 16 healthy male volunteers. The subjects received 180 mg peppermint oil and 100 mg caraway oil, once as 2 enteric coated capsules of the fixed enteric coated combination preparation containing 90 mg peppermint oil (WS 1340) and 50 mg caraway oil (WS 1520) each (test) and once in the form of 5 capsules of an immediate release formulation (reference) containing 36 mg peppermint (WS 1340) oil and 20 mg caraway oil (WS 1520) each. The capsules were taken with 250 ml water after a 10 h fast. Both substances were determined in plasma by GC/MS after extraction. The limit of quantification was 10 ng/ml for menthol and 0.5 ng/ml for carvone. The mean maximum plasma levels for menthol were 1196 ng/ml after administration of the test medication and 1492 ng/ml after administration of the reference medication. The bioavailability with respect to the AUC was comparable after administration of test and reference preparation, the 90% confidence interval was 97 to 105%. As expected, there were considerable differences for Tmax. After application of the enteric coated form the maximum concentration was reached significantly later (3.0 h vs. 1.7 h) compared to the immediate release capsule. Corresponding data were also calculated for carvone. After application of the test medication the maxima of 14 ng/ml for both formulations were reached later (2.5 h vs. 1.3 h). The 90% confidence interval of the AUC for carvone was 79 to 119% and therefore slightly outside the acceptable range for bioequivalence of 80 to 125%. However, this fact should not be relevant, in particular since the dosage of the enteric coated capsule lies at the upper limit of the model text and positive clinical studies, also on the therapeutic equivalence of the two formulations, are available.
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PMID:Pharmacokinetics of menthol and carvone after administration of an enteric coated formulation containing peppermint oil and caraway oil. 1145 77

Dyspepsia is defined as chronic or recurrent pain or discomfort centred in the upper abdomen. Early satiety, nausea, vomiting, or bloating are often also present. Dyspepsia should be differentiated from gastro-oesophageal reflux disease, whose predominant symptoms are heartburn and acid regurgitation. Prevalence rates vary between 25% and 40%, and dyspepsia is the main reason for consulting GPs: 3-5% of all visits. Older patients and patients presenting with alarm symptoms (weight loss, anaemia, jaundice, dysphagia, bleeding) should undergo endoscopy, but apart from this no other management strategy has been agreed upon. Management strategies based on non-invasive H. pylori testing will probably prove cost-effective and safe. However, the results of clinical trials are awaited before guidelines can be offered. The symptomatic effects of treating patients with functional dyspepsia with either acid inhibitors, prokinetics, or H. pylori eradication therapy are difficult to predict and are usually quite modest.
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PMID:[Dyspepsia. Investigation and treatment]. 1157 69

Although a strong association exists between gastroesophageal reflux (GER) and asthma, results of studies designed to maximize the likelihood of identifying that GER worsens pulmonary function in patients with asthma have been negative or inconclusive. Asthma symptoms worsen during symptomatic reflux episodes, and asthma symptom severity correlates with the severity of symptomatic reflux. Various reasons have been proposed to explain these findings. Discomfort associated with GER can cause reflux-associated respiratory symptoms even when pulmonary function is normal. New findings suggest that increases in minute ventilation rather than inhibition of diaphragm activity are responsible for the changes in respiratory sensation during acid perfusion of the esophagus in nonasthmatic subjects. These results may also pertain to asthmatic patients, because increasing minute ventilation can cause dyspnea and bronchospasm in this population. Treating GER, either medically or surgically, may improve asthma symptoms by preventing GER-induced changes in minute ventilation.
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PMID:Underlying mechanisms of respiratory symptoms with esophageal acid when there is no evidence of airway response. 1174 22

Opioid bowel dysfunction (OBD) is a common adverse effect associated with opioid therapy. OBD is commonly described as constipation; however, it is a constellation of adverse gastrointestinal (GI) effects, which also includes abdominal cramping, bloating, and gastroesophageal reflux. The mechanism for these effects is mediated primarily by stimulation of opioid receptors in the GI tract. In patients with pain, uncontrolled symptoms of OBD can add to their discomfort and may serve as a barrier to effective pain management, limiting therapy, or prompting discontinuation. Patients with cancer may have disease-related constipation, which is usually worsened by opioid therapy. However, OBD is not limited to cancer patients. A recent survey of patients taking opioid therapy for pain of noncancer origin found that approximately 40% of patients experienced constipation related to opioid therapy (<3 complete bowel movements per week) compared with 7.6% in a control group. Of subjects who required laxative therapy, only 46% of opioid-treated patients (control subjects, 84%) reported achieving the desired treatment results >50% of the time. Laxatives prescribed prophylactically and throughout opioid therapy may improve bowel movements in many patients. Nevertheless, a substantial number of patients will not obtain adequate relief of OBD because of its refractory nature. Naloxone and other tertiary opioid receptor antagonists effectively reduce the symptoms of constipation in opioid-treated patients. However, because they also act centrally, they may provoke opioid withdrawal symptoms or reverse analgesia in some patients. There are 2 peripherally selective opioid receptor antagonists, methylnaltrexone and ADL 8-2698 (Adolor Corporation, Exton, PA, USA), that are currently under investigation for their use in treating OBD. Early studies confirm that they are effective at normalizing bowel function in opioid-treated patients without entering the central nervous system and affecting analgesia. With a better understanding of the prevalence of OBD and its pathophysiology, a more aggressive approach to preventing and treating OBD is possible and will likely improve the quality of life of patients with pain.
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PMID:Incidence, prevalence, and management of opioid bowel dysfunction. 1175 92

Functional (nonulcer) dyspepsia refers to upper abdominal pain or discomfort with or without symptoms of early satiety, nausea, or vomiting with no definable organic cause. The current Rome II criteria help to diagnose functional dyspepsia and avoid misdiagnosis of gastroesophageal reflux disease and irritable bowel syndrome as functional dyspepsia. Assessment of gastric emptying with scintigraphy or breath testing may be useful in identifying delayed gastric emptying in patients with dyspeptic symptoms and may be helpful in patient management. Electrogastrography is a noninvasive test that evaluates for gastric dysrhythmias. Satiety testing is being evaluated as an indirect test for impaired fundic relaxation and visceral hypersensitivity. The symptom response to Helicobacter pylori therapy in patients with functional dyspepsia and a negative endoscopy examination but a positive H. pylori test is marginal. Lifestyle modifications often are suggested for initial treatment of functional dyspepsia. Dietary changes such as frequent small meals, low-fat diet, and avoidance of certain aggravating foods may improve symptoms. Additional measures include cessation of smoking, avoiding excess alcohol intake, and minimizing coffee intake. Antacids and over-the-counter histamine type 2 receptor antagonists may be helpful as an "on-demand" therapy for intermittent symptoms. They are safe and relatively inexpensive. Different subgroups of functional dyspepsia are based on the predominant symptom and may help in choosing an appropriate drug to initiate therapy. If the predominant symptom is epigastric pain (ulcer-like functional dyspepsia), histamine-2 receptor antagonists or proton pump inhibitors are the initial treatment of choice. If fullness, bloating, early satiety or nausea is the predominant complaint (dysmotility-like functional dyspepsia), a prokinetic agent may help. Metoclopramide is the only available effective prokinetic agent at present. If metoclopramide is used, short-term treatment and discussion of possible side effects with the patient are advised. If there is no response to these initial treatments, switching therapy from proton pump inhibitor to prokinetic or vice versa can be tried. If these treatment options fail, patient re-evaluation for other disorders (including other functional bowel disorders) is advised. A low-dose tricyclic antidepressant at bedtime may be helpful for treatment of visceral hypersensitivity.
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PMID:Functional (Nonulcer) Dyspepsia. 1187 96

Gastro-oesophageal reflux disease (GERD) is common in obese patients. Apart from the physical discomfort and the economic burden, GERD may increase morbidity and mortality through its association with oesophageal carcinoma. The pathophysiology of GERD differs between obese and lean subjects. First, obese subjects are more sensitive to the presence of acid in the oesophagus. Second, hiatal hernia, capable of promoting GERD by several mechanisms, is more prevalent among the obese. Third, obese subjects have increased intra-abdominal pressure that displaces the lower oesophageal sphincter and increases the gastro-oesophageal gradient. Finally, vagal abnormalities associated with obesity may cause a higher output of bile and pancreatic enzymes, which makes the refluxate more toxic to the oesophageal mucosa. The altered body composition associated with obesity affects the pharmacokinetics of drugs. There are no data regarding the efficacy of any of the drugs used for GERD treatment. The dosages of cimetidine and ranitidine should be calculated according to the patient's ideal body weight, not their actual weight. Of the operative procedures used for weight loss, Roux-en-Y gastric bypass was found to be most effective for GERD, while gastric banding was associated with a high prevalence of reflux. This review outlines the pathophysiology and the treatment of GERD in obesity with emphasis on the therapeutic considerations in this population of patients.
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PMID:Gastro-oesophageal reflux disease in obesity: pathophysiological and therapeutic considerations. 1211 61

The discomfort caused by persistent cough compels a great number of patients to seek medical aid. Persistent cough interferes with the patient's sleep, professional and social activities. The pathogenic triad of asthma, post nasal drip syndrome and gastroesophageal reflux disease, alone or in combination, is responsible for the majority of cases of chronic cough. Investigation of chronic cough, according to a rational protocol leads to the identification of the cause for chronic cough in approximately 90% of the cases.
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PMID:[Chronic cough]. 1218 56


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