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)

Persisting retrosternal pain of sudden onset is suggestive of a drug-induced oesophageal lesion, particularly if it starts at night. After exclusion of a myocardial infarction, a carefully taken history and oesophagoscopy will rapidly clarify the cause and severity of the injury. Since almost any pill may produce oesophageal lesions, care has to be taken that tablets, capsules and other pills are always taken in an upright position together with a fluid chaser of at least 120 ml. If possible, less harmful liquid preparations of the drugs should be preferred. Lesions in the oesophageal wall and perioesophageal tissue are almost unavoidable side-effects of sclerotherapy of oesophageal varices. The patient and the doctor should be particularly aware of bleeding from oesophageal ulcers during the first week after sclerotherapy. Numerous drugs may weaken or strengthen contractions of the oesophagus and lower oesophageal sphincter. These potentially unwanted motor effects of the drugs have to be kept in mind, especially in patients with pre-existing gastro-oesophageal reflux disease and hypermotility states.
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PMID:Drug-induced oesophageal lesions. 304 62

An examination of esophageal function using manometric techniques and long-term pH measurement was carried out on 14 patients suffering from cirrhosis of the liver who had esophageal varices. The resting pressure in the lower esophageal sphincter was found to be slightly reduced in 50 per cent of those examined, while 100 per cent showed a slightly reduced contraction amplitude in the distal tubular esophagus which became progressively lower in the distal direction, and a pathological gastro-esophageal reflux was observed in 57 per cent. We were able to carry out a control examination on 10 of these patients after sclerosing procedure. Sclerotherapy was found to have lowered resting pressures in the lower esophageal sphincter in 80 per cent of those patients, while all of them showed a grossly impaired tubular peristalsis in the form of simultaneous, mostly repetitive contractions with a considerably lowered contraction amplitude, however it had no negative influence on gastro-esophageal reflux patterns.
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PMID:[Esophageal function in portal hypertension before and after sclerotherapy]. 325 34

Esophageal manometry was performed before and after the operations for esophageal disorders in children to evaluate lower esophageal sphincter (LES) function and motility of the esophagocardiac region in each disease. Patients who underwent radical operations for gross C-type esophageal atresia (EA) and those with hiatal hernias considered to have gastroesophageal reflux (GER) showed reduction in LESP and LESL and eosphagocardiac motor abnormalities. Lower esophageal sphincter pressure and length, and motility of the esophagocardiac region improved in six patients who underwent an antireflux operation. Abnormal esophageal waves in EA patients persisted even after improvements in LES function by the antireflux operation and were considered to be a congenital problem, as the literature suggests. Effects of surgical intervention on the esophagus on the LES function were studied. Lower esophageal sphincter and esophagocardiac function were preserved, and GER did not develop after Livaditis' procedure for EA or esophageal transection and sectioning the esophageal branch of the vagus nerve for esophageal varices. Anatomic abnormalities that lead to LES dysfunction are considered to cause GER.
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PMID:Evaluation of lower esophageal sphincter function in infants and children following esophageal surgery. 337 45

Pressure in oesophageal varices was measured endoscopically in 52 patients, in 16 of them central portal-vein pressure additionally by percutaneously introduced transhepatic portal-vein catheter. Only in the region of the cardia occlusion segment was the portal-vein pressure the same as that in the oesophageal varices. The larger the varices the higher the average variceal pressure. Depending on the time interval since a meal there were marked pressure variations during the day in portal-vein pressure. Intra-abdominal pressure rise (e.g. on coughing, choking or vomiting) induces a sudden and marked pressure rise in the portal vein as well as the oesophageal varices. The larger the varices the greater the danger of rupture when these pressure rises occur. Gastro-oesophageal reflux plays no role in the pathogenesis of bleeding from oesophageal varices.
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PMID:[Pathogenesis of bleeding esophageal varices]. 348 19

Rebleeding, the long time high occurrence of encephalopathy and the impairment of hepatic function in the successful cases have led to increasing dissatisfaction in the last years with portasystemic shunt procedures. In the past 12 years we have operated on 14 children for bleeding esophageal varices using the Sugiura procedure (esophageal transection with paraesophagogastric devascularization); in two cases the entire procedure was performed through the thoracic approach. We had no mortality. Complications include bleeding in the early postoperative period in two children and partial leakage from the esophageal suture in two others. Patient follow-up has been between 16 months and 11 1/2 years with an average of 6 1/2 years. The long term controls have been gratifying in 12 patients with disappearance of the varices and no evidence of rebleeding, esophageal strictures, gastroesophageal reflux, encephalopathy or impairment of the hepatic function; in two other patients the operations was unsuccessful. In our opinion the Sugiura procedure should be the elected operation in the surgical treatment of esophageal varices bleeding in pediatric age, after an attempt with sclerotherapy.
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PMID:[Sugiura's operation in the treatment of hemorrhaging esophageal varices]. 349 85

The paper describes the physiology of swallowing, the methods for the assessment of esophageal motility, and the motility disorders of the tubular part and the lower sphincter of the esophagus, except for gastroesophageal reflux disease. Primary esophageal motility disorders are achalasia (incomplete relaxation of the lower sphincter in response to swallowing), diffuse esophagospasm (simultaneous repetitive contractions), and the nutcracker esophagus (propulsive peristalsis with abnormally high amplitude). Besides, there are non-specific as yet unclassified contraction abnormalities. Since hypermotile contraction abnormalities can mimic chest pain of cardiac origin, differential diagnosis of anginal chest pain should include esophageal motility disorders. Contraction abnormalities of the esophagus may occur in diffuse scleroderma, after therapeutic radiation of the mediastinum, and possibly after sclerotherapy of esophageal varices.
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PMID:[Motility disorders of the esophagus]. 356 Nov 40

Since 1974, 112 patients with ruptured esophageal varices, have undergone resection-anastomosis of the supracardial esophagus using the circular suture stapler. Recently, preliminary splenic artery ligature has also been associated, if possible, with systematic ligature of the gastric coronary vein and followed by cardioplasty, to prevent gastro-esophageal reflux and block subcardial venous flow. This highly selective portal decompression (HSPD) procedure provides lasting reduction in blood pressure (confirmed by manometric recordings) in the esophago-cardial region, without any reduction in the distal hepatic flow (no portocaval shunt) or increase in the proximal flow (raised portal pressure). Results were compared with those of the initial, already encouraging, protocol, and demonstrated a tangible improvement after more than one year follow-up. In 50 cases (Child A:16, B:29 and C:5), postoperative mortality was 10% (5 cases) during the first month and 7.5% (3 cases/40) during the first year. There was no specific morbidity due to the additional procedure nor cases of portocaval encephalopathy. During the first postoperative year, the frequency of hemorrhagic complications was one tenth of that during the year before surgery. These very encouraging results suggest the possibility of extending the indications for HSPD in the treatment of recurrent digestive hemorrhages from ruptured esophago-cardial varices, replacing porto-systemic shunts which are sometimes well tolerated but always anti-physiological.
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PMID:Highly selective portal decompression for bleeding esophageal varices. 387 25

Portal hypertension is defined as an increase of the portal venous pressure over 20 cm H2O or 7 mm Hg, respectively. It may be induced by different types of portal venous stenosis or obstruction, primarily by cirrhosis and fibrosis of the liver and, less frequent by posthepatic disorders such as the Budd-Chiari-syndrome or congestive heart failure. Portal hypertension is followed by ectasia and phlebosclerosis of the portal vein, by splenomegaly, ascites and by various types of collateral circulation. Among these, oesophageal varices, are most important since they often lead to acute upper gastrointestinal haemorrhage, the major complication of portal hypertension. Bleeding from oesophaeal varices is essentially based on atrophy of the squamous epithelium, caused by ischemia from local hypoxia and venous stasis. Portal hypertension and the frequently compromised blood clotting mechanism due to reduced synthesis of clotting factors in the liver aggravate the bleeding. Atrophy of the esophageal mucosa presents an area of decreased resistance likely to ulcerate with easy erosion of the varices--usually lying very superficially--; with mechanical irritation by food or peptic erosion from gastroesophageal reflux being frequent inducers of hemorrhage.
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PMID:[Pathologic-anatomic reflections on portal hypertension (author's transl)]. 624 21

Review of 98 endoscopies done over a 4-year period demonstrated that these procedures aided in the diagnosis and management of infants and children with upper gastrointestinal disorders. Endoscopic indications included evaluation of the esophagus in gastroesophageal reflux, achlasia, and lye ingestion; and evaluation of biliary and pancreatic diseases. Other indications included diagnosis of the site of upper gastrointestinal bleeding and treatment of esophageal varices with sclerotherapy, esophageal strictures with steroid injection and removal of foreign bodies. The majority of the procedures were done under sedation. There were no complications.
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PMID:Indications and techniques of upper gastrointestinal endoscopy in infants and children. 648 91

Eighty-eight patients with bleeding esophageal varices due to portal hypertension underwent splenectomy and devascularization of the upper half of the stomach and the abdominal esophagus. A Hegar dilator no. 17 was introduced into the esophagus through a gastrotomy. A ring of separated stitches was applied at cardia level, the needle being inserted as far as the metallic surface so as to include the entire wall of the esophagus. Complete interruption of all gastroesophageal vascular communication was thus obtained. After suture of the gastrotomy, a Nissen or Lind's fundoplication was performed. In 62 (70.45%) patients, the immediate postoperative course was uneventful, 21 had non-lethal complications, 13 had abdominal evisceration, six pulmonary complications, four subphrenic abscesses, five patients died, two in hepatic coma, two after reoperation for subphrenic abscess and one after massive hemorrhage due to an acute gastric ulcer. Forty-three patients (48.8%) developed transient ascites which disappeared before they were discharged from the hospital. In thirteen patients (15.6%), the hemorrhage recurred. Of the 32 patients operated one to two years ago, only one rebled. Of the 35 patients operated three to five years ago, nine rebled and three, of the 16 patients operated from five to seven years ago, rebled. With radiological and endoscopic investigations, reduced varices were seen above the suture line, in many cases, passively filled up with blood returning from the azygos vein. Reflux esophagitis was observed in 17 patients who had had a Lortat-Jacob procedure to reduce the His angle; of these, eight rebled later. No gastroesophageal reflux was seen after Nissen or Lind's fundoplication. No fistulae, dysphagia or stenosis was observed.
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PMID:A new procedure for the treatment of bleeding esophageal varices by transgastric azygo-portal disconnection. 660 5


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