Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Reflux esophagitis and anastomotic ulcer are potential complications associated with surgery for esophagogastric lesions. This study compared 10 cases following terminal esophagoproximal gastrectomy (TEPG) for esophageal varices and 20 cases following esophageal transection (ET) for esophageal varices with respect to postoperative motor function and mucosal blood supply, to ascertain the reason for the development of anastomotic ulcer. Endoscopic findings showed that anastomotic ulcers were detected more often after TEPG than after TR. Maximum swallowing pressure, high pressure zone pressure, and length did not differ between the two groups. However, maximum swallowing pressure in the lower esophagus after both procedures was significantly lower than in the control group (20 cases; p < 0.01). The results, measured by reflectance spectrophotometry, showed that the index of esophageal mucosal blood volume following TEPG is significantly lower than that following ET and in non-operated esophageal varices (10 cases; p < 0.01). Yet the index of oxygen saturation of hemoglobin was similar in the three groups. This study has demonstrated that patients undergoing TEPG have mucosal ischemia of the lower esophagus, causing the development of anastomotic ulcers.
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PMID:Postoperative motor function and mucosal blood flow of lower esophagus: comparison between terminal esophagoproximal gastrectomy and esophageal transection for esophageal varices. 831 7

Cameron lesions are seen in 5.2% of patients with hiatal hernias who undergo EGD examinations. The prevalence of Cameron lesions seems to be dependent on the size of the hernia sac, with an increased prevalence the larger the hernia sac. In about two thirds of the cases, multiple Cameron lesions are noted rather than a solitary erosion or ulcer. Historically, Cameron lesions present clinically with chronic GI bleeding and associated iron deficiency anemia. With increased awareness of the existence of this lesion, however, it is now more frequently seen as an incidental finding during EGD. Cameron lesions can also present as acute upper GI bleeding, occasionally life-threatening, in up to one third of cases. Therefore, Cameron lesions should be considered in any patient in whom a hiatal hernia is noted during endoscopic examination. Concomitant acid-peptic diseases are seen in a majority of individuals, especially reflux esophagitis and its complications. Mechanical trauma, ischemia, and acid mucosal injury may play a role in the pathogenesis of Cameron lesions. The choice of therapy of Cameron lesions, medical or surgical, should be individualized for each patient. Of those patients who were treated with a spectrum of medical therapy and who have had long-term follow-up, about one third have had a recurrence of the lesion and 17% (8/48) have developed complications, most commonly either acute upper GI bleeding (6.3%) or persistent and recurrent iron deficiency anemia (8.3%).
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PMID:Hiatal hernia with cameron ulcers and erosions. 889 1

Our objective was to assess the complications of laparoscopic fundoplication in 77 patients older than 70 years of age. The indications for surgery were (1) complications of reflux esophagitis (n = 17), (2) large hiatal hernia (n = 10), (3) asthma and bronchitis (n = 7), (4) the need for other surgery (n = 13), and (5) a patient's desire to discontinue medical treatment that was controlling reflux esophagitis (n = 30). Operative time varied from 34 to 250 minutes (mean [standard deviation], 116 +/- 20). Hospital stay varied from 12 hours to 19 days (mean, 1.2). No patient needed conversion to open operation. Intraoperative complications were observed in 4 patients (5.2%): left pneumothorax in 2, major operative bleeding in 1, and minor spleen lesion in 1. The most common postoperative complications were gas-bloating syndrome and dysphagia. Gastric ulcer was diagnosed in two. Other postoperative complications included acute delirium, acute urinary retention, and acute ischemia of the lower extremity. One patient died of congestive heart failure. It is concluded that laparoscopic fundoplication is an effective procedure for treating geriatric patients with reflux esophagitis and may be performed with low morbidity and mortality rates.
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PMID:Complications of laparoscopic fundoplication in the elderly. 1259 50

In esophagogastrostomy during laparoscopically assisted proximal gastrectomy, some problems have occurred; the main ones being reflux esophagitis and the technical difficulty in anastomosis. We have had good results with a hemidouble stapling technique; the center rod of circular stapler is pierced through the left end of the staple line of the stomach. The longest distance from the pylorus to the esophagogastrostomy can be fired in this position. The distance is longer, so alkaline esophagitis is rarer. When the center rod is pierced through the anterior or posterior gastric wall, the operator may be worried about ischemia of the area surrounded by the linear stapler and circular stapler. In hemidouble stapling, an ischemic area is not created at all structurally. Any surgeon can perform a reproducible anastomosis because the place pierced with the center rod is fixed. This technique is easy and safety to operate via minilaparotomy.
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PMID:Hemidouble stapling for esophagogastrostomy during laparoscopically assisted proximal gastrectomy. 1692 4

Systemic sclerosis and its subtypes differ significantly from other diseases in rheumatology and clinical immunology, as the aberrant activation of the immune system does not result in an inflammation-driven destruction but in a progressive matrix synthesis, especially of the skin. Owing to the recently established networks in Germany (DNSS) as well as in Europe (EUSTAR), a detailed profile of the affected patients could be determined. No specific predictive markers for the disease exist in the early phases of the disease although a Raynaud phenomenon can be present up to ten years prior to the first organ manifestations. On the other hand, distinct clinical features and laboratory parameters can be independent predictive markers for the outcome of a given patient. Therefore, monitoring should be performed on a regular basis in the preclinical and early stages of the disease, as early diagnosis can reduce morbidity and mortality of the affected patients significantly, especially with regard to pulmonary hypertension, digital ischemia, reflux esophagitis and sclerodermal renal crisis.
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PMID:[Systemic sclerosis]. 1821 18

Melatonin is a potent reactive oxygen metabolite scavenger and antioxidant that has been shown to influence many physiological functions of the gastrointestinal (GI) tract including secretion, motility, digestion and absorption of nutrients. The role of melatonin in gastroduodenal defense and ulcer healing has been the subject of recent investigations. Melatonin produced in the GI mucosa plays an important role in protection against noxious agents thus contributing to the maintenance of GI integrity and to esophageal protection, gastroprotection and ulcer healing. This review was designed to summarize the involvement of melatonin, conventionally considered as a major hormone of the pineal gland, in the maintenance of gastric mucosal integrity, gastroprotection, ulcer healing and intestinal disorders. Melatonin was originally shown to attenuate gastric mucosal lesions but controversy exists in the literature as to whether melatonin derived from the pineal gland, considered as the major source of this indole, or rather gastrointestinal melatonin plays predominant role in gastroprotection. Intragastric and central administration of exogenous melatonin and L-tryptophan, this indoleamine precursor, affords protection against gastric hemorrhagic damage caused by the exposure of gastric mucosa to variety of non-topical and topical ulcerogens such as stress, ethanol and ischemia-reperfusion. The speed of ulcer healing in experimental animals and humans is accelerated by melatonin. This indoleamine could be also effective against the esophageal lesions provoked by reflux esophagitis in animal models and prevents the incidence of GERD in humans. The melatonin-induced gastroprotection is accompanied by an increase in gastric blood flow, plasma melatonin concentration, enhancement in mucosal generation of PGE2, luminal NO content and plasma gastrin levels. Melatonin scavenges reactive oxygen metabolites, exerts anti-oxidizing and anti-inflammatory actions and inhibits the formation of metalloproteinases- 3 and -9; both implicated in the pathogenesis of gastrointestinal injury and formation of gastric ulcers. Blockade of MT2 receptors by luzindole, significantly attenuated melatonin- and L-tryptophan-induced protection and increased the speed of ulcer healing and these effects were accompanied by an increase in the GBF and luminal content of NO suggesting that melatonin exhibits gastroprotection and hyperemia via activation of MT2 receptors and release of NO. The accumulated evidence indicates that the melatonin-induced gastroprotection and the enhancement in healing rate of gastric ulcers may involve the gastroprotective factors derived from the activation of PG/COX and NO/NOS systems as well as gastrin which also was shown to exhibit protective and trophic effects in the upper GItract. Interestingly, pinealectomy, which suppressed plasma melatonin levels, markedly exacerbated gastric lesions induced by topical and non-topical ulcerogens and these effects are counteracted by a concurrent supplementation with melatonin. Evidence is provided that exogenous melatonin and that converted from its precursor, L-tryptophan, attenuates acute gastric lesions and accelerates ulcer healing via interaction with MT2 receptors due to an enhancement of gastric microcirculation, probably mediated by NO and PG derived from NOS and COX-1 and COX-2 overexpression and activity. The pineal gland plays an important role in the limitation of gastric mucosal injury and the acceleration of ulcer healing via releasing endogenous melatonin, which attenuates oxidative stress and exerts anti-inflammatory action.
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PMID:Mechanisms of esophageal protection, gastroprotection and ulcer healing by melatonin. implications for the therapeutic use of melatonin in gastroesophageal reflux disease (GERD) and peptic ulcer disease. 2425 71