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In a 6.5 year period starting January 1982, 121 patients (74 male, 47 female; 1.6:1) with complicated gastroesophageal reflux referred to Alberta Children's Hospital, University of Calgary, required a Nissen fundoplication at a mean age of 35.5 months (range 3 weeks to 18 years). The median age of onset of symptoms was less than 1 month. Symptoms and indications for surgery included regurgitation (88%), failure to thrive (52%), reflux-associated pulmonary symptoms and aspiration (48%), biopsy evidence of esophagitis (35%) with heartburn (17%), dysphagia (18%), hematemesis (17%), anemia (13%), and hypoproteinemia (22%). Sixty-four percent of the patients had a syndrome or chromosomal abnormality, respiratory disease, or neuromuscular disorder. The barium contrast upper-gastrointestinal radiographic series, performed in all patients, identified structural [gastric outlet obstruction (2%), esophageal stricture (11%), erosive esophagitis (9%)], and functional abnormalities [gastroesophageal reflux (90%), barium aspiration (8%), esophageal hypoperistalsis (30%), delayed gastric emptying (4%)]. Barium contrast upper gastrointestinal radiographic series identified gastroesophageal reflux with a sensitivity of 90% (compared to history), was 50% sensitive and 92% specific for erosive esophagitis (compared to biopsy), was 59% sensitive and 74% specific for esophageal dysmotility (compared to esophageal manometry), and there was a significant (p less than 0.01) association between barium aspiration and prior evidence of aspiration pneumonitis. Esophageal manometry demonstrated a significantly (p less than 0.001) lower esophageal sphincter pressure in patients compared with controls, but no significant correlation with failure to thrive, aspiration pneumonia, biopsy evidence of esophagitis, or parameters of the 24-hour esophageal pH study. Twenty-four hour pH monitoring showed significantly (p less than 0.05) more reflux episodes than in asymptomatic controls and there was significant (p less than 0.05) correlation between the percentage of time pH was less than 4 and the presence of hypoalbuminemia, and biopsy-proven erosive esophagitis or Barrett's esophagus. Endoscopic appearance was 91% sensitive and 60% specific for esophagitis when compared to biopsy. Nissen fundoplication was completely effective at resolving gastroesophageal reflux in 83%, and associated with marked improvement in 15%. No patient died as a result of fundoplication. Major complications included: recurrence of symptoms requiring reoperation (2%), subsequent mechanical bowel obstruction (8%), wound infection or pneumonia (12%).
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PMID:Investigation and outcome of 121 infants and children requiring Nissen fundoplication for the management of gastroesophageal reflux. 227 17

Long-term results are presented in 60 patients (4 to 50 years old) who underwent a diaphragmatic graft procedure for relief of cardiospasm (achalasia) from 1962 through 1987. The operative technique involves construction of a pedicle flap of diaphragm. The muscular defect on the lower segment of the esophagus and the transplanted diaphragmatic pedicle that is sutured to the defect must be the same size. Immediate operative results were good. Only one complication developed, a case of pneumonia that was cured. The patients were followed up from 11 months to 25 years. Two patients were lost to follow-up, 55 had excellent results, and three patients still had nausea and heartburn but were better than before the operation. This procedure has three advantages: (1) It prevents the development of fistulas and diverticula at the site of the esophageal muscular defect; (2) it effectively eliminates both restenosis resulting from scar tissue and reflux esophagitis; and (3) it allows the cardia to recover its normal function and the esophagus to return to normal size at the site of the operation.
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PMID:Treatment of esophageal achalasia (cardiospasm) with diaphragmatic graft. Twenty-five years' experience. 292 62

Results with the use of a diaphragmatic graft in the surgical relief of achalasia are reported for 44 patients. The operative technique involves construction of a pedicle flap of diaphragm the size of the muscular defect on the lower segment of the esophagus and suture of the transplanted diaphragmatic pedicle to the site of the esophageal muscular defect. Immediate operative results were good; there was only one complication, a case of pneumonia that was cured. Patients were followed from 3 months to 19 years. Two patients were lost to follow-up. Excellent results were obtained in 39 patients; 3 patients still had nausea and heartburn, but were better than before operation. This procedure has three advantages: (1) it prevents occurrence of fistula and diverticulum at the site of the esophageal muscular defect; (2) it effectively eliminates formation of restenosis due to scar and reflux esophagitis; and (3) it allows the cardia to recover its normal function and the esophagus to return to normal size at the site of operation.
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PMID:Treatment of esophageal achalasia (cardiospasm) with diaphragmatic graft: report of 44 patients. 640 96

One hundred and sixty two laparoscopic fundoplications were performed between may 1991 and december 1993 by the first author. No perioperative death was observed. There were 4 intraoperative complications (3%): 1 gastric perforation, 2 pleural perforations and 1 liver laceration. There were 3 conversions to laparotomy: 2 for left liver hypertrophy and 1 for needle holder defect. The duration of the operation ranged from 40 minutes to 5 hours (median 120 minutes). The median postoperative stay was 2 days. Five postoperative complications occurred: 2 cases of pneumonia and 3 cases necessitating second-look laparatomy (1 necrosis of the valve, 1 small bowel perforation and 1 obstruction due to migration of the entire stomach into the chest). The follow-up ranges from 4 to 897 days (median 10 months). Long-term complications were: one recurrence of heartburn reoperated laparoscopically and two cases of long-term postoperative dysphagia.
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PMID:[Nissen's fundoplication by celiovideoscopy]. 774 66

Surgery is indicated when gastro-oesophageal reflux disease (GORD) is resistant to medical treatment. Manometry, upper GI series, pH-metry, gastric emptying studies and gastric acid sampling are performed in order to demonstrate that GORD is caused by a deficient gastro-oesophageal valve mechanism, and hence that surgical treatment will be beneficial. The surgical principle is restoring an anti-reflux barrier by recreating a sufficient pressure gradient in the distal oesophagus, and by correcting the gastro-oesophageal Hiss. Nissen' fundoplication is probably the most efficient anti-reflux procedure. However, it can cause dysphagia, gas bloating and inability to burp. One hundred and fifty-six laparoscopic Nissen fundoplications have been performed by the author. Operating time average 120 min. No perioperative death was observed. There were 3 conversions to laparotomy and 4 peroperative complications: 1 gastric perforation, 2 lesions of the pleura and 1 liver laceration. Four postoperative complications occurred: 1 pneumonia, 1 necrosis of the wrap, 1 small bowel perforation and 1 obstruction due to migration of the entire stomach into the chest. Hospitalisation time ranged between 2 and 14 days (median 2), with a follow up of a median of 10 months. Long-term postoperative complications were: 1 recurrent heartburn 6 months postoperatively and 2 severe dysphagia.
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PMID:[Anti-reflux surgery: indications, principles and contribution of laparoscopy]. 819 Nov 68

Characteristics of 10-year survival after esophagectomy for carcinoma were studied retrospectively in 161 patients who underwent curative operation between 1973 and 1984. Of the 161 patients, 44 (27.3%) survived for 10 years after operation (right transthoracic approach with cervical anastomosis in 36 patients and left thoracoabdominal approach with jejunoesophagostomy in 8 patients). Females survived significantly longer than males; 10-year survival was observed in 10 (50%) of 20 females and 34 (24.1%) of 141 males. TNM factors were significantly linked to the 10-year survival for 25 patients (56.8%) whose tumors invaded the adventitia and 20 patients (45.5%) who had lymph node metastases, where the total number of involved nodes was less than eight. A questionnaire mailed 10 years after operation revealed that about one-fifth of the 10-year survivors could not go up one flight of stairs without taking a rest, and that the daily activity significantly deteriorated if the patient's age at the time of surgery was more than 66 years. One-third of the 10-year survivors were not satisfied with the daily quantity of food intake, resulting in no gain of body weight after discharge from the hospital. This complaint was significantly correlated with either weekly reflux or heartburn, resulting in the increasing number of nonmalignancy deaths. Of 13 ten-year survivors who were alive at 10 years but died after that, 11 (84.6%) died of pneumonia or malnutrition. Duodenogastroesophageal reflux may eventually cause nonmalignancy death 10 years after esophagectomy for carcinoma.
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PMID:Appraisal of ten-year survival following esophagectomy for carcinoma of the esophagus with emphasis on quality of life. 901 71

Idiopathic pulmonary fibrosis (IPF) is a progressive, fatal interstitial lung disease (ILD) of unknown etiology. Introduction of acid into the respiratory tree can produce pulmonary fibrosis. Gastroesophageal reflux (GER) has previously been associated with several other respiratory conditions, including pneumonia, bronchitis, and asthma. To investigate prospectively the possible association of GER and IPF, 17 consecutive patients with biopsy-proven IPF and eight control patients with ILD other than IPF underwent dual-channel, ambulatory esophageal pH monitoring. Sixteen of 17 patients with IPF had abnormal distal and/or proximal esophageal acid exposure compared with four of eight control patients (p = 0.02). In the patients with IPF, mean percent distal total (13.6 versus 3.34, p = 0.006), distal upright (12.4 versus 5.1, p = 0.04), distal supine (14.7 versus 0.88, p = 0.02), and proximal supine (7.48 versus 0.24, p = 0.04) esophageal acid exposure times were significantly greater than those in control patients. Only four patients with IPF (25%) with increased acid exposure had typical reflux symptoms such as heartburn or regurgitation. Patients with IPF have a high prevalence of increased esophageal acid exposure, usually without typical GER symptoms. GER in these patients tends to occur at night and extend into the proximal esophagus. Acid reflux may be a contributing factor in the pathogenesis of IPF.
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PMID:Increased prevalence of gastroesophageal reflux in patients with idiopathic pulmonary fibrosis. 984 71

A 75-year-old man visited our hospital complaining of heartburn in November 1997. Gastroscopical examination revealed ulcerous protruding extended from the gastric antrum to body and a flat, elevated lesion in the greater curvature of the stomach. Biopsy specimens revealed a CD4-positive malignant lymphoma. The serum anti-human T-lymphotrophic virus type I (HTLV-I) antibody test was positive. He was diagnosed as having primary gastric adult T-cell leukemia/lymphoma (ATLL; acute type). Complete remission was achieved with chemotherapy. In December 1998, the patient experienced a relapse. The lesions were limited to the region between the upper gastric body and the fornix and disappeared with radiation therapy. A second relapse was detected in the gastric greater curvature and descending portion of the duodenum in May 1999 but spontaneously disappeared in 5 months. The third relapse in May 2000 was systemic. Monoclonal integration of the HTLV-I provirus was observed in DNA extracted from ascitic lymphocytes. Chemotherapy was resumed, but the response was poor. The patient subsequently died of respiratory failure as a result of pneumonia. Although gastrointestinal involvement is frequent in ATLL, this appears to be a rare case of an idolent clinical course with lesions limited to the stomach and duodenum for 30 months.
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PMID:[Indolent primary gastric adult T-cell leukemia/lymphoma with recurrent lesions limited to the stomach and duodenum]. 1222 25

For a long time heartburn was not considered a symptom for serious illness. By now, however, it is accepted that the incidence of secondary carcinoma of the esophagus caused by chronic GERD has increased dramatically since the nineteen-seventies. Mechanisms leading to GERD are complex and its incidence is not necessarily pathological. However pathological reflux in the lower esophagus (pH lower than 4 in 6 % of 24 hours), caused by decreased sphinctertonus, impaired peristalsis and clearance of the esophagus, may lead to complications. Helicobacter pylori may play a key role in GERD. There is strong evidence for a protective effect of Hp-infection in the development of GERD. In pangastritis, caused by Hp-infection, gastric acid production is inhibited resulting in a reduction of stomach-acid-concentration. This may be caused by either the chronic infection itself and the resulting atrophy of the stomach-mucosa, by the ammonia-producing HP-bacteria, or an increase in acid re-absorbtion of gastric epithelium. Laryngopharyngeal reflux (LPR) often results in atypical manifestations with oral, pharyngeal, laryngeal, and pulmonary disorders. Laryngopharyngeal reflux is known to contribute to posterior acid laryngitis and laryngeal contact ulceration or granuloma formation, laryngeal cancer, chronic hoarseness, pharyngitis, asthma, pneumonia, nocturnal choking, and dental diseases. Today, PPI are the medication of choice in both acute and long-term (prophylactic) therapy of GERD. The so called "step-up-strategy" of medication is no longer recommended. Here, patients were first treated with antacids, then prokinetics followed by H2-blockers and finally low-dose PPI. Only in the case of persisting symptoms medication was further increased to high-dose PPI therapy. In the past this increase in medication lead to a prolonged healing process and consequently to higher medication costs. Studies have shown that a "step-down"-therapy, beginning with high dose PPI, is highly preferable, since it is much more effective. Depending on the degree of the symptoms, however, medication may also be applied "on-demand". The BfArM has approved this kind of medication application only for Esomeprazol (Nexium mups 20 mg).
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PMID:[Gastroesophageal reflux -- a common illness?]. 1262 41

Adverse reactions to acetylsalicylic acid (aspirin, ASA) and other non-steroidal anti-inflammatory drugs (NSAIDs) are the second most important cause of adverse drug reactions (ARDs) after beta-lactams. They produce various clinical manifestations and can affect different organs. Gastrointestinal reactions (pyrosis, vomiting, gastralgia), neurological reactions (tinnitus, deafness, vertigo), blood dyscrasias, and nephrotoxic and hepatotoxic reactions are well known.NSAIDs are the drugs of choice in the treatment of chronic arthropathies and other childhood connective-tissue diseases and are also commonly used in the treatment of febrile and acute inflammatory processes. Not all NAIDs are authorized for use in the pediatric population but their spectrum of use varies according to the entity for which they are indicated and the legislation of the country. Published studies on the prevalence of aspirin intolerance in patients with bronchial asthma show a fair amount of disagreement. This may be due to (i) the method of selecting asthmatic patients for the study, which differs according to whether all asthmatic patients are included or only those dependent on corticoids; (ii) the diagnostic method used, whether based on clinical criteria or oral provocation tests, which will affect the number of patients with a diagnosis of intolerance. In children aged less than 10 years, including children with asthma, the prevalence is low, while among children and young adults aged 10-20 years old, the prevalence is estimated at 10 %. Some hypotheses attempt to explain the mechanisms through which adverse reactions to NAIDs take place. One hypothesis attributes the reaction to a reaginic immunological mechanism but this hypothesis has only been confirmed in exceptional cases. The theory of the cyclooxygenase pathway, currently the most widely accepted, is based on the ability of NSAIDs to inhibit the cyclooxygenase pathway of arachidonic acid metabolism, leading to prostaglandin depletion and an increase in leukotrienes. The discovery of two isoforms of the cyclooxygenase enzymes, COX-1 and COX-2, has represented a great advance in our understanding of the mechanism of action of NSAIDs and has also elucidated the problem of cross-reactivities. According to the theory of viral infection, aspirin-induced asthma could be caused by chronic viral infection since, after initial exposure to the virus, cytotoxic lymphocytes are produced. Their activity is inhibited by prostaglandin E2 (PGE2); aspirin and other NSAIDs block PGE2 production and allow cytotoxic lymphocytes to attack and eliminate the respiratory tract cells infected by the virus. During this reaction lysosomal enzymes and mediators are released, which could precipitate an asthmatic crisis.Clinically, five types of reaction have been identified: 1. Respiratory illness with aspirin sensitivity. 2. Aspirin-induced urticarial disease. 3. Allergic reactions to NSAIDs and aspirin. 4 and 5. Aseptic meningitis and pneumonitis due to hypersensitivity. The latter are exceptional and are published as case reports. They have never been associated with aspirin or acetaminophen and usually occur in patients undergoing prolonged treatment. Diagnosis is based on a detailed history. Skin tests are not valid and in vitro tests are not widely used. Provocation tests with aspirin and NSAIDs definitively identify sensitized patients but their indications and limitations should be kept in mind. In children, certain features of adverse reactions to NSAIDs are observed in relation to their incidence and clinical manifestations. Acetaminophen is considered the drug of choice but further studies of other alternatives in children are required.
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PMID:[Special features of NSAID intolerance in children]. 1278 61


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