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Treatment aims to ease and eliminate symptoms, reversal of squamous cell esophageal columnar epithelium, prevention and treatment of complications, reduce the incidence of esophageal adenocarcinoma. 1. General treatment into easy to digest foods should avoid the symptoms induced by body position and food are spicy food, overweight should lose weight. 2. Drug treatment (1) Proton pump inhibitors (PPIs): the drug of choice for the medical treatment, the dose should be large, such as omeprazole 20 ~ 40mg, 2 times a day orally, symptom control after low-dose maintenance therapy, treatment more than six months. There is evidence that, PPIs can reduce long-term treatment length of Barrett mucosa, in some cases there BE squamous mucosa covered, suggesting that PPIs can BE partially reversed, but it is difficult to achieve complete reversal. PPIs in the treatment of intestinal metaplasia also enable BE and dysplasia subsided, suggesting that PPIs can prevent the progression of BE to increase the chance of reversal of squamous epithelium, reducing the risk of malignant transformation. (2) of prokinetic drugs (domperidone, cisapride, etc.): these drugs can reduce reflux and control symptoms, but longer course of treatment. Such as domperidone 10 ~ 20mg, 3 to 4 times a day, often with PPIs also applied to increase the efficacy. (3) Other: such as sucralfate, Smecta mucosal protective agents, etc. have a certain effect, can improve symptoms, PPIs combined with better effect. 3. Endoscopic therapy with endoscopic therapy technology, in recent years, endoscopic ablation therapy (endoSCopic ablation therapies, EATs) has been used clinically. EATs can be divided into thermal ablation, chemical ablation, and mechanical ablation of three categories. Thermal ablation, including multipolar electrocoagulation and surgery (MPEC), argon photocoagulation (APC) and laser (KTP, YAG, etc.). Ablation mainly refers to photodynamic therapy (PDT), The basic principle is first blood porphyrin photosensitizer such as intravenous injection located in the esophagus metaplasia to dysplasia or carcinoma, or epithelial, through non-thermal photochemical reaction cause local tissue necrosis. This approach is that light can cause skin allergies. Recently reported the non-specific and sensitive skin of 5 - aminolevulinic acid (ALA) treatment associated with mucosal dysplasia or carcinoma in the case of 100% can disappear dysplasia, intramucosal cancer cure rate was 72% The average follow-up 9 months. Endoscopic ablation, including the use of mechanical suction extraction, removal and other methods. EATs plus PPIs acid suppression therapy is the treatment of dysplasia in BE and BE with an effective way to make BE epithelium disappeared or reversed to squamous epithelium, efficacy up to 70% to 100%, low complication rate. But EATs use not long, small number of cases, follow-up time is shorter, the time needed to test its efficacy, but also to reverse the metaplastic epithelium can red
Alias names of diseases Barrett Barrett Esophageal Diseases Esophagitis, Barrett's esophagus, columnar epithelium of esophageal mucosa of medical disease Digestive disease classification description of abnormal esophageal columnar epithelium covering, known as Barrett esophagus. Generally considered to be acquired, and with reflux esophagitis is closely related to, and adenocarcinoma may occur. First proposed in 1950, Norman Barrett, 1957 do
Esophageal model recognition, concern for people gradually. Barrett esophagus is suspected see endoscopic columnar epithelium and by histological examination confirmed the need for the existence of intestinal metaplasia. Also suggested that Barrett esophagus is a congenital, due to fetal development period, after esophageal columnar epithelium replaced by squamous epithelium. Ectopic columnar epithelium remaining in the esophagus can occur in any part of the esophagus. Barrett's esophagus symptoms and signs of age from birth to 1 month to 88 years are being reported, the age distribution curve showed a double peak, first peak in the 0 to 15 years old, another peak at 48 to 80 years old, but more common in clinical the elderly. Incidence of Barrett's esophagus more common in men, male to female ratio is 3:1 ~ 4:1. Only patients with esophageal columnar metaplasia usually asymptomatic, so most
Books can be life-long non-symptomatic patients. Barrett's esophagus and gastroesophageal reflux symptoms are mainly caused by complications, gastroesophageal reflux symptoms are retrosternal burning sensation, chest pain and nausea, heartburn typical clinical appear and nausea before going to treatment, partly because of esophageal stricture or cancer appear diagnosis of dysphagia led to symptoms. Difficulty swallowing because: â‘ scales - narrow columnar epithelial junction; â‘¡ wall fibrosis caused by chronic esophagitis, esophageal motility dysfunction; â‘¢ acute inflammation of the esophagus in esophageal spasm; â‘£ occurred in columnar epithelium of esophageal adenocarcinoma lumen due to obstruction. Some patients early days of heartburn symptoms, after a long asymptomatic period after the onset of symptoms until complications occur, because the columnar epithelium of the digestive squamous cell stimulation as sensitive. Barrett esophagus bleeding can be substantial, but often has chronic iron deficiency anemia. Small perforation or fistula or invasion into the pleural cavity causing symptoms of other adjacent organs. Cause of Barrett's esophagus causes of disease so far not fully understood. Although Barrett esophagus and gastroesophageal reflux on the relationship between the majority of scholars have been accepted, but the exact pathogenesis of Barrett esophagus is still unclear. Say this is because in reflux patients, only 10% of the development of Barrett esophagus, and 90% of patients did not change. What factors affect the conversion between the two is still a mystery. But no matter what, said the stomach - esophageal reflux is the most important and fundamental pathological basis, in addition to the duodenum - stomach - esophageal reflux and esophageal motor dysfunction but also with the pathogenesis of Barrett's esophagus. There are two theories has long been that the theory of congenital and acquired theories. 1. Congenital doctrine from the perspective of embryology, human embryonic development to the 3 ~ 34mm (for 4 months ago), the original foregut (esophagus, the predecessor) mucosal lining columnar epithelium. Developed to the 130 ~ 160mm (18 ~ 20 weeks), the squamous epithelium began to replace
Columnar epithelium of the human digestive system, this change started from the center of the esophagus and the stomach and mouth gradually to both ends of development, to be completed before birth. This extension, such as by any obstruction, may result in lower esophagus in columnar epithelium after birth, still covered, and left upper esophageal columnar epithelial cells. Based on this theory, the congenital theory that Barrett esophagus is due to the body during embryonic development of columnar epithelium was not completely replace the squamous epithelium caused by, the left lower esophageal columnar epithelium during embryo. Some clinical observations also support the congenital theory. An autopsy confirmed that the stillborn baby's esophagus to columnar epithelium were found. Borrie and put forward, Barrett's esophagus incidence peak has two stages, a group of children (0 to 10 years), the other is the adult group (40 years old), and therefore group of children is a congenital etiology. In addition, a pathology report, Barrett esophagus was not found in the doctrine that acquired chronic inflammation and tissue fibrosis. 2. Acquired more and more current theories of animal experiments and clinical research evidence that, Barrett esophagus is an acquired disease that is closely related with gastroesophageal reflux disease. Long-term exposure of esophageal acid solution, gastric enzymes and bile, causing inflammation and destruction of esophageal mucosa, causing acid substitution squamous columnar epithelium. Study confirmed that the majority of patients with Barrett esophagus reflux esophagitis exist. Clinical also found that some surgery, such as esophageal muscle incision, total gastrectomy plus gastric esophageal anastomosis and esophageal side to side anastomosis Barrett esophagus may occur after surgery. Its mechanism is mainly due to surgery destroyed the integrity of the lower esophageal sphincter, resulting in gastric acid and bile reflux or esophageal and gastric emptying. There are also reports of chemotherapy drugs can damage esophageal mucosa, leading to Barrett esophagus. Barrett esophagus animal model to study the etiology and pathogenesis play a very important role. The late 20th century, there are 60 scholars trying to establish an animal model of Barrett esophagus, but without success. Bremner and Gillen, respectively, in the basis of previous animal models, an increase of long-term high-acid reflux condition, successfully established animal model of Barrett's esophagus, the results strongly support the theory of acquired Barrett's esophagus. Since then, a number of different animal models have appeared. 3. Columnar epithelium of Barrett esophageal columnar epithelium on the source of the source has not yet conclusive. There are several views: â‘ from the basal cells of squamous epithelium; â‘¡ from the esophageal gland cells; â‘¢ from the gastric mucosa or the original stem cells. Clinical pathophysiology of gastroesophageal reflux of acid found in gastric juice and gastric resection alkaline intestinal fluid reflux after esophageal mucosal damage can occur, there columnar epithelium on the move. Reflux esophagitis after the contraction of the lower esophageal sphincter and food
Down tube clearance drug treatment two factors have led the formation of Barrett's esophagus. Materials including acid reflux, pepsin, trypsin, one or more bile acid to promote squamous metaplasia of esophageal reflux patients. Squamous epithelium after destruction of the gastric cardia to the head end of the columnar epithelium damaged area and then transferred to the epithelium of the esophagus. Other rare cases by the corrosive esophageal burns or long-term application of anti-cancer chemotherapy, esophageal mucosal damage can also occur in Barrett esophagus. Esophageal dysmotility esophageal columnar epithelium with a causal relationship is not fully understood. Followed up long-term esophageal columnar epithelium found in the possibility of cancer, but pre-malignant columnar epithelial predisposing factors potentially dangerous unknown. Diagnosis Diagnosis: Barrett's esophagus in patients with clinical diagnosis should be based on history, clinical manifestations, esophageal manometry, pH monitoring, endoscopy and biopsy, one of the most valuable methods for the diagnosis of endoscopy and biopsy. Laboratory tests: detection of BE in patients with esophageal motility dysfunction, lower esophageal sphincter, lower esophageal pressure, easy to form reflux and acid reflux decreased scavenging ability, so by the pressure and esophageal pH monitoring in , the presence of BE suggest a certain reference value. Generally believed that the lower esophageal sphincter pressure of less than 1.33kPa to dysfunction.
Esophagoscopy Ranson, etc. The experimental determination of normal human lower esophageal sphincter pressure 2.6kPa Â± 7kPa, patients in the generalized BE 0.97kPa Â± 3.46kPa, was significantly lower than the control group. When endoscopy can not determine the boundary of the lower esophagus, but also under the guidance of biopsy in manometry. Other laboratory examinations: 1.X-ray examination difficult to find Barrett esophagus, a hiatal hernia and reflux esophagitis performance, not the specificity of this disease. Found to have peptic esophageal stricture or ulcers body should be suspected of having Barrett esophagus. 2. Esophageal endoscopy in patients with Barrett esophagus may appear above the gastroesophageal junction granular, red columnar epithelium, and esophageal reflux occurred signs of injury. Biopsy can confirm that and find the columnar metaplasia. 3. Esophageal manometry and pH monitoring of patients with Barrett's esophagus and esophageal acid and alkaline reflux in contact for a long time to see the performance of gastroesophageal reflux in the pressure measurement, the lower esophageal sphincter pressure in reflux patients than the average lower. Treatment of Barrett's esophagus treatment programs designed to control gastroesophageal reflux, relieve symptoms, prevent complications and reduce the risk of malignant transformation. 1. Medical treatment of choice for the treatment of Barrett's esophagus. Of symptom-free and without complications, no surgical treatment, mainly to change the bad habits such as diet should reduce the intake of pungent, raising the bed, smoking and drinking, Jichi inhibition of lower esophageal sphincter chocolate and other food, to avoid physical overweight. Drug treatment of multiple choice H2 receptor antagonists and proton pump inhibitors, combined with prokinetic medication. For Barrett Ulcer: Clinical data show that although some patients significantly reduced acid secretion and ulcer healing, gastroesophageal reflux, but there are still, after further study found that patients with Barrett esophagus, acid reflux is not only physical, but also basic substances. So people speculate that the current treatment methods by changing the pH value of the esophagus and stomach to reduce the reflux symptoms, but can not prevent the flow of basic anti-esophageal gastric contents, so the drug treatment, the symptoms caused by acid under control, and alkaline reflux persists, continue to undermine the esophageal mucosa. Narrow for most patients with Barrett, on the expansion of therapy and medication have a good response. Especially in the repeated expansion, difficulty swallowing can be eased. 2. Surgical treatment for medical therapy, persistent symptoms and complications of patients, surgical treatment is aimed at curbing anti-flow, to prevent the continued development of columnar epithelium and extending upward. Starnes so that only 15% of clinical patients with Barrett esophagus after treatment by medication is better, and the remaining 85% is ineffective. At present, most scholars advocate of Barrett esophagus patients, regardless of a symptom, as long as the objective existence of gastroesophageal reflux (esophageal pH monitoring positive), biopsy, intestinal metaplasia or epithelial dysplasia of any degree, must be anti- reflux surgery, particularly those with reflux esophagitis, ulcers, or stenosis, must be thoroughly correct reflux. So that, for patients with Barrett's esophagus, with surgery as long as the conditions, especially in young patients, short and drug treatment history of poor or difficult to control the development of complications in patients, the line should be considered anti-reflux surgery. Surgical treatment of Barrett's esophagus with Nissen fundoplication for the surgical choice. The effects of various treatments should be determined by 24h pH esophagus, endoscopy and clinical performance in evaluation. In addition, after surgery should endoscopy and biopsy on a regular basis. Successful anti-reflux surgery, columnar epithelium can be degenerated, such as anti-reflux reflux persists after surgery, the risk of cancer is no doubt continue to exist. However, the success of anti-reflux surgery, still in the columnar epithelium lining the esophageal epithelium occurring adenocarcinoma. Barrett esophagus is currently considered the most effective treatment is surgery. Where it is confirmed by endoscopy and pathology Barrett esophageal cancer surgery should be as soon as possible. Surgical resection with esophageal cancer, gastrointestinal reconstruction of multi-use residual stomach or colon, a few with the jejunum. Operative mortality was 0 ~ 10%. Disease prevention and prognosis: Barrett esophageal cancer with poor prognosis, mainly due to advanced stage at diagnosis, most patients with lymph node metastasis and local. The overall 5-year survival was 21% to 55%, lymph node negative group was 91% 5-year survival rate was significantly higher than other groups. Barrett esophageal cancer staging and tumor size is an important factor of long-term survival, we analyzed 51 cases of Barrett esophageal cancer survival, â…¡ tumors and tumor diameter <6cm's 5-year survival rates were 25% and 21%, while â…¢ and â…£, and tumor diameter> 6cm who were 4.5% and 0. Prognosis and tumor differentiation and foreign invasion conditions, but not with tumor site, patient age, gender, and related surgical methods. Prevention: There is no relevant information. Concurrent symptoms of Barrett esophagus can be serious complications, benign complications include reflux esophagitis, esophageal stricture, ulceration, perforation, hemorrhage, and aspiration pneumonia. Common complications are: 1. Ulceration caused by Barrett esophagus ulcer incidence rate from 2% to 54%, esophageal columnar epithelium of digestive juice by acid corrosion can occur after the ulcer, gastric ulcer similar symptoms, pain may radiate to the back and can cause perforation, hemorrhage, infiltration, ulcer healing occurred after the narrow, poor swallowing symptoms appear. Even penetrate the aorta led to bleeding and rapid death. Barrett ulcer pathology type, there are two, the most common to occur in superficial squamous ulcer segment, this type of reflux esophagitis because of ulcers caused similar. Another rare to occur in the deep section of columnar epithelial ulceration, and peptic ulcer similar. 2. Stricture esophageal stenosis, Barrett esophagus is the most common complication rate was 15% to 100%. Stenosis in the upper esophagus than the scales - the junction of columnar epithelium, and gastroesophageal reflux in the esophagus caused by lower and more narrow. Reflux
Esophageal stricture incidence of esophagitis was 29% to 82%. Lesions involving the columnar epithelium can be individually, but also involved the squamous and columnar epithelium. 3. Malignant Barrett's esophagus cancer incidence occurred in less precise, long-term reflux material into the malignant transformation of Barrett esophagus may play a role. However, some studies that patients with Barrett esophagus patients practiced anti-reflux surgery does not make these columnar epithelium subsided, nor to reduce the risk of malignancy. Columnar epithelium of Barrett's esophagus dysplasia can occur the region, the degree can be from low to high, sometimes low-grade dysplasia difficult to distinguish from normal columnar epithelium, a high degree of dysplasia and carcinoma in situ is sometimes difficult to distinguish, and may progress to invasive carcinoma . The Department of malignant cancer tumors. Have found that GCA is associated with benign endoscopic columnar epithelium columnar epithelial dysplasia and adenocarcinoma is different. Barrett's esophagus is a precancerous condition dysplasia has been recognized by most people. 4. Gastrointestinal tract bleeding can be manifested as hematemesis or blood in the stool, accompanied by iron deficiency anemia, occur in approximately 45% of the source of bleeding esophagitis and esophageal ulcers. Epidemiology Cameron et al (1992) in the implementation of 51,311 cases of upper gastrointestinal endoscopy was found in 377 cases of esophageal columnar epithelium â‰¥ 3cm long, that rate was 0.89%, 0.74% of the other, so endoscopy rate of about 1%. With age, incidence increased. The average age of those in the more common 40 years old. Reflux esophagitis patients, Barrett's esophagus to high incidence, chronic peptic stricture of the cases reported up to 44%. It was issued in the autopsy Barrett esophagus for more than the clinical findings, confirmed diagnosis of Barrett esophagus during his lifetime most of the failure, because most patients are asymptomatic. The incidence rates quoted material from the West, it was considered a lower incidence in Asians because of reflux esophagitis incidence is also lower than the West, its causes the accumulation of material yet to be verified. Prescription Pianfangyanfang: Hara film (commercially available), the anti-infective drugs for the respiratory tract, however, used in treatment of Henan Medical College
Hara films get better treatment of esophageal cancer patients. Usage: 5 / each. 3 times a day orally. Were treated in 36 patients with advanced esophageal cancer, 2 cases markedly effective in 11 cases, 6 cases were lost, the effective rate was 36.1%. Recipe: â‘ Actinidiae 30g, Qu dishes per 10g, 10g water Aozhi barbata dark red, to the residue concentrated syrup made of 2 times a day, every 10ml oral. â‘¡ borer jinsong 4g, Scorpion 2g, 4g dried grub joint research to fine, two eggs and mix thoroughly with the powder, Wen steam heat, 1 served, day 1.
Cause of Barrett's esophagus has not yet entirely clear, although the Barrett esophagus and the relationship between gastroesophageal reflux has been accepted by most scholars, but the exact pathogenesis of Barrett esophagus is still unclear, say this is because in gastroesophageal reflux patients, only 10% of the development of Barrett esophagus, and 90% of patients does not change, what factors affect the conversion between the two is still a mystery, but no matter how that the stomach - esophageal reflux is the most essential and basic pathology, in addition to the duodenum - stomach - esophageal reflux and esophageal motor dysfunction but also with the pathogenesis of Barrett's esophagus.
There are two theories has long been that the theory of congenital and acquired theories.
1. Congenital doctrine from the perspective of embryology, human embryonic development to the 3 ~ 34mm (for 4 months ago), the original foregut (the predecessor of the esophagus) mucosa lining the columnar epithelium, and development to the 130 ~ 160mm (18 ~ 20 ), the squamous epithelium began to replace columnar epithelium, the change started from the center of the esophagus and the stomach and mouth gradually to both ends of development, to be completed before birth, subject to any such extension, such as obstruction, may lead to esophageal birth covered even after the upper esophageal columnar epithelium and residual columnar epithelial cells, based on this theory, the congenital theory that Barrett esophagus is due to the body during embryonic development of columnar epithelium was not completely replace the squamous epithelium caused by lower esophageal therefore left the embryonic period columnar epithelium, some clinical observations also support the congenital theory, an autopsy confirmed that the stillborn baby's esophagus to columnar epithelium were found, Borrie and put forward, Barrett's esophagus incidence peak has two stages, a children's group ( 0 to 10 years), the other is the adult group (40 years old), and therefore the incidence of children due to congenital group, in addition, a pathology report, Barrett esophagus was not found in the doctrine that acquired chronic inflammation and tissue fibrosis (Table 1).
2. Acquired more and more current theories of animal experiments and clinical research evidence that, Barrett esophagus is an acquired disease that is closely related with gastroesophageal reflux disease, lower esophageal long-term exposure to acidic solution, the stomach enzymes and bile, causing inflammation and destruction of esophageal mucosa, causing acid substitution squamous columnar epithelium, studies confirm that most patients with Barrett esophagus reflux esophagitis exists, clinical also found that some surgical procedures, such as the esophageal muscle layer incision total gastrectomy plus gastric esophageal anastomosis and esophageal side to side anastomosis can occur after surgery Barrett esophagus and its mechanism was mainly due to surgery destroyed the integrity of the lower esophageal sphincter, resulting in gastric acid and bile reflux or esophageal and gastric emptying disorders, in addition, there are reports of chemotherapy drugs can damage esophageal mucosa, leading to Barrett esophagus (Table 2).
Barrett esophagus animal model to study the etiology and pathogenesis play a very important role in the late 20th century, there are 60 scholars trying to establish an animal model of Barrett esophagus, but without success, Bremner, and Gillen, respectively, in previous animal models Based on the increase of long-term high-acid reflux condition, successfully established animal model of Barrett's esophagus, the results strongly support the theory of acquired Barrett's esophagus, since there are a number of different animal models have appeared.
(B) of the pathogenesis
Barrett esophageal columnar epithelium on the source has not yet conclusive, there are several views: â‘ from the basal cells of squamous epithelium; â‘¡ from the esophageal gland cells; â‘¢ from the gastric mucosa or the original stem cells.
BE is the main pathological features of the columnar epithelium extends upward from the stomach into the lower esophagus 1 / 3 to 1 / 2, mostly limited to within the lower esophageal 6cm, while the normal submucosa and muscular structure, the columnar epithelium of 3 histologic types:
1. Fundic gland type similar to the gastric body and gastric epithelium and mucus glands containing small concave, with the primary cells and parietal cells, secretion of gastric acid and pepsin to the original, but compared with normal mucosa, these glands scarce and short.
2. Gastric cardia junction type is characterized by cardi
3. Special type of columnar epithelium similar to the intestinal epithelium, the surface of villi and lacunae, the columnar cells and goblet cells, columnar cells and normal cells in different intestinal absorption, no clear brush border, the cytoplasm to the top with sugar and protein secretion particles do not have the fat absorption, and thus corresponds to incomplete intestinal metaplasia epithelium, the most common of this type.
Barrett esophagus may be the formation of ulcers, known as Barrett ulcer, is considered a precancerous lesion of esophageal adenocarcinoma, BE than deep ulcers, it is easy to perforation, such as ulcers penetrate the esophageal wall, may be complicated by purulent infection of the pleura and mediastinum or mediastinal tissue fibers inflammation of the surrounding lymph nodes.