注: 食管癌预防，食管癌治疗（成人），以及癌症筛查和预防研究的证据等级的独立的PDQ总结也已可以获取。
在美国，基于中等强度证据，筛查对降低食管癌死亡率无效（或收效甚微）。
基于强有力的证据，食管癌筛查会导致少见但严重的内镜相关副作用，包括穿孔、心肺功能异常、误吸及出血等需要住院治疗的状况。另外，对于明确诊断为巴雷特食管的患者，尽管其患癌风险较低，但仍有可能使得他们误以为自己病情较重，从而带来潜在的精神心理伤害。
Note: Separate PDQ summaries on Esophageal Cancer Prevention, Esophageal Cancer Treatment (Adult), and Levels of Evidence for Cancer Screening and Prevention Studies are also available.
Based on fair evidence, screening would result in no (or minimal) decrease in mortality from esophageal cancer in the U.S. population.
Based on solid evidence, screening would result in uncommon but serious side effects associated with endoscopy which may include perforation, cardiopulmonary events and aspiration, and bleeding requiring hospitalization. Potential psychological harms may occur in those identified as having Barrett esophagus who may consider themselves to be ill even though their risk of developing cancer is low.
在2020年，预计美国将有18,440例食管癌新发病例，16,170例患者将死于食管癌。新发病例中，预计有14,350例男性患者，4090例女性患者。
据估计，2015年中国有24.6万例食管癌新发病例，18.8万例死亡病例。新发病例中，估计有17.7万例男性患者，6.9万例女性患者。
绝大多数食管癌可分为食管腺癌、食管鳞癌两大组织类型。不同类型食管癌的流行病学特征具有显著差异。在20世纪60年代，食管鳞癌在所有食管癌中占比超过90%。在过去20年间，食管腺癌的发病率明显升高，目前，在美国和西欧地区，好发于食管末端的腺癌的发病率已经超过鳞癌。在我国，90%以上的食管癌是食管鳞癌。
虽然食管鳞癌的总发病率有所下降，但是食管鳞癌型在黑人男性中的发病率是白人男性发病率的6倍以上。我国食管腺癌在所有食管癌中所占比例低于10%。
食管鳞癌的发病率通常在所有人群种族中均随着年龄增长而增加，但食管鳞癌在黑人中的发病率则始终高于同年龄段白人。55-69岁黑人男性的食管鳞癌发病率与70岁以上白人男性的发病率相近。而55-69岁黑人女性的食管鳞癌发病率则稍高于其70岁以上白人女性的食管鳞癌发病率。
虽然食管鳞癌的危险因素已被证实（包括烟草、酒精、营养不良及人乳头瘤病毒感染），
但是，食管腺癌的危险因素尚不明确。食管腺癌和鳞癌的流行病学特点的最重要的不同之处在于胃食管反流病（GERD）与腺癌密切相关。一项基于人群的病例对照研究结果提示症状性胃食管反流症状是食管腺癌的高危因素。反流症状的发生频率、严重程度、持续时间均与食管腺癌的发生风险增加有关。
长期的胃食管反流容易诱发巴雷特食管，出现肠上皮替代食管下端鳞状上皮的情况。
巴雷特食管的肠型上皮的内镜下典型表现与鳞状上皮截然不同。
巴雷特食管上皮的不典型增生表现为柱状上皮化生，而柱状上皮可能进展为侵袭性腺癌。
在西方国家，一个有趣的假说认为食管腺癌的发生率增加与幽门螺杆菌的感染率下降有关。研究发现，胃部幽门螺杆菌感染可预防胃食管反流病以及并发症发生。
这一假说认为幽门螺杆菌感染在引起全胃炎的同时，也导致胃酸分泌减少，从而预防胃食管反流病发生。
十二指肠溃疡患者使用抗生素完全治愈后发生反流性食管炎的几率是感染持续存在患者的2倍。
食管腺癌的发病风险增加亦与既往使用食管下括约肌（LES）松弛性药物正相关。长期（＞5年）每日使用LES松弛性药物的人群食管腺癌的发病率是从未使用此类药物的人群的3.8倍（95%置信区间[CI]，2.2-6.4）。但胃贲门腺癌及食管鳞癌与使用LES松弛性药物无关。
食管腺癌的发生与体重指数（BMI）间存在明显相关性。与BMI最低四分位区间人群相比，BMI最高四分位区间人群的校正优势比（OR）为7.6（95%CI，3.8-15.2）。与消瘦人群（BMI＜22 kg/m2）相比，肥胖人群（BMI＞30Kg/m2）的OR为16.2（95%CI，6.3-41.4）。 而食管鳞状细胞癌与BMI之间并无类似相关性。
In 2020, it is estimated that 18,440 Americans will be diagnosed with esophageal cancer, and 16,170 will die of this malignancy. Of the new cases, it is estimated that 14,350 will occur in men and 4,090 will occur in women.
Two histologic types account for the majority of malignant esophageal neoplasms: adenocarcinoma and squamous carcinoma. The epidemiology of these types varies markedly. In the 1960s, squamous cell cancers comprised more than 90% of all esophageal tumors. The incidence of esophageal adenocarcinomas has risen considerably for the past 2 decades, such that it is now more prevalent than squamous cell cancer in the United States and Western Europe, with most tumors located in the distal esophagus.
Although the overall incidence of squamous cell carcinoma of the esophagus is declining, this histologic type remains six times more likely to occur in black males than in white males.
Incidence rates generally increase with age in all racial/ethnic groups but squamous cell cancer is consistently more common in blacks than in whites. Among black men, the incidence rate for those aged 55 to 69 years is close to that of white men aged 70 years and older. In black women aged 55 to 69 years, the incidence rate is slightly higher than white women aged 70 years and older.
While risk factors for squamous cell carcinoma of the esophagus have been identified (such as tobacco, alcoholism, malnutrition, and infection with human papillomavirus),
the risk factors associated with esophageal adenocarcinoma are less defined. The most important epidemiological difference between squamous cell cancer and adenocarcinoma, however, is the strong association between gastroesophageal reflux disease (GERD) and adenocarcinoma. The results of a population-based case-control study suggest that symptomatic gastroesophageal reflux is a risk factor for esophageal adenocarcinoma. The frequency, severity, and duration of reflux symptoms were positively associated with increased risk of esophageal adenocarcinoma.
Long-standing GERD predisposes to Barrett esophagus, the condition in which an abnormal intestinal epithelium replaces the stratified squamous epithelium that normally lines the distal esophagus.
The intestinal-type epithelium of Barrett esophagus has a characteristic endoscopic appearance that differs from squamous epithelium.
Dysplasia in Barrett epithelium represents an alteration of the columnar epithelium that may progress to invasive adenocarcinoma.
An interesting hypothesis relates the rise in incidence of esophageal adenocarcinoma to a declining prevalence of Helicobacter pylori infection in Western countries. Reports have suggested that gastric infection with H. pylori may protect the esophagus from GERD and its complications.
According to this theory, H. pylori infections that cause pangastritis also cause a decrease in gastric acid production that protects against GERD.
Patients whose duodenal ulcers were treated successfully with antibiotics developed reflux esophagitis twice as often as those in whom infection persisted.
Past use of lower esophageal sphincter (LES)-relaxing drugs was positively associated with risk of esophageal adenocarcinoma. Among daily, long-term users (>5 years) of LES-relaxing drugs, the estimated incidence rate ratio was 3.8 (95% confidence interval [CI], 2.2–6.4) compared with persons who had never used these drugs. Gastric cardia adenocarcinoma and esophageal squamous cell carcinoma were not associated with use of LES-relaxing drugs.
There exists a strong relationship between body mass index (BMI) and esophageal adenocarcinoma. The adjusted odds ratio (OR) was 7.6 (95% CI, 3.8–15.2) among persons in the highest BMI quartile compared with persons in the lowest. Obese persons (those with BMI >30 kg/m2) had an OR of 16.2 (95% CI, 6.3–41.4) compared with the leanest persons (BMI <22 kg/m2). Esophageal squamous cell carcinoma was not associated with BMI.
尽管尚未发现食管鳞癌常见诱发因素，但已发现多个与食管鳞癌发病率增加相关的因素，包括：长期暴露于烟草或酒精、贲门失弛缓症、长期酒精和（或）烟草暴露引起的头颈部鳞状细胞癌、胼胝症、碱液摄入史、乳糜泻与好发于南美及中国的热饮摄入史。
此外，人乳头瘤病毒感染对鳞癌发生的病因学影响仍在研究之中。
在食管鳞癌发病率高的国家，食管鳞癌的早期筛查工作主要集中于目标人群的细胞学或内镜筛查。这些检查可以在无症状的早期阶段发现鳞癌，一项中国的研究评估了终身一次内镜筛查对食管癌患者的影响。研究采用非随机的方式选取了河北省磁县的一些乡镇/社区；干预组是北部的14个村庄，对照组是南部的10个村庄。研究的干预措施是由专家进行的终身一次性内窥镜检查，并使用卢戈氏碘染色鉴别不典型增生或隐性癌。对取活检并读片后确诊的不典型增生和隐性癌，进行了内镜下黏膜切除或氩离子凝固术。在干预组的6827名40至69岁受试者中，有3319例接受筛查。在对照组的6200名40岁至69岁受试者中，有797例接受了访谈。通过监测各组结局来评估食管鳞癌的发生率和死亡率。在10年的随访中，共有542例食管鳞癌(ESCC)死亡病例，干预组的累积死亡率比对照组有所下降，对照组为5.05%，而干预组为3.35%(P<0.001)，且干预组ESCC的发生率较低(5.92%vs.4.17%，P<0.001)。但本研究存在以下局限性:
中国，伊朗，南非，意大利，和日本等多个国家相继发表了食管癌细胞学筛查相关研究报道。
在美国，类似的研究工作主要在食管癌高危人群中开展。
此外，法国和日本则发表了内镜初筛的相关研究结果。
对比中国和美国的研究均发现，细胞学联合组织学检查，检出已经活检确诊的肿瘤敏感性较低（14%-36%）。特异性为90-99%，而其阳性预测值为23%-94%。
因此，统一且准确的食管病灶细胞学诊断标准，需要正式的细胞学-组织学相关性研究。随着内镜筛查在高危人群中的普及率逐步提升，上述研究将变得更为可行。
对于患胼胝症或长期贲门失弛缓症的高危人群，进行细胞学或内镜检测的有效性尚不明确。
对于巴雷特食管患者发生癌症的风险尚存在争议。一些已发表的前瞻性研究发现巴雷特食管患者的食管腺癌年发病率在0.2%到1.9%之间。
考虑到存在文献发表偏倚，部分学者认为真实的发病率可能会低于文献报道的数据。
目前普遍认为在巴雷特食管患者中，比较合理的食管腺癌发病率在0.5%左右。
巴雷特食管与胃食管反流病（GERD）显著相关，约10%的胃食管反流病患者有巴雷特食管。但胃食管反流病本身非常普遍，研究发现约20%的美国成年人出现过烧心等胃食管反流症状，且每周至少一次。
内镜下发现巴雷特食管可能与胃食管反流症状的持续时间相关。一项纳入701例受试者的研究发现，在胃食管反流症状持续不足1年的患者中，经内镜检查仅有4%出现了巴雷特食管；而在胃食管反流症状持续超过10年的患者中，这一比例高达21%。据估计，医生仅诊断或发现了约5%的巴雷特食管患者。
尚未有足够证据提示针对巴雷特食管的人群筛查可以降低癌症的死亡率。
巴雷特食管的监测包括通过在确诊巴雷特食管的患者中检查出癌前病变或可治愈的肿瘤。监测的有效实施必须满足多个必要因素，包括采用风险低的监测方法、对不典型增生的正确组织学诊断、证明高度不典型增生的手术切除能降低患癌风险，和成功的肿瘤切除。内镜随访的时间间隔取决于组织学结果，以胃肠道疾病协会发表的指南为准则。
为了减少胃食管反流病本身的炎症反应对活检结果判读的干扰，应在实施内镜检查前先治疗胃食管反流病。部分临床医生推荐采用随机四象限活检的方法作为组织学评估标准，该技术将食管柱状上皮取材区域分为四个象限，分别取材一次，各取材点间隔2cm。对于无不典型增生的患者，推荐每隔2到3年复查一次内镜。
对于轻度不典型增生患者，指南建议自诊断起第一年内每隔6个月复查一次内镜，如果不典型增生的严重程度没有进展，自第二年起可延长至每年一次复查内镜。对于高度不典型增生患者，指南有两个建议：直接手术切除或者重复内镜评估直至诊断为黏膜下癌。尽管上述指南建议在临床实践中被广泛采用，仍需注意上述建议主要是基于非对照病例系列研究及胃肠道疾病的内镜专科医师和病理学家的意见。
其他有望识别不典型增生上皮且可以可以广泛采样的技术包括染色内镜检查
和激光诱导荧光光谱法。
采用盲法非内镜引导球囊细胞学采样对食管鳞状细胞癌进行筛查很少引起不便或不适。食管腺癌的内镜筛查较为昂贵、不方便且常需药物镇静。
我国的大量科学证据表明，上消化道内镜检查是食管癌筛查的有效手段，而且内镜检查对于食管鳞癌的检出效果优于食管腺癌。因此，上消化道内镜检查是预防食管癌发生的有效方法。
内镜检查可能出现穿孔或出血等并发症。穿孔、呼吸骤停及心肌梗死三大并发症的发生率约为0-13/万次操作，死亡率0-0.8例/万次操作。
尽管巴雷特食管的患癌风险较低，诊断为巴雷特食管的患者仍会以为自己生病了。
Squamous cell carcinoma of the esophagus does not have a highly prevalent predisposing condition, although the incidence increases in persons who have had long-standing exposure to tobacco and alcohol,achalasia, head and neck squamous cell cancer attributable most likely to long-standing alcohol and/or tobacco exposure,tylosis, history of lye ingestion, celiac sprue, and, in South America and China, hot liquid ingestion.
The etiological role of human papillomavirus infection in squamous cell cancer is under study.
Efforts at early detection of squamous cell cancer of the esophagus have concentrated on cytological or endoscopic screening of populations in countries where there is a high incidence. While these programs have demonstrated that it is possible to detect squamous cell cancers in an early asymptomatic stage, a study from China assessed one-time endoscopic screening on the outcome of patients with esophageal cancer. In this study, communities were chosen nonrandomly in Cixian County, Hibei Province; 14 villages in the north were intervention communities and ten villages in the south were control communities. The intervention was one-time endoscopy, completed by experts, using Lugol’s iodine staining to identify dysplasia or occult cancer. After biopsy was obtained and read, dysplasia and occult cancers were treated by endoscopic mucosal resection or argon plasma coagulation. Among the 6,827 participants aged 40 to 69 years in the intervention group, 3,319 volunteers were screened. Among the 6,200 participants aged 40 to 69 years in the control group, 797 individuals were interviewed. Outcome in each group was monitored to assess incidence and mortality of esophageal squamous cancer. In a 10-year follow-up, there were 542 cases of fatal esophageal squamous cell carcinoma (ESCC), a reduction in cumulative mortality from 5.05% in the control group to 3.35% in the intervention group (P < .001), and lower incidence of ESCC in the intervention group (5.92% vs. 4.17%, P < .001). Potential weaknesses of the study include the following:
Esophageal cytological screening studies have been reported from China,Iran, South Africa,Italy,and Japan.
In the United States, such efforts have been focused on individuals perceived to be at higher risk.
Studies of primary endoscopic screening have been reported from France and Japan.
Comparisons of both Chinese and U.S. cytological diagnoses with concurrent histological findings showed low (14% to 36%) sensitivities for the cytological detection of biopsy-proven cancers. Specificity ranged from 90% to 99% with a positive predictive value of 23% to 94%.
The development of uniform and accurate cytological criteria will require formal cytological-histological correlation studies of esophageal lesions. Such studies should become more feasible with the increasing availability of endoscopy in high-risk populations.
The efficacy of surveillance cytology or endoscopy for high-risk patients with tylosis or long-standing achalasia is not known.
Considerable debate has ensued concerning the risk of cancer in patients with Barrett esophagus. Prospective studies have reported annual esophageal cancer incidence rates ranging from 0.2% to 1.9%.
Concern over publication bias has led some authors to suggest that the risk may be lower than the literature suggests.
A risk of 0.5% per year for development of adenocarcinoma is now thought to be a reasonable estimate for Barrett esophagus.
Barrett esophagus is strongly associated with gastroesophageal reflux disease (GERD), and the changes of Barrett esophagus can be found in approximately 10% of patients who have GERD. However, GERD is very common; surveys have found that approximately 20% of adult Americans experience symptoms of GERD, such as heartburn, at least once each week.
The likelihood of finding Barrett esophagus on endoscopy is related to the duration of symptoms of gastroesophageal reflux. In a series of 701 individuals, 4% of those with symptoms for less than 1 year had Barrett esophagus on endoscopy, whereas Barrett esophagus was found in 21% of those with more than 10 years of symptoms of GERD. It has been estimated that physicians identify only approximately 5% of the population who have Barrett esophagus.
There is insufficient evidence that population screening for Barrett esophagus reduces cancer mortality.
Surveillance of Barrett esophagus involves the use of tests to identify preneoplastic changes or curable neoplasms in patients who are known to have Barrett esophagus. Certain factors are essential in the implementation of an effective surveillance protocol, including low risk of the surveillance method, correct histological diagnosis of dysplasia, proof that surgical resection for high-grade dysplasia will decrease the risk of cancer, and successful resection of cancer. The interval between endoscopic evaluations is typically determined by histologic findings, in accordance with published guidelines by gastroenterological committees.
GERD should be treated prior to surveillance endoscopy to minimize confusion caused by inflammation in the interpretation of biopsy specimens. The technique of random, four-quadrant biopsies taken every 2 cm in the columnar-lined esophagus for standard histological evaluation has been recommended by some clinicians. For patients with no dysplasia, surveillance endoscopy at an interval of every 2 to 3 years has been recommended.
For patients with low-grade dysplasia, surveillance every 6 months for the first year has been recommended, followed by annual endoscopy if the dysplasia has not progressed in severity. For patients with high-grade dysplasia, two options have been recommended: surgical resection or repeated endoscopic evaluation until the diagnosis of intramucosal carcinoma is made. Although widely adopted in clinical practice, these practices are based on uncontrolled series and the opinion of expert gastrointestinal endoscopists and pathologists.
Other techniques to potentially identify dysplastic epithelium that could then be sampled extensively include chromoendoscopy
and laser-induced fluorescence spectroscopy.
Screening for esophageal cancer by the use of blind nonendoscopically directed balloon cytological sampling for squamous cell carcinoma is minimally inconvenient and uncomfortable. Endoscopic screening for esophageal adenocarcinoma is expensive, inconvenient, and usually requires sedation.
Complications such as perforation and bleeding can occur. The incidence of complications including perforation, respiratory arrest, and myocardial infarction, has been estimated to be 0 to 13 per 10,000 procedures with an associated mortality of 0 to 0.8 per 10,000 procedures.
Individuals who are informed they have Barrett esophagus may consider themselves to be ill even though their risk of developing cancer is very low.
PDQ癌症信息库会定期审核，并在出现新信息时进行更新。本节描述了截至上述日期前对该信息库所做的最新更改。
更新了2020年新发病例与死亡病例的统计学估计数据（引用美国癌症研究所参考文献1）。
该信息库由PDQ筛查和预防编辑委员会撰写和维护，该委员会在编辑上独立于NCI。本信息库为独立的文献综述，不作为NCI或NIH的政策声明。关于总结政策和PDQ编辑委员会的更多信息请参见关于本PDQ总结和 PDQ® - NCI综合性癌症数据库页面。
The PDQ cancer information summaries are reviewed regularly and updated as new information becomes available. This section describes the latest changes made to this summary as of the date above.
Updated statistics with estimated new cases and deaths for 2020 (cited American Cancer Society as reference 1).
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This PDQ cancer information summary for health professionals provides comprehensive, peer-reviewed, evidence-based information about esophageal cancer screening. It is intended as a resource to inform and assist clinicians who care for cancer patients. It does not provide formal guidelines or recommendations for making health care decisions.
This summary is reviewed regularly and updated as necessary by the PDQ Screening and Prevention Editorial Board, which is editorially independent of the National Cancer Institute (NCI). The summary reflects an independent review of the literature and does not represent a policy statement of NCI or the National Institutes of Health (NIH).
Board members review recently published articles each month to determine whether an article should:
Changes to the summaries are made through a consensus process in which Board members evaluate the strength of the evidence in the published articles and determine how the article should be included in the summary.
Any comments or questions about the summary content should be submitted to Cancer.gov through the NCI website's Email Us. Do not contact the individual Board Members with questions or comments about the summaries. Board members will not respond to individual inquiries.
Some of the reference citations in this summary are accompanied by a level-of-evidence designation. These designations are intended to help readers assess the strength of the evidence supporting the use of specific interventions or approaches. The PDQ Screening and Prevention Editorial Board uses a formal evidence ranking system in developing its level-of-evidence designations.
PDQ is a registered trademark. Although the content of PDQ documents can be used freely as text, it cannot be identified as an NCI PDQ cancer information summary unless it is presented in its entirety and is regularly updated. However, an author would be permitted to write a sentence such as “NCI’s PDQ cancer information summary about breast cancer prevention states the risks succinctly: [include excerpt from the summary].”
The preferred citation for this PDQ summary is:
PDQ® Screening and Prevention Editorial Board. PDQ Esophageal Cancer Screening. Bethesda, MD: National Cancer Institute. Updated
Images in this summary are used with permission of the author(s), artist, and/or publisher for use within the PDQ summaries only. Permission to use images outside the context of PDQ information must be obtained from the owner(s) and cannot be granted by the National Cancer Institute. Information about using the illustrations in this summary, along with many other cancer-related images, is available in Visuals Online, a collection of over 2,000 scientific images.
The information in these summaries should not be used as a basis for insurance reimbursement determinations. More information on insurance coverage is available on Cancer.gov on the Managing Cancer Care page.
More information about contacting us or receiving help with the Cancer.gov website can be found on our Contact Us for Help page. Questions can also be submitted to Cancer.gov through the website’s Email Us.