Columnar epithelization of lower esophageal mucosa is more common in middle-aged and elderly people. The incidence is mostly male, and the ratio of male to female is 3 ∶ 1 ~ 4 ∶ 1. Symptoms are mainly caused by gastroesophageal reflux and complications. The symptoms of gastroesophageal reflux are burning sensation behind sternum, chest pain and nausea. Serious complications can occur, and benign complications include reflux esophagitis, esophageal stenosis, ulcer, perforation, bleeding and aspiration pneumonia. The purpose of Barrett's esophageal therapy is to control gastroesophageal reflux, relieve symptoms, prevent complications and reduce the risk of malignant transformation. It can be treated by internal medicine or surgery. The prognosis is very poor.
See Gastroesophageal Reflux Disease Test Paper.
2 disease name columnar epithelization of lower esophageal mucosa
3 English name Barrett esophagus
Barrett's esophagus; , another name for columnar epithelization of lower esophageal mucosa; Barrett esophagitis; Barrett's esophagus; Barrett's esophagus; barrett's esophagus
5 classification of gastroenterology >; Esophageal diseases > other diseases of esophagus.
Thoracic surgery > esophageal diseases > esophageal injury and esophagitis diseases >: esophagitis diseases
6 ICD number K20
7 Epidemiology Cameron et al. (1992) found 377 cases of esophageal columnar epithelium ≥3cm in 5 1 0/case of upper gastrointestinal endoscopy, the detection rate was 0.89%, and that of another author was 0.74%, so the detection rate of endoscopy was about1. With the increase of age, the incidence rate increases. The average age is about 40 years old. Barrett's esophagus has a high incidence in patients with reflux esophagitis, and as many as 44% cases of chronic peptic stenosis are reported. Some people found more Barrett's esophagus in autopsy than in clinic, which confirmed that Barrett's esophagus was mostly undiagnosed before his death because most patients were asymptomatic. The above-mentioned incidence rates are all quoted from western data, and it is considered that the incidence rate of reflux esophagitis in the East is lower, because the incidence rate of reflux esophagitis is also lower than that in the West, and the reasons need to be verified by accumulated data.
According to the literature, 65,438+0 pairs of twin women and the elderly suffer from BE, 65,438+0 cases of 40-year-old men and their two sons suffer from BE, 65,438+0 cases of 80-year-old men and their 65,438+0 sons and two daughters also suffer from BE, and three fathers, sons and grandchildren in 65,438+0 families are BE cases. These reports show that there is indeed a blood relationship.
8 Etiology The etiology of Barrett's esophagus is unknown. Although the relationship between Barrett esophagus and gastroesophageal reflux has been accepted by most scholars, the exact pathogenesis of Barrett esophagus is still unclear. This is because only 10% patients with gastroesophageal reflux developed Barrett's esophagus, while 90% patients did not change. What factors have influenced the transformation between the two is still a mystery. But in any case, gastroesophageal reflux is the most important and basic pathological basis. In addition, duodenogastroesophageal reflux and esophageal motor dysfunction are also related to Barrett's esophagus.
There have been two theories for a long time, namely, congenital theory and acquired theory.
8. 1 Congenital theory From the embryological point of view, when the human embryo develops to 3 ~ 34 mm (4 months ago), the mucosa of the primitive foregut (the predecessor of the esophagus) is covered with columnar epithelium. When it develops to130 ~160 mm (18 ~ 20 weeks), squamous epithelium begins to replace columnar epithelium. This change starts from the center of esophagus, gradually develops to both ends of stomach and mouth, and is completed before birth. If this extension is hindered in any way, it may lead to the lower part of the esophagus being covered with columnar epithelium and the upper part of the esophagus retaining columnar epithelial cells after birth. Based on this theory, congenital theory holds that Barrett's esophagus is caused by columnar epithelium not being completely replaced by squamous epithelium during human embryonic development, so columnar epithelium remains in the lower part of esophagus during embryonic period. Some clinical observations also support the congenital theory. Autopsy confirmed that columnar epithelium was found in the esophagus of stillborn infants. Borrie et al. proposed that Barrett's esophagus has two stages, one is children (0 ~ 10 years old) and the other is adults (over 40 years old). Therefore, the etiology of Barrett's esophagus is congenital. In addition, a pathological study reported that no chronic inflammation and tissue fibrosis mentioned in the acquired theory were found in Barrett's esophagus (table 1).
8.2 Acquired Theory At present, more and more animal experiments and clinical research evidence show that Barrett's esophagus is an acquired disease, which is closely related to gastroesophageal reflux disease. Long-term exposure of the lower esophagus to acidic solution, gastric enzyme and bile causes inflammation and destruction of esophageal mucosa, which leads to acid-resistant columnar epithelium replacing squamous epithelium. Studies have confirmed that most Barrett's esophageal patients have reflux esophagitis. It is also found that Barrett's esophagus can occur after some surgical operations, such as myotomy, total gastrectomy plus esophagojejunostomy and gastroesophageal side-to-side anastomosis. The main mechanism is that the operation destroys the integrity of the lower esophageal sphincter, leading to gastric acid and bile reflux or esophageal and gastric emptying disorder. In addition, it has also been reported that chemotherapy drugs can damage the esophageal mucosa, leading to Barrett's esophagus (Table 2).
Animal models play a very important role in studying the etiology and pathogenesis of Barrett's esophagus. In the late 1960s, some scholars tried to establish an animal model of Barrett's esophagus, but failed. On the basis of previous animal models, Brenner and Gillen respectively established Barrett's esophageal animal models by increasing the condition of long-term high acid reflux, which strongly supported Barrett's acquired esophageal theory. Since then, some different animal models have appeared one after another.
The origin of Barrett's esophageal columnar epithelium has not been determined. At present, there are several viewpoints: ① Basal cells are derived from squamous epithelium; ② glandular cells from esophagus and cardia; ③ From gastric mucosa or primitive stem cells.
The main pathological feature of BE is that columnar epithelium extends upward from the stomach to the lower esophagus 1/3 ~ 1/2, mostly within 6cm of the lower esophagus, while the submucosa and muscularis are normal in structure. There are three histological types of columnar epithelium:
9. 1 The gastric fundus gland type is similar to the gastric fundus epithelium, containing pits and mucous glands, with main cells and parietal cells, which can secrete gastric acid and pepsinogen, but compared with normal mucosa, these glands are rare and short.
9.2 The gastric cardia junction is characterized by mucinous glands of cardia, with pits and villi on the surface, pits and glands covered by mucinous cells, and lack of main cells and parietal cells.
9.3 Special columnar epithelium is similar to small intestine epithelium, with villi and pits on the surface, and consists of columnar cells and goblet cells. Columnar cells are different from normal small intestinal absorptive cells, which have no clear brush border, and the top of cytoplasm contains glycoprotein secretory granules, which have no fat absorption function, equivalent to incomplete intestinal metaplasia epithelium, and are the most common types.
Barrett's esophagus can form ulcer, called Barrett's ulcer, which is considered as a precancerous lesion of esophageal adenocarcinoma. The ulcer is deep and easy to perforate. If the ulcer penetrates the esophageal wall, it may be complicated with purulent infection of pleura and mediastinum or mediastinal fibrosis and peripheral lymphadenitis.
10 clinical manifestations of columnar epithelization of lower esophageal mucosa Barrett's esophagus itself does not produce symptoms, and the symptoms of patients are mainly caused by reflux esophagitis and its accompanying lesions. The most common symptoms are acid reflux and heartburn, followed by retrosternal pain and epigastric pain. When the esophagus is narrow, the prominent symptom is dysphagia. The reasons for dysphagia are as follows: ① the junction of squamous columnar epithelium is narrow; (2) Chronic esophagitis leads to tube wall fibrosis and decreased esophageal peristalsis; ③ Esophageal spasm caused by acute esophageal inflammation; ④ Lumen obstruction caused by columnar intraepithelial esophageal adenocarcinoma. Some patients have heartburn symptoms in the early stage, and after a long period of asymptomatic period, symptoms do not appear until complications occur, because columnar epithelium is not as sensitive to digestive juice as squamous epithelium. Barrett's esophageal bleeding can be massive, but it is often chronic iron deficiency anemia. A small number of perforation or invasion of pleural cavity cause fistula or enter other adjacent organs to appear symptoms.
11Complications of columnar epithelization of esophageal mucosa in the lower esophagus Barrett's esophagus can have serious complications, including reflux esophagitis, esophageal stenosis, ulcer, perforation, bleeding and aspiration pneumonia. The incidence of Barrett's esophageal complications is shown in Table 3.
Common complications are:
1 1. 1 Ulcer The incidence of Barrett's esophageal ulcer is 2% ~ 54%. After the columnar epithelium of esophagus is corroded by acidic digestive juice, ulcer may occur, pain may radiate to the back, and perforation, bleeding, infiltration, stenosis after ulcer healing and dysphagia may be caused. It can even penetrate the aorta, causing massive bleeding and rapid death. Barrett ulcer has two pathological types, the most common is superficial ulcer of squamous epithelial segment, similar to ulcer caused by reflux esophagitis. Another rare type is deep ulcer of columnar epithelial segment, which is similar to peptic ulcer.
1 1.2 Stenosis Esophageal stenosis is the most common complication of Barrett's esophagus, and the incidence rate is 15% ~ 100%. Most of the strictures are located at the junction of squamous columnar epithelium in the middle and upper esophagus, while most of the strictures caused by gastroesophageal reflux are located in the lower esophagus. The incidence of reflux esophagitis is 29% ~ 82%. Lesions can only involve columnar epithelium, or both squamous epithelium and columnar epithelium.
11.3 The incidence of cancer in Barrett's esophagus is not exact, and long-term reflux may have a malignant effect on Barrett's esophagus. However, some studies believe that anti-reflux surgery for Barrett's esophageal disease patients can not make these columnar epithelium disappear, nor can it reduce the risk of malignant transformation. Barrett's esophageal columnar epithelium can produce dysplasia, and the degree can be from low to high. Low-grade dysplasia is sometimes indistinguishable from normal columnar epithelium, and high-grade dysplasia is sometimes indistinguishable from carcinoma in situ, which can progress to invasive carcinoma. These malignant tumors are adenocarcinoma. It should be pointed out that the endoscopic manifestations of cardiac adenocarcinoma with benign columnar epithelium are different from those of atypical hyperplasia of columnar epithelium as adenocarcinoma. Barrett's esophageal dysplasia is a precancerous lesion, which has been recognized by most people.
1 1.4 gastrointestinal bleeding can be manifested as hematemesis or bloody stool, accompanied by iron deficiency anemia, the incidence rate is about 45%, and the bleeding sources are esophagitis and esophageal ulcer.
12 esophageal motility laboratory examination showed that the function of the lower esophageal sphincter was impaired and the pressure of the lower esophageal segment decreased in BE patients, which was easy to form gastroesophageal reflux and the ability to remove reflux acid substances decreased. Therefore, monitoring the esophageal pressure and pH value of patients has certain reference significance for suggesting the existence of BE. It is generally considered that the lower esophageal sphincter pressure is lower than 1.33kPa as dysfunction. Ranson et al. measured that the lower esophageal sphincter pressure of normal people was 2.6 kpa±7 kpa, while that of patients with systemic BE was 0.97 kpa±3.46 kpa, which was significantly lower than that of normal control group. When endoscope can't determine the boundary of the lower esophagus, biopsy can also be performed under the guidance of manometry.
13 auxiliary examination 13. 1 X-ray examination is difficult to find Barrett's esophagus, with esophageal hiatal hernia and reflux esophagitis, which is not the specificity of this disease. Barrett's esophagus should be suspected if peptic stenosis or body ulcer is found in the esophagus.
13.2 Endoscopy can easily diagnose Barrett's mucosa. Normal esophageal mucosa is pink with gray, while columnar epithelium is orange-red like gastric mucosa. There are significant differences between them. Endoscopic BE can be divided into three types:
(1) Peripheral type: the red mucosa extends to the esophagus and involves the whole circumference, with no obvious boundary with the gastric mucosa, and its free edge is more than 3cm away from the lower esophageal sphincter.
(2) Island type: red mucosal plaque appeared above dentate line 1cm.
(3) Tongue type: connected with the dentate line and extending to the esophagus in a peninsula shape. Barrett epithelium can appear congestion, edema, erosion or ulcer, and repeated ulcer can cause esophageal stenosis.
13.3 esophageal manometry and pH monitoring Barrett esophageal patients can see the manometry of gastroesophageal reflux after long-term contact with acid-base reflux, and the pressure of lower esophageal sphincter is lower than that of ordinary reflux patients.
The clinical diagnosis of 14 Barrett's esophagus should be based on the patient's medical history, clinical manifestations, esophageal manometry, pH monitoring, endoscopy and biopsy, among which the most valuable methods are endoscopy and biopsy.
The differential diagnosis between Barrett esophagus and 15 is sometimes differentiated from early gastric ulcer.
16 The treatment of columnar epithelium in lower esophageal mucosa aims at relieving and eliminating symptoms, reversing columnar epithelium into squamous epithelium, preventing and treating complications and reducing the incidence of esophageal adenocarcinoma.
16. 1 Generally speaking, it is advisable to eat digestible food and avoid food that induces symptoms. Overweight people should lose weight.
16.2 drug therapy (1) proton pump inhibitors (PPIs): the first choice for medical treatment is to take a large dose, such as losec 20 ~ 40 mg orally twice a day, and maintain a small dose of treatment after symptom control for more than half a year. There is evidence that PPIs can shorten the length of Barrett mucosa after long-term treatment, and some BE mucosa is covered by squamous epithelium, suggesting that PPIs can partially reverse BE, but it is difficult to achieve complete reversal. PPIs treatment can also make intestinal metaplasia and dysplasia in BE subside, indicating that PPIs can prevent the development of BE, increase the chance of squamous epithelial reversal and reduce the risk of malignant transformation.
(2) prokinetic drugs (domperidone, cisapride, etc. ): These drugs can reduce gastroesophageal reflux and control symptoms, but the course of treatment is longer. For example, domperidone 10 ~ 20 mg, 3 ~ 4 times a day, is often used at the same time with PPIs to increase the curative effect.
(3) Others: Mucosal protectants such as sucralfate and smecta also have certain curative effects, which can improve symptoms, especially when combined with PPIs.
16.3 endoscopic therapy with the development of endoscopic therapy technology, in recent years, endoscopic ablation therapy (EATs) began to be applied in clinic. EATs can be divided into three categories: thermal ablation, chemical ablation and mechanical ablation. Thermal ablation includes multipole electrocoagulation (MPEC), argon laser coagulation (APC) and laser (KTP, YAG, etc. ). Chemical ablation mainly refers to photodynamic therapy (PDT). Its basic principle is to localize it in the metaplasia or dysplasia or adenocarcinoma epithelium of esophagus by intravenous injection of photosensitizer such as Viola yedoensis, and then make local tissue necrosis through non-thermal photochemical reaction. The disadvantage of this method is that it will cause skin photosensitive reaction. Recently, it has been reported that the application of 5- aminolevulinic acid (ALA) with strong specificity and no skin sensitivity can make 100% dysplasia disappear, and the cure rate of mucosal cancer is 72%, with an average follow-up of 9 months. Mechanical ablation uses methods such as aspiration and endoscopic resection. At present, EATs plus PPIs is an effective method to treat BE and BE with atypical hyperplasia, which can make BE epithelium disappear or reverse to squamous epithelium. The curative effect can reach 70% ~ 100% and the incidence of complications is low. However, EATs has not been used for a long time, the number of cases is small and the follow-up time is short. Its curative effect needs time to test, and whether it can reduce the incidence of adenocarcinoma after epithelial metaplasia reversal needs further evaluation. Esophageal bougie or balloon dilatation can be performed for patients with obvious esophageal stenosis, but the effect is short-lived and may need multiple dilatation.
16.4 surgical indications are:
(1) was accompanied by severe symptomatic reflux, and medical treatment was ineffective.
(2) Esophageal stenosis is ineffective after dilation.
(3) Refractory ulcer.
(4) Severe dysplasia or canceration.
There are many surgical methods, Nissen fundoplication is generally selected, and esophagectomy is suitable for patients with severe dysplasia or canceration. The therapeutic effect of anti-reflux surgery is still controversial. Some scholars believe that although anti-reflux surgery can relieve reflux symptoms, heal ulcers and improve stenosis, it can not reverse BE epithelium, let alone reverse dysplasia into adenocarcinoma. However, another scholar reported that abdominal or laparoscopic anti-reflux surgery can not only relieve symptoms, but also stabilize the coverage of columnar epithelium, control the development of dysplasia, and even reverse the atypical columnar epithelium into squamous epithelium, reducing the risk of being cancerous. It seems that the curative effect of anti-reflux surgery needs a lot of clinical research to further evaluate.
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17 prognosis Barrett's esophageal cancer has a poor prognosis, mainly because it was advanced at the time of diagnosis, mostly accompanied by lymph nodes and local metastasis. The overall 5-year survival rate was 265,438+0% ~ 55%, and the 5-year survival rate of lymph node negative group was 965,438+0%, which was significantly higher than other groups. The clinical stage and tumor size of Barrett's esophageal cancer are important factors affecting the long-term survival rate. We analyzed the survival of 565,438+0 cases of Barrett's esophageal cancer. The 5-year survival rates of stage ⅱ tumors and tumors with diameters less than 6 cm were 25% and 265,438+0%, respectively, while the 5-year survival rates of stage ⅲ and ⅳ tumors with diameters greater than 6 cm were 4.5% and 0, respectively. The prognosis is related to the degree of tumor differentiation and infiltration, but has nothing to do with the tumor site, patient's age, sex and surgical method.
Richter pointed out that the average age of BE patients at diagnosis was 55 years old, and the average age of esophageal adenocarcinoma patients at diagnosis was at least 10 years old. About 25% of patients are not suitable for surgery because of their aging accompanied by cardiopulmonary diseases. Whether surgery can eliminate BE or prevent the occurrence of adenocarcinoma needs further study.
18 prevention of columnar epithelialization of lower esophageal mucosa There is no special method to prevent columnar epithelialization of lower esophageal mucosa. In life, it is mainly to change bad habits, such as reducing the intake of sexual diet, improving the bedside, quitting smoking and drinking, avoiding eating chocolate and other foods that inhibit the tension of lower esophageal sphincter, and avoiding being overweight.
19 related drugs pepsin, domperidone, domperidone, cisapride, sucralfate.
20 related inspection