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Query: UMLS:C0002871 (anemia)
 52,094 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gastro-oesophageal reflux occurs when the pressure barrier of the lower oesophageal sphincter (LOS) fails due to a low basal pressure (less than or equal to 6 mm Hg), sphincteric relaxations or a noncompensated increase in intragastric pressure. This reflux becomes pathological when it leads to symptoms severe enough for the patient to seek medical help or results in reflux oesophagitis or its complications. Damage to the oesophageal mucosa develops when the balance between aggressive and defensive factors is no longer in equilibrium. The main aggressive factor is acid-pepsin or alkaline bile secretion. Defence against this aggression is based on rapid removal of the refluxate from the oesophagus (oesophageal clearance) and on poorly understood mucosal resistance. The length of time acid is in contact with the oesophageal mucosa is shortened by adoption of an upright position, by swallow-induced oesophageal peristalsis and saliva. Treatment of pathological reflux aims (1) to decrease acid aggression by means of H2-receptor antagonists or proton pump inhibitors; (2) to strengthen the anti-reflux barrier and improve oesophageal clearance by prokinetic drugs that increase the LOS pressure and enhance peristaltic contractions; and (3) to boost mucosal resistance by sucralfate or prostaglandin analogues. Initial treatment of gastro-oesophageal reflux disease may be symptomatic provided that there are no alarming symptoms, such as dysphagia, anaemia or weight loss. Usually either H2-receptor blockers or prokinetic drugs are used. Endoscopy is indicated whenever alarming symptoms are present and when there is insufficient symptomatic improvement after a 4-6-week therapeutic trial. Moderate oesophagitis may be treated in the same way.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Pathophysiology and treatment of gastro-oesophageal reflux disease. 257 7

A 50-year-old woman who had been on maintenance hemodialysis for 5 years developed severe anemia resistant to treatment with iron supplements and erythropoietin 4 months prior to hospital admission. Her stool occult blood test was positive, and an initial panendoscopy revealed evidence of possible antral gastritis. However, repeated administration of sucralfate, H2 blockers and a proton pump inhibitor was not effective in preventing further gastrointestinal tract blood loss and subsequent refractory anemia. She required multiple blood transfusions and hospital admissions during this period. There was no obvious coagulopathy or thrombocytopenia. After her third admission, a second panendoscopy demonstrated the typical picture of watermelon stomach. A trial of hormone therapy with estrogen and progesterone increased the hemoglobin level within a month without further evidence of active gastrointestinal bleeding. From our experience with this case, we found that the diagnosis of antral vascular ectasia (watermelon stomach) with bleeding requires a high degree of clinical alertness and careful endoscopic examination. Estrogen and progesterone therapy may provide a good option for treating the disease in uremic patients without an obvious complication. To the best of our knowledge, this is the first report demonstrating the use of maintenance hormone therapy in a female uremic patient to successfully treat watermelon gastric bleeding.
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PMID:Watermelon stomach--an unusual cause of recurrent upper gastrointestinal bleeding in a uremic patient receiving estrogen-progesterone therapy: case report. 1007 34

Gastroesophageal reflux disease (GORD) is more frequent among people with intellectual disability than among the intellectually normal population. Also GORD is more serious in this population. The diagnosis is often missed, because most intellectually disabled cannot express their complaints of GORD. For that reason a multidisciplinary working group of the Dutch Association of physicians active in the care of persons with a mental handicap has developed guidelines. The working group recommends endoscopy in case of a (alarm) symptoms: haematemesis, prolonged vomiting, irondeficiency anaemia e.c.i., and a 24 hour oesophageal pH test in case of b (aspecific) symptoms: recurrent pneumonia, refusal of food, regurgitation, rumination, dental erosions. In general most patients are cured with drug treatment (omeprazol or another proton pump inhibitor). If symptoms are not improved after 6 months of optimal treatment, surgical treatment may be considered.
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PMID:[Diagnosis and treatment of gastroesophageal reflux disease in the mentally retarded: guidelines of a multidisciplinary consensus work group. Dutch Association of Physicians in Care of Mentally Handicapped]. 1087 95

Gastroesophageal reflux is a very common disorder. Typical symptoms are heartburn, regurgitation and chest pain. Recently, it has been demonstrated that gastroesophageal reflux may generate or worse extraesophageal symptoms such as asthma, chronic bronchitis, posterior laryngitis, and chronic cough. The diagnosis of gastroesophageal reflux is suggested by typical symptoms which improve under a therapy with proton pump inhibitors. pH-monitoring over 24 hours is able to establish directly the diagnosis by measuring acid reflux into the esophagus. Manometry detects the two most common causes of gastroesophageal reflux: insufficiency of the lower esophageal sphincter or esophageal motility abnormalities. Gastroesophageal reflux can lead to reflux esophagitis, which is diagnosed endoscopically. An endoscopy should routinely be performed in case of dysphagia, anemia, or loss of weight. A long-term sequela of gastroesophageal reflux is the development of Barrett's-esophagus, a condition which has to be verified by endoscopy and biopsy. This premalignant lesion is defined by a metaplastic change from the normal squamous mucosa to a specialized intestinal epithelium characterized by goblet cells. Because dysplasia in these metaplastic areas can lead to esophageal adenocarcinoma, regular endoscopic surveillance with biopsies is recommended. Gastroesophageal reflux can significantly impair the quality of life and can cause complications that include the neoplastic progression from Barrett's esophagus to carcinoma. Therefore, appropriate diagnostic procedures and adequate therapy are required. This article summarizes the diagnostic approach to patients with gastroesophageal reflux, reflux esophagitis and Barrett's-esophagus. The impact of endoscopy, pH-monitoring, esophageal manometry, radiology and scintigraphy are reviewed.
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PMID:[Diagnosis of gastroesophageal reflux and Barrett esophagus]. 1092 25

Serum hypergastrinemia promotes the growth of colorectal adenocarcinoma. Some colorectal adenomas express cholecystokinin B/gastrin receptor mRNA, and thus hypergastrinemia may increase progression through the adenoma-carcinoma sequence. This was investigated in the multiple intestinal neoplasia APC(Min-/+) mouse. Serum gastrin levels in APC(Min-/+) mice were elevated 5-6-fold by oral administration of omeprazole (75 mg/kg). Terminal tumor burden was monitored by onset of anemia. A labeling index was generated by immunohistochemical detection of bromodeoxyuridine incorporation. Serum gastrin was neutralized by antigastrin antibodies raised in situ by use of a gastrin immunogen, Gastrimmune. Hypergastrinemia resulted in reduced survival of the APC(Min-/+) mice from a median survival of 13 weeks in the controls to 10 weeks following omeprazole treatment (P < 0.00001, log-rank test). The labeling indices of adenomas from the small and large intestines of omeprazole-treated mice were increased 35 and 29%, respectively (P < 0.05 and P < 0.025, respectively). Gastrimmune immunization reversed both the survival effect and the increased proliferation resulting from serum hypergastrinemia. Hypergastrinemia may promote the progression of existing premalignant colonic lesions by increasing proliferation. Clinical investigations should determine whether this occurs in the human scenario, considering the widespread use of proton pump inhibitors.
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PMID:Hypergastrinemia promotes adenoma progression in the APC(Min-/+) mouse model of familial adenomatous polyposis. 1121 60

Usual gastroesophageal reflux (GER) presentations are heartburn and acid regurgitation. The prevalence in occidental population ranges from 5 to 45% according to symptoms frequency. Oesophagitis is observed in 30 to 50% of examined patients and only erosive and ulcerative lesions must be considered. Distinction is made between non-severe oesophagitis (isolated loss of substance), severe oesophagitis (circonferential loss of substance) and complicated oesophagitis (stenosis, ulcerations, brachyoesophagus). 24-hour pH-monitoring analyses reflux duration and relations between symptoms and reflux specially in unusual extraoesophageal presentations. Symptoms and quality of life are the main criteria for staging. In few patients, oesophagitis is severe. Complications (stenosis, ulcerations, bleeding, endobrachyoesophagus) are observed in 10 to 15% of cases. Endobrachyoesophagus with intestinal metaplasia is a risk for neoplasia. The consensus conference proposes this initial therapeutic strategy. In cases of time-spaced symptoms: antiacids, alginic acid or low doses of anti-H2 with life style changes. In cases of typical frequent symptoms, in patients younger than 50 years: 4-weeks treatment with half dosed proton pump inhibitors (PPI) or standard doses of anti-H2 or prokinetics. Nowadays, the majority of the experts propose empiric full-dose treatment. This attitude is more logical as total symptoms suppression with full dose PPI brings positive clues for exact GOR diagnostic without endoscopy. In patients older than 50 years or with alarming symptoms (weight loss, dysplagia, bleeding, anemia): endoscopy must be performed. Patients with non severe oesophagitis: PPI without checking endoscopy. In patients with severe or complicated oesophagitis: 8-weeks treatment following by endoscopy; in non relieved patients: doses are increased. In cases of extraoesophageal presentations: standard PPI treatment during 4 to 8 weeks if GER is well established. In long term strategy, if recidives are rare: intermittent treatment. In early and frequent recidives: long term adapted PPI or surgery. Stenosis are treated by PPI, pneumatic dilatation or surgery if unsuccessful. Brachyoesophagus must be checked by endoscopy every 2 years (malignancy risk).
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PMID:[Diagnosis and treatment of gastroesophageal reflux in the adult: guidelines recommended by French and Belgian consensus]. 1125 2

Gastrointestinal stromal tumors (GISTs) are rare neoplasms arising from connective tissue elements of the gastrointestinal wall. They show a great heterogeneity with respect to their histogenetic, morphologic and prognostic characteristics. GISTs are known with myoid, neural or mixed features of differentiation. Clinical findings are gastrointestinal bleeding, abdominal pain and weight loss. We report on the case of a 50-year-old male patient who presented with melena and acute anemia (hemoglobin 10.5 g/dl). Esophagogastroduodenoscopy revealed a broad-based, centrally ulcerated polypoid formation of 3 cm in the gastric corpus as the cause of the upper gastrointestinal bleeding. Multiple endoscopic biopsies were negative for neoplastic changes. Because of no tendency of healing after triple eradication therapy of Helicobacter pylori and following proton pump inhibitor medication, the patient underwent distal gastrectomy with gastrojejunostomy. GIST of combined smooth muscle and neural type was diagnosed by histological and immunohistochemical examination. The features with increased mitotic activity and cellularity were those of a borderline stromal tumor. 6 months after surgery the patient is well with no signs of residual malignancy. This case demonstrates that rare stromal neoplasms have to be taken into account in the differential diagnosis of gastrointestinal tumors even if endoscopic biopsies are negative for neoplastic changes. Because of the uncertain biological behavior of the GISTs an early surgical intervention is recommended.
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PMID:Gastric stromal tumor--a rare cause of an upper gastrointestinal bleeding. 1147 2

Venous malformations of blue rubber bleb nevus syndrome (BRBNS) may involve any area of the gastrointestinal tract. Gastrointestinal blood loss and anemia brings these patients to the attention of gastroenterologists. Effective treatment of these malformations throughout the gastrointestinal tract requires aggressive management to ultimately decrease blood loss and restore the patient's hemoglobin to a near-normal level. Treatment of patients with BRBNS includes supportive measures, endoscopic ablation, and surgery. Supportive therapy consists of proton pump inhibitors and octreotide to decrease blood loss, iron replacement, and blood transfusions. The effective management of patients with anemia demands aggressive treatment of venous malformations in the small bowel. This requires a collaboration between the surgeon and the therapeutic endoscopist, ie, laparotomy and excision of larger lesions with surgically assisted enteroscopy and thermal ablation of smaller lesions via enterotomy. There is no effective systemic therapy for treatment of the vascular malformations in patients with BRBNS.
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PMID:Blue Rubber Bleb Nevus Syndrome. 1156 Jul 90

Omeprazole is a proton pump inhibitor that is used commonly in the treatment of acid-peptic disorders. Although omeprazole is generally well tolerated, serious adverse effects such as renal failure have been reported. Thus far, 17 cases of acute interstitial nephritis (AIN) secondary to omeprazole have been described. Another case of AIN is described in a 36-yr-old woman presenting with nausea, vomiting, weight loss, and a rising serum creatinine concentration. Omeprazole therapy had ceased 2 wk before admission. AIN was diagnosed by renal biopsy and corticosteroid therapy was initiated. After 4 wk of therapy the serum creatinine concentration had normalized. Among the reported cases in the literature, AIN was diagnosed after an average of 2.7 months of therapy with 20-40 mg of omeprazole daily. Recurrence was universal on rechallenge. Common symptoms included fatigue, fever, anorexia, and nausea. The classic triad of fever, rash, and eosinophilia was uncommon. Typical laboratory features included hematuria, proteinuria, pyuria, eosinophilia, and anemia. Management consisted of withdrawal of omeprazole and corticosteroid therapy in some patients. All but one patient recovered normal renal function. Corticosteroid therapy was well tolerated and may have been beneficial.
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PMID:Acute interstitial nephritis due to omeprazole. 1177 62

Upper gastrointestinal bleeding is a potentially fatal condition at times due to loss of large volumes of blood. Common sources of upper gastrointestinal bleeding in children include mucosal lesions and variceal hemorrhage (most commonly extra hepatic portal venous obstruction) and, in intensive care settings infections and drugs are other etiological factors associated with bleeding. Massive upper GI bleeding is life threatening and requires immediate resuscitation measures in the form of protection of the airways, oxygen administration, immediate volume replacement with ringer lactate or normal saline, transfusion of whole blood or packed cells and also monitoring the adequacy of volume replacement by central venous lines and urine output. Upper GI endoscopy is an effective initial diagnostic modality to localize the site and cause of bleeding in almost 85-90% of patients. Antacids supplemented by H2- receptor antagonists, proton pump inhibitors and sucralfate are the mainstay in the treatment of bleeding from mucosal lesion. For variceal bleeds, emergency endoscopy is the treatment of choice after initial haemodynamic stabilization of patient. If facilities for endoscopic sclerotherapy (EST) are not available, pharmacotherapy which decreases the portal pressure is almost equally effective and should be resorted to. Shunt surgery is reserved for patients who do not respond to the above therapy. Beta blockers combined with sclerotherapy have been shown to be the most effective therapy in significantly reducing the risk of recurrent rebleeding from varices as well as the death rates, as compared to any other modality of treatment. Based on studies among adult patients, presence of shock, co-morbidities, underlying diagnosis, presence of stigmata of recent hemorrhage on endoscopy and rebleeding are independent risk factors for mortality due to upper GI bleeding. Rebleeding is more likely to occur if the patient has hematemesis, liver disease, coagulopathy, hypotension and or anemia. There is a great need for conducting therapeutic trials as well as identifying predictors of outcome of upper GI bleeding in children to develop evidence based management protocols.
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PMID:Upper gastrointestinal bleeding: etiology and management. 1192 33


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