Tuesday, August 17, 2010

Recognize Closer Barrett's Esophagus Disease

Barrett's esophagus (called Barrett's syndrome, cello, epithelium along the bottom of the esophagus or colloquially) Barrett refers to the abnormal change (metaplasia) in the cells of the lower esophageal considered caused by damage by chronic acid exposure or esophageal comments. Barrett's esophagus occurs in approximately 10% of patients who seek medical care for heartburn (GERD). It is considered a precancerous lesion and is associated with an increased risk of cancer of the esophagus.
The name comes from the state, Dr. Norman Barrett (1903-1979), actor, hospital surgeon at St Thomas', which describes a state in 1957.
Causes and Symptoms
Barrett's esophagus is caused by gastroesophageal reflux, reflux (UK: GORD), which allows stomach contents to damage the cells lining the lower esophagus. However, any person who has GERD will develop Barrett's esophagus. Scientists are unable to predict who suffer from heartburn will develop Barrett's esophagus. Although there is no relationship between severity of heartburn and the development of Barrett's esophagus, there is a relationship between chronic heartburn and Barrett's esophagus development. Sometimes people with Barrett's esophagus have no symptoms of heartburn at all. In rare cases, damage to the esophagus can be caused by ingestion of corrosive substances such as laundry.
Change in normal cells, precancerous Barrett's esophagus shows does not cause specific symptoms. However, the warning signs that should not be ignored are:
  • Frequent heartburn and long-term
  • Swallowing problems (dysphagia)
  • Blood, vomiting
  • Pain under the breastbone where the esophagus meets the stomach 
  • Involuntary weight loss because eating is painful

Barrett's esophagus is marked by the presence of epithelium of the lower esophagus, replacing the normal cells such as squamous metaplasia. secretory epithelium may be more resistant to the erosive effects of gastric acid secretion, however, this metaplasia confers an increased risk of adenocarcinoma.

Metaplastic cells may be of two types: gastric (similar to those of the stomach, which is not technically Barrett's esophagus) or intestines (such as cells in the intestine). Biopsy of the region often contain a mixture of both. Type of intestinal metaplasia is a kind of metaplasia associated with cancer risk in people genetically predisposed.
Metaplasia of Barrett's esophagus is quite visible through the gastroscope, but biopsy should be examined microscopically to determine whether the cells of the stomach or intestine into the wild. colonic metaplasia is usually identified by the research of goblet cells of the epithelium and is necessary for a true diagnosis of Barrett.
There are many histologic mimics of Barrett's esophagus (ie goblet cells in normal epithelium of the esophagus transition channels of submucosal glands, cells pseudogoblet "in which rich foveolar (gastric) -type mucin simulates the acid mucin goblet cell true). Notes to submucosal glands and epithelium transition type analysis of different levels of tissue may allow the pathologist to reliably distinguish between goblet cells, submucosal glands and ducts true esophagus (Barrett's metaplasia cylindrical specialist). Using the histochemical stain Alcian blue pH 2.5 is often used to distinguish true intestinal-type mucin their histological mimics. Recently, immunohistochemistry with antibodies against CDX-2 (specific medium and rear exit of the intestine) has also been used to identify true intestinal-type metaplastic cells.
After an initial diagnosis of Barrett's esophagus is present, about people being monitored annually to detect changes that indicate an increased risk of progression to cancer: development of dysplasia. There are significant differences in the assessment of dysplasia among pathologists. Recently, gastroenterology societies and gastrointestinal disease has recommended that the diagnosis of high grade dysplasia in Barrett to be confirmed by at least two trained pathologists IM communities before definitive treatment of patients.
Current recommendations for routine endoscopy and biopsy (looking for dysplastic changes) every 12 months or if the esophagus is controlled by a basic inhibitor proton pump drugs in combination with measures to prevent reactions. Proton pump inhibitors have not yet been proven to prevent esophageal cancer. Laser treatment is used in severe dysplasia and cancer may require open surgery, radiotherapy or systemic chemotherapy. In addition, a recent 5-year study showed that randomized controlled photodynamic therapy using Photofrin is statistically more effective in eliminating areas of dysplasia of the growth of the exclusive use of the inhibitor of the proton pump. There is currently no reliable way to determine which patients with Barrett's esophagus go on the development of esophageal cancer, but recent studies have shown that the detection of three different genetic diseases have been associated with a maximum 79% risk of developing cancer within 6 years. Endoscopic mucosal resection (EMR) has also been evaluated as management techniques.
Removal BARRX
HALO radio-frequency ablation system current technology has been tested in clinical trials since 2003. Complete eradication rate of non-dysplastic and dysplastic over 90% has been demonstrated in several studies.
HALO ablation technology is designed to remove Barrett's epithelium in short, the endoscopic procedure well tolerated and offers an alternative to "watchful waiting" for patients with intestinal metaplasia, dysplasia, low grade dysplasia and high grade. This procedure is now commonly performed in an outpatient procedure in many hospitals across the United States.
In addition to acting as a Nissen fundoplication can reduce the return of stomach acid into the esophagus.
In many studies, anti-inflammatory drugs (NSAIDs) like aspirin, have shown prevention of cancer of the esophagus in patients with Barrett esophagus. However, none of these studies were randomized, placebo-controlled studies, which are considered the gold standard in evaluating medical intervention. In addition, the best dose of NSAIDs in preventing cancer is not yet known.

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