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)

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

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

Human papillomavirus infection is important for both the development of papilloma and the progression of the papilloma-carcinoma sequence in the cervix, larynx, lung, and colon. Esophageal squamous cell papilloma is rare but important as a possible precancerous lesion. Esophageal papilloma has previously been thought to develop mainly as a result of chemical irritation by chronic gastroesophageal reflux. However, a few recent studies suggested a role for papillomavirus infection in esophageal tumorigenesis, although the exact route of transmission and invasion of the virus has not been fully elucidated. A case of esophageal squamous papilloma at the site of endoscopic injection sclerotherapy (EIS) for varices is reported. Papilloma development was followed up clinically during a 2-year period, and the papilloma was removed by endoscopic mucosal resection. Histological examination of the tissue confirmed the diagnosis of squamous cell papilloma. DNA analysis of the tumor showed integration of papillomavirus type 16 but not types 18 and 33. The surrounding normal mucosa did not contain any of the three virus types. Injury such as ulceration resulting from EIS may have provided a locus susceptible to the viral infection. The clinical course after EIS should be monitored carefully to detect papilloma formation.
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PMID:Human papillomavirus type 16-positive esophageal papilloma at an endoscopic injection sclerotherapy site. 783 98

Esophageal replacement by a segment of isoperistaltic ileum with cecum or by transverse or left colon will allow near-normal swallowing for many years. The authors reviewed the course of 59 children who had bypass of their entire esophagus and of four whose distal esophagus was resected and replaced. The follow-up period ranges from 1 to 37 years; in 36 cases, it exceeds 5 years. Thirty children had caustic strictures and 25 had either isolated esophageal atresia or atresia with fistula. Two children with esophageal injury caused by foreign body ingestion and two with congenital strictures also required complete bypass. Four patients required resection and replacement of the distal esophagus only; two had acquired strictures from gastroesophageal reflux, one had varices, and one had a teratoma involving the esophagus. A retrosternal isoperistaltic ileocolic segment is our preference for complete esophageal replacement. Forty-eight patients underwent esophageal reconstruction with this procedure. The esophagus damaged by caustic ingestion was left in place in all patients, without any subsequent problem. The authors have not used the distal esophagus for anastomosis in patients with atresia, because this segment may be abnormal; and, in any case, an isoperistaltic cologastric anastomosis does not reflux. The right or left colon or jejunum was used in the other cases. Three children lost an interposed intestinal segment from necrosis even though the bowel appeared to be well vascularized at the end of the operation. Each patient had successful reconstruction using another type of interposition. An intrathoracic leak occurred in one infant. A cervical anastomotic leak developed in 11 children, and a stricture in 13. Strictures were more common in patients who had caustic burns. Three patients required surgery for adhesive intestinal obstruction. A redundant colon transplant with ulceration, and the herniation of an ileal segment into the pleural cavity with obstruction prompted reoperation in two other patients. There were two deaths early in the series, one of which was secondary to postoperative respiratory arrest. The other death occurred in a child who had a caustic pharyngeal burn and chronic aspiration. All patients were seen in our office recently, or they or their parents were interviewed by phone. All of them are taking all of their nutrition by mouth. Forty-three of the 61 survivors have had no difficulty with swallowing. One required reoperation to enlarge the thoracic inlet. Seventeen other have mild dysphagia that does not require treatment. The patients with esophageal atresia or atresia and fistula consistently have not grown as well as those who required replacement for an acquired condition or injury.
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PMID:Intestinal bypass of the esophagus. 863 84

Endoscopic variceal sclerotherapy (EVS) has been considered the mainstay of therapy for bleeding esophageal varices in adults. However, recent data have shown that endoscopic variceal ligation (EVL) is just as efficacious and has fewer complications than EVS. Although there are many reports concerning EVL in adults, only a few studies have been done in children. This report describes experience with EVL in 22 children with esophageal variceal hemorrhage. Eighty-seven EVL procedures were performed during a 9-year period in 22 children. The causes of portal hypertension were biliary atresia (10), portal vein thrombosis (8), chronic active hepatitis (1), cirrhosis secondary to cystic fibrosis (2), and primary sclerosing cholangitis (1). The age range at the onset of variceal bleeding was 8 months to 19 years. Twelve patients had EVS before EVL treatment was begun. Distal esophageal varices (one to four per session) were mechanically ligated using an elastic band ligature device attached to a flexible endoscope. The aim of therapy was obliteration of distal esophageal varices by EVL, every 2 to 4 weeks, until eradication. Subsequent EVL was dictated by the status of the varices. Outcome was assessed with respect to survival, rebleeding, status of varices, and complications. The patients underwent a mean of four sessions of EVL (range, one to eight). Four patients subsequently underwent liver transplantation. Of the 18 patients remaining (average follow-up period, 5.3 years), 12 had their varices eradicated (average of four EVL sessions), four are still in treatment, one has not been evaluated in the past 4 years, and one died of liver failure. Complications included bleeding between sessions (6 patients), cervical esophageal perforation (1 patient), and transient fever (2 patients). No child has experienced symptoms of esophageal stenosis or gastroesophageal reflux. Two patients died of liver disease, unrelated to bleeding from portal hypertension. EVL is effective in controlling variceal hemorrhage in children with portal hypertension, regardless of etiology. The complication rate is low, and EVL is an acceptable and perhaps preferable alternative to EVS in children with esophageal varices.
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PMID:Management of esophageal varices in children by endoscopic variceal ligation. 886 33

The effects of transjugular intrahepatic portosystemic shunt (TIPS) placement on esophageal motor function and gastroesophageal reflux were investigated in patients with esophageal varices. In six men with esophageal varices, esophageal manometry and upper gastrointestinal endoscopy were performed before and 15-20 days after TIPS placement. Intraesophageal pH monitoring was performed in the four patients with severe esophageal varices (defined as the largest sized varices) following TIPS placement. Findings were compared with those in six healthy men (controls) who underwent esophageal manometry and intraesophageal pH monitoring. The esophageal varices resolved or were reduced after TIPS placement. Resting lower esophageal sphincter (LES) pressures were similar in the study group before and after TIPS placement and in the control subjects. The incidence and progression of esophageal contractions were similar in the study group before and after TIPS placement and in the control subjects. At 3 cm above the LES, the amplitude of esophageal contraction after TIPS placement was significantly higher than that before TIPS placement. At 3 and 8 cm above the LES, the amplitude of esophageal contraction in the control subjects was significantly higher than that in the study group before and after TIPS placement. Esophageal acid exposure time after TIPS placement was similar to that in the controls. TIPS placement is a useful treatment that improves esophageal motor function without the occurrence of pathologic gastroesophageal reflux.
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PMID:Effects of transjugular intrahepatic portosystemic shunt (TIPS) on esophageal motor function and gastroesophageal reflux. 965 6

In asthma patients, microaspiration of acid into the lower airways (ie, airway acidification) causes such respiratory responses as cough and bronchoconstriction. The mechanism of bronchoconstriction induced by airway acidification is unknown, although evidence is emerging that increasing proton concentrations in airway tissues can activate a subpopulation of primary sensory neurons, so-called capsaicin-sensitive primary sensory neurons, that contain such neuropeptides as the tachykinins substance P (SP) and neurokinin A (NKA). Protons activate a capsaicin-operated channel/receptor, located in the afferents of capsaicin-sensitive neurons, with the subsequent opening of ion channels that are permeable to sodium, potassium, and calcium ions. This event initiates a propagated action potential that antidromically depolarizes collateral fibers and triggers neuropeptide release from nerve fiber varicosities. The tachykinins SP and NKA, released from terminals of primary sensory neurons in peripheral tissues, cause all the major signs of inflammation (neurogenic inflammation) by means of activation of NK(1) and NK(2) receptors. Exposure of the airways to acidic solutions stimulates sensory nerve endings of capsaicin-sensitive sensory neurons and causes different airway responses, including bronchoconstriction. Recently, the NK(2), and to a lesser extent the NK(1), receptors have been shown to be involved with citric acid-induced bronchoconstriction in the guinea pig, which is in part mediated by endogenously released bradykinin. Tachykinins and bradykinin, released by airway acidification, could also modulate citric acid-induced bronchoconstriction by their ability to subsequently release the epithelially derived bronchoprotective nitric oxide (NO). Further study with selective tachykinin NK(1) and NK(2) agonists demonstrated that only the septide-insensitive tachykinin NK(1) receptor releases NO. Thus, bronchoconstriction induced by citric acid inhalation in the guinea pig, mainly caused by the tachykinin NK(2) receptor, is counteracted by bronchoprotective NO after activation of bradykinin B(2) and tachykinin NK(1) receptors in airway epithelium. If a similar mechanism is involved in the pathogenesis of bronchial asthma associated with gastroesophageal reflux in the respiratory tract, new therapeutic strategies should be investigated.
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PMID:Mechanisms of citric acid-induced bronchoconstriction. 1174 19

Proximal gastric relaxation is a vago-vagal reflex upon food intake. The efferent neurons involved at the level of the stomach are nonadrenergic noncholinergic. Deficient proximal gastric relaxation is observed in a portion of patients with functional dyspepsia, while exaggerated relaxation might contribute to the development of gastroesophageal reflux disease via triggering of transient lower esophageal sphincter relaxations. Nitric oxide (NO) is mediating, together with vasoactive intestinal polypeptide (VIP) as parallel cotransmitter, the nonadrenergic noncholinergic neurotransmission of the proximal stomach. Evidence for a sequential link between VIP as neurotransmitter and muscular NO generation was obtained when studied in isolated gastric smooth muscle cells; inducible NO synthase seems expressed. The endogenous gastric nitrergic neurotransmitter is not sensitive to superoxide anion generators and NO scavengers, that reduce the relaxation to exogenous NO. This is not due to the release of a nerve-derived hyperpolarizing factor in addition of NO, nor to binding to thiols, but Cu/Zn superoxide dismutase is involved in the protection of endogenous NO versus superoxide anions and scavenging. The release of NO from gastric nitrergic neurons is not sensitive to negative feedback but is inhibited via presynaptic alpha 2-adrenoceptors. Nitric oxide functionally antagonizes acetylcholine in the smooth muscle cells but does not influence the release of acetylcholine at the cholinergic varicosities. Stimulating or inhibiting the gastric nitrergic neurons might be a target for drug therapy in functional dyspepsia or gastro-esophageal reflux, respectively.
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PMID:Pharmacological characterization of the nitrergic innervation of the stomach. 1223 40

Gastroesophageal reflux disease (GERD) is a condition where stomach acids are chronically regurgitated into the esophagus and oral cavity, resulting in pathology, such as esophagitis, varices or ulcers. Continual exposure of the teeth to these acids can also cause severe dental erosion. This condition frequently is asymptomatic, and the only evident sign may be the irreversible erosion of tooth structure. The dentist often is the first health care professional to identify the affected dentition. Knowledge of this cause and effect relationship between GERD and dental erosion will better prepare the practitioner to refer patients for appropriate diagnosis and treatment of the underlying medical condition and provide treatment for the affected teeth. This article presents a case report where dental erosion was present due to GERD. After management of the disease with medication, dental treatment of the eroded dentition is described, including diagnosis, treatment planning and restorative reconstruction.
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PMID:Restoring erosion associated with gastroesophageal reflux using direct resins: case report. 1598 62

The barium esophagram is a valuable diagnostic test for evaluating structural and functional abnormalities of the esophagus. The study is usually performed as a multiphasic examination that includes upright double-contrast views with a high-density barium suspension, prone single-contrast views with a low-density barium suspension, and, not infrequently, mucosal-relief views with either density of barium suspension. The double-contrast phase optimizes the ability to detect inflammatory or neoplastic diseases, whereas the single-contrast phase optimizes the ability to detect hiatal hernias and lower esophageal rings or strictures. Fluoroscopic examination of the esophagus is also important for assessing motility disorders such as achalasia and diffuse esophageal spasm. This article is a review of gastroesophageal reflux disease, other types of esophagitis, benign and malignant esophageal tumors, varices, lower esophageal rings, diverticula, and esophageal motility disorders, all of which can be diagnosed with the aid of esophagography.
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PMID:Diseases of the esophagus: diagnosis with esophagography. 1617 17


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