Epidemiologic risk factors for Barrett’s esophagus and associated adenocarcinoma
2005; Elsevier BV; Volume: 3; Issue: 1 Linguagem: Inglês
10.1016/s1542-3565(04)00602-0
ISSN1542-7714
AutoresAngela Wong, Rebecca C. Fitzgerald,
Tópico(s)Esophageal and GI Pathology
ResumoThe incidence of esophageal adenocarcinoma (AC) has increased dramatically in the Western world over the past 20 years and the majority of these cancers arise on the background of the preinvasive lesion Barrett's esophagus. The epidemiologic factors that contribute to an individual's susceptibility for Barrett's esophagus and associated cancer are likely to be multifactorial. However, the short time frame over which the incidence of adenocarcinoma has increased, and the increase across populations, provides a strong argument for environmental factors as etiologic agents, perhaps interacting with genetically determined characteristics that define personal susceptibility. In this review we discuss the epidemiologic evidence for the proposed demographic and environmental risk factors for the development of both Barrett's esophagus and AC. The current evidence suggests that significant risk factors include male sex, Caucasian race, and the presence of duodenogastroesophageal reflux disease. The susceptibility for reflux disease may in turn be influenced by factors such as obesity, the use of drugs that lower the lower-esophageal sphincter tone, and a protective effect of Helicobacter pylori colonization. There appears to be a weak association between smoking and AC. The role of dietary factors has not been studied adequately and deserves further attention. An understanding of the factors that predispose to the development and progression of Barrett's esophagus is crucial to the implementation of effective screening and prevention programs. The incidence of esophageal adenocarcinoma (AC) has increased dramatically in the Western world over the past 20 years and the majority of these cancers arise on the background of the preinvasive lesion Barrett's esophagus. The epidemiologic factors that contribute to an individual's susceptibility for Barrett's esophagus and associated cancer are likely to be multifactorial. However, the short time frame over which the incidence of adenocarcinoma has increased, and the increase across populations, provides a strong argument for environmental factors as etiologic agents, perhaps interacting with genetically determined characteristics that define personal susceptibility. In this review we discuss the epidemiologic evidence for the proposed demographic and environmental risk factors for the development of both Barrett's esophagus and AC. The current evidence suggests that significant risk factors include male sex, Caucasian race, and the presence of duodenogastroesophageal reflux disease. The susceptibility for reflux disease may in turn be influenced by factors such as obesity, the use of drugs that lower the lower-esophageal sphincter tone, and a protective effect of Helicobacter pylori colonization. There appears to be a weak association between smoking and AC. The role of dietary factors has not been studied adequately and deserves further attention. An understanding of the factors that predispose to the development and progression of Barrett's esophagus is crucial to the implementation of effective screening and prevention programs. Over the past 25 years there has been a dramatic increase in the incidence of esophageal adenocarcinoma (AC) of 350% and 300% in Caucasian men and Caucasian women, respectively.1Blot W. Devesa S. Fraumeni J. Continued climb in rates of esophageal adenocarcinoma an update.JAMA. 1993; 270: 1320Crossref PubMed Scopus (391) Google Scholar Currently, 60% of all esophageal cancers are adenocarcinomas.1Blot W. Devesa S. Fraumeni J. Continued climb in rates of esophageal adenocarcinoma an update.JAMA. 1993; 270: 1320Crossref PubMed Scopus (391) Google Scholar In contrast, the incidence of squamous cell carcinoma is quite stable in Western countries,2Enzinger P.C. Mayer R.J. Esophageal cancer.N Engl J Med. 2003; 349: 2241-2252Crossref PubMed Scopus (2461) Google Scholar, 3Liabeuf A. Faivre J. Time trends in oesophageal cancer incidence in Cote d'Or (France), 1976–93.Eur J Cancer Prev. 1997; 6: 24-30Crossref PubMed Scopus (25) Google Scholar and the incidence of noncardia gastric tumors is decreasing.4Hansson L.E. Bergstrom R. Sparen P. et al.The decline in the incidence of stomach cancer in Sweden 1960–1984 a birth cohort phenomenon.Int J Cancer. 1991; 47: 499-503Crossref PubMed Scopus (45) Google Scholar Most ACs present at an advanced stage when lymph node invasion already has occurred and the overall 5-year survival is less than 20%.5Lund O. Kimose H. Augaard M. et al.Risk stratification and long-term results for carcinoma of the esophagus.J Thorac Cardiovasc Surg. 1990; 99: 200-209PubMed Google Scholar, 6Landis S. Murray T. Bolden S. et al.Cancer statistics.CA Cancer J Clin. 1999; 49: 8-31Crossref PubMed Scopus (3127) Google Scholar As a result of the increasing incidence and poor survival of this disease, attention has focused on prevention and early diagnostic strategies.Barrett's esophageal epithelium (BE) is a known risk factor for the development of AC, however, the reasons why only a small proportion (10%) of patients with gastroesophageal reflux develop BE and a smaller proportion still progress to adenocarcinoma are unknown. The causative factors that contribute to an individual's susceptibility for this condition are likely to be multifactorial. It has been suggested that the increased incidence of AC is in part related to an age effect in that an individual's risk is greater by virtue of increasing age. In addition, a trend toward a birth cohort effect also has been shown, with higher incidence rates in younger cohorts.7El-Serag H.B. Mason A.C. Petersen N. et al.Epidemiological differences between adenocarcinoma of the oesophagus and adenocarcinoma of the gastric cardia in the USA.Gut. 2002; 50: 368-372Crossref PubMed Scopus (219) Google Scholar The latter effect would tend to support exposure to a common risk factor(s) in early life, predisposing to an increased risk for AC at all subsequent ages within the age cohort. This together with the increase in incidence of AC across populations provides a strong argument for environmental factors as causative agents, perhaps interacting with genetically determined characteristics that define personal susceptibility.It is thought that only 5% of patients with BE are diagnosed, with the silent majority of people with BE remaining unrecognized in the general population. Therefore, the majority of cancers present de novo,8Conio M. Cameron A.J. Romero Y. et al.Secular trends in the epidemiology and outcome of Barrett's oesophagus in Olmsted County, Minnesota.Gut. 2001; 48: 304-309Crossref PubMed Scopus (224) Google Scholar, 9Cameron A. Zinsmeister A. Ballard D. et al.Prevalence of columnar-lined (Barrett's) esophagus. Comparison of population-based clinical and autopsy findings.Gastroenterology. 1990; 99: 1918-1922Google Scholar, 10Bytzer P. Christensen P.B. Damkier P. et al.Adenocarcinoma of the esophagus and Barrett's esophagus a population-based study.Am J Gastroenterol. 1999; 94: 86-91Crossref PubMed Scopus (253) Google Scholar and the current surveillance programs have minimal impact at the population level. Because gastroesophageal reflux is common, endoscopic screening of an untargeted population is undesirable in view of the high associated costs and because endoscopy is not without risk. Therefore, an understanding of the factors that predispose to the development and progression of BE is crucial to the implementation of effective screening and chemoprevention programs. The epidemiologic evidence for the proposed risk factors for the development of BE and AC are discussed in turn.Age, sex, and raceBE is an acquired disorder. There is a very low prevalence in childhood,11Cameron A.J. Lomboy C.T. Barrett's esophagus age, prevalence and extent of columnar epithelium.Gastroenterology. 1992; 103: 1241-1245PubMed Google Scholar and when it occurs it frequently is associated with mental retardation.12Snyder J.D. Goldman H. Barrett's esophagus in children and young adults. Frequent association with mental retardation.Dig Dis Sci. 1990; 35: 1185-1189Crossref PubMed Scopus (39) Google Scholar Half the maximum prevalence of BE is reached at age 40, so this may be the mean age of developing the condition.13Gruppo Operativo per lo Studio delle Precancerosi dell'Esofago (GOSPE)Barrett's esophagus epidemiological and clinical results of a multicentric survey.Int J Cancer. 1991; 48: 364-368Crossref PubMed Scopus (111) Google Scholar However, because the mean age for diagnosing BE in Europe is in the 60s, this suggests that most patients have unrecognizable BE for many years before diagnosis. The UK BE registry found that there is geographic variation such that in a comparison of over 5000 patients from 27 hospitals spread geographically throughout the United Kingdom, male patients in Scotland were diagnosed at an average age of 57.4 compared with 61.6 years for male patients in England.14Caygill C.P. Watson A. Reed P.I. et al.Characteristics and regional variations of patients with Barrett's oesophagus in the UK.Eur J Gastroenterol Hepatol. 2003; 15: 1217-1222Crossref PubMed Scopus (28) Google Scholar The mean age for diagnosis of BE-associated AC is 64.7 years for men and 74 years for women in the United Kingdom,14Caygill C.P. Watson A. Reed P.I. et al.Characteristics and regional variations of patients with Barrett's oesophagus in the UK.Eur J Gastroenterol Hepatol. 2003; 15: 1217-1222Crossref PubMed Scopus (28) Google Scholar which is similar for data from Europe and the United States, although there has been a significant increase in incidence among the 45–65 age group.7El-Serag H.B. Mason A.C. Petersen N. et al.Epidemiological differences between adenocarcinoma of the oesophagus and adenocarcinoma of the gastric cardia in the USA.Gut. 2002; 50: 368-372Crossref PubMed Scopus (219) Google ScholarBE is more common in men than in women, with a male:female ratio of about 2:1 (Table 1). All the studies suggest that this male predominance increases with the development of Barrett's adenocarcinoma with a ratio of at least 3:1.14Caygill C.P. Watson A. Reed P.I. et al.Characteristics and regional variations of patients with Barrett's oesophagus in the UK.Eur J Gastroenterol Hepatol. 2003; 15: 1217-1222Crossref PubMed Scopus (28) Google Scholar, 15Menke-Pluymers M.B. Hop W.C. Dees J. et al.The Rotterdam Esophageal Tumor Study GroupRisk factors for the development of an adenocarcinoma in columnar-lined (Barrett) esophagus.Cancer. 1993; 72: 1155-1158Crossref PubMed Scopus (215) Google Scholar, 16Sarr M.G. Hamilton S.R. Marrone G.C. et al.Barrett's esophagus its prevalence and association with adenocarcinoma in patients with symptoms of gastroesophageal reflux.Am J Surg. 1985; 149: 187-193Abstract Full Text PDF PubMed Scopus (188) Google Scholar, 17Rogers E. Goldkind S. Iseri O. et al.Adenocarcinoma of the lower esophagus. A disease primarily of white men with Barrett's esophagus.J Clin Gastroenterol. 1986; 8: 613-618Crossref PubMed Scopus (54) Google ScholarTable 1Summary of the Studies That Have Examined the Male to Female Ratio for Esophageal AdenocarcinomaStudyMenWomenM:FBytzer et al,10Bytzer P. Christensen P.B. Damkier P. et al.Adenocarcinoma of the esophagus and Barrett's esophagus a population-based study.Am J Gastroenterol. 1999; 94: 86-91Crossref PubMed Scopus (253) Google Scholar 19994201044:1GOSPE,13Gruppo Operativo per lo Studio delle Precancerosi dell'Esofago (GOSPE)Barrett's esophagus epidemiological and clinical results of a multicentric survey.Int J Cancer. 1991; 48: 364-368Crossref PubMed Scopus (111) Google Scholar 19991%.39%2.6:1Cameron and Lomboy,11Cameron A.J. Lomboy C.T. Barrett's esophagus age, prevalence and extent of columnar epithelium.Gastroenterology. 1992; 103: 1241-1245PubMed Google Scholar 1992.97%.29%2:1Caygill et al,14Caygill C.P. Watson A. Reed P.I. et al.Characteristics and regional variations of patients with Barrett's oesophagus in the UK.Eur J Gastroenterol Hepatol. 2003; 15: 1217-1222Crossref PubMed Scopus (28) Google Scholar 19993231851.7:1 Open table in a new tab Despite possible selection bias in those attending for endoscopy, it has been observed that BE is more common in Caucasians and this ratio increases with the development of adenocarcinoma.1Blot W. Devesa S. Fraumeni J. Continued climb in rates of esophageal adenocarcinoma an update.JAMA. 1993; 270: 1320Crossref PubMed Scopus (391) Google Scholar, 16Sarr M.G. Hamilton S.R. Marrone G.C. et al.Barrett's esophagus its prevalence and association with adenocarcinoma in patients with symptoms of gastroesophageal reflux.Am J Surg. 1985; 149: 187-193Abstract Full Text PDF PubMed Scopus (188) Google Scholar, 17Rogers E. Goldkind S. Iseri O. et al.Adenocarcinoma of the lower esophagus. A disease primarily of white men with Barrett's esophagus.J Clin Gastroenterol. 1986; 8: 613-618Crossref PubMed Scopus (54) Google Scholar Recent studies showed that the incidence of AC continues to increase in Caucasian men,7El-Serag H.B. Mason A.C. Petersen N. et al.Epidemiological differences between adenocarcinoma of the oesophagus and adenocarcinoma of the gastric cardia in the USA.Gut. 2002; 50: 368-372Crossref PubMed Scopus (219) Google Scholar, 18Younes M. Henson D.E. Ertan A. et al.Incidence and survival trends of esophageal carcinoma in the United States racial and gender differences by histological type.Scand J Gastroenterol. 2002; 37: 1359-1365Crossref PubMed Scopus (105) Google Scholar and, interestingly, an increase also has been observed in Hispanics in the United States.18Younes M. Henson D.E. Ertan A. et al.Incidence and survival trends of esophageal carcinoma in the United States racial and gender differences by histological type.Scand J Gastroenterol. 2002; 37: 1359-1365Crossref PubMed Scopus (105) Google Scholar Adenocarcinoma is rare in the Pacific Rim, comparable with the low incidence in the United States before 1970. In a review of the Japanese literature it was found that the incidence of AC was increasing slowly, although it was still much less common than squamous cell cancer of the esophagus.19Hongo M. Shoji T. Epidemiology of reflux disease and CLE in East Asia.J Gastroenterol. 2003; 38: 25-30PubMed Google Scholar Similarly, the prevalence of long-segment BE in Japan is less than 2% of the number reported in the US series.19Hongo M. Shoji T. Epidemiology of reflux disease and CLE in East Asia.J Gastroenterol. 2003; 38: 25-30PubMed Google Scholar A study from Taiwan indicated a trend toward an increasing prevalence of BE in the indigent population. The investigators proposed Westernization of diet, an increasing elderly population, and obesity as possible explanations.20Yeh C. Hsu C.T. Ho A.S. et al.Erosive esophagitis and Barrett's esophagus in Taiwan a higher frequency than expected.Dig Dis Sci. 1997; 42: 702-706Crossref PubMed Scopus (126) Google Scholar In Singapore, heartburn or acid reflux occurred at least monthly in only 1.6% of adults, compared with 29%–44% in the West.21Ho K.Y. Kang J.Y. Seow A. Prevalence of gastrointestinal symptoms in a multiracial Asian population, with particular reference to reflux-type symptoms.Am J Gastroenterol. 1998; 93: 1816-1822Crossref PubMed Scopus (274) Google Scholar In a recent study in the United States, Caucasian and African American people had a similarly high prevalence of gastroesophageal reflux disease (GERD). However, African American people had a lower prevalence of esophagitis. BE was rare in this study.22El-Serag H.B. Petersen N.J. Carter J. et al.Gastroesophageal reflux among different racial groups in the United States.Gastroenterology. 2004; 126: 1692-1699Abstract Full Text Full Text PDF PubMed Scopus (213) Google Scholar It is too early to know whether non-Caucasian ethnic groups have a genetic variation that is protective against the complications of reflux disease or whether the epidemic increase seen in the West may be beginning to occur in other racial groups as a result of environmental factors such as changes in diet and lifestyle.SmokingThe role of smoking and BE is controversial. This may be related to variations in study methodology; the role of smoking has often not been the primary end point of studies. Many small studies have not shown an association with smoking.23Conio M. Filiberti R. Blanchi S. et al.Risk factors for Barrett's esophagus a case-control study.Int J Cancer. 2002; 97: 225-229Crossref PubMed Scopus (140) Google Scholar, 24Eloubeidi M. Provenzale D. Clinical and demographic predictors of Barrett's esophagus among patients with gastroesophageal reflux disease a multivariable analysis in veterans.J Clin Gastroenterol. 2001; 33: 306-309Crossref PubMed Scopus (120) Google Scholar, 25Caygill C.P. Johnston D.A. Lopez M. et al.Lifestyle factors and Barrett's esophagus.Am J Gastroenterol. 2002; 97: 1328-1331Crossref PubMed Google Scholar, 26Avidan B. Sonnenberg A. Schnell T.G. et al.Hiatal hernia size, Barrett's length, and severity of acid reflux are all risk factors for esophageal adenocarcinoma.Am J Gastroenterol. 2002; 97: 1930-1936Crossref PubMed Google Scholar, 27Gray M.R. Donnelly R.J. Kingsnorth A.N. The role of smoking and alcohol in metaplasia and cancer risk in Barrett's columnar lined oesophagus.Gut. 1993; 34: 727-731Crossref PubMed Scopus (86) Google Scholar For example, in a study comparing the smoking habits between different patient groups, patients with nondysplastic BE were significantly more likely to be nonsmokers than patients with both severe esophagitis and AC.27Gray M.R. Donnelly R.J. Kingsnorth A.N. The role of smoking and alcohol in metaplasia and cancer risk in Barrett's columnar lined oesophagus.Gut. 1993; 34: 727-731Crossref PubMed Scopus (86) Google ScholarWith regard to AC, studies have produced mixed results. Even for those studies in which an association was found (Table 2), it is clear that the odds ratio (OR) for adenocarcinoma (OR, 1.5–3.4) is much lower than the risk associated with squamous cell carcinoma (OR, 16.9).28Vaughan T.L. Davis S. Kristal A. et al.Obesity, alcohol, and tobacco as risk factors for cancers of the esophagus and gastric cardia adenocarcinoma versus squamous cell carcinoma.Cancer Epidemiol Biomarkers Prev. 1995; 4: 85-92PubMed Google ScholarTable 2Association With Tobacco, Alcohol, and Esophageal AdenocarcinomaStudy detailsOR (95% CI) for tobaccoOR (95% CI) for alcoholGammon et al,29Gammon M. Schoenberg J. Ahsan H. Tobacco, alcohol and socioeconomic status and adenocarcinoma of the esophagus and gastric cardia.J Natl Cancer Inst. 1997; 89: 1277-1284Crossref PubMed Scopus (522) Google Scholar 1997, n > 500 cases, n > 500 controlsCurrent smokers 2.4 (.8–1.4)Beer .8 (.6–1.1)Little decrease after 30 y cessationLiquor 1.1 (.8–1.4)Wine .6 (.5–.8)Kabat et al,30Kabat G.C. Ng S.K. Wynder E.L. Tobacco, alcohol intake, and diet in relation to adenocarcinoma of the esophagus and gastric cardia.Cancer Causes Control. 1993; 4: 123-132Crossref PubMed Scopus (259) Google Scholar 1993, n = 173 cases, n > 4000 controlsCurrent smokers 2.3 (1.4–3.9)2.3 (1.3–4.3)Ex-smokers 1.9 (1.2–3.0)Zhang et al,79Zhang Z.F. Kurtz R.C. Sun M. et al.Adenocarcinomas of the esophagus and gastric cardia medical conditions, tobacco, alcohol, and socioeconomic factors.Cancer Epidemiol Biomarkers Prev. 1996; 5: 761-768PubMed Google Scholar 1996, n = 95 cases, n = 132 controls1.5–2.4No associationBrown et al,31Brown L.M. Silverman D.T. Pottern L.M. et al.Adenocarcinoma of the esophagus and esophagogastric junction in white men in the United States alcohol, tobacco, and socioeconomic factors.Cancer Causes Control. 1994; 5: 333-340Crossref PubMed Scopus (180) Google Scholar 1994, n = 171 cases, n > 500 controls2.11.6No risk reduction on quittingDose gradientVaughn et al,28Vaughan T.L. Davis S. Kristal A. et al.Obesity, alcohol, and tobacco as risk factors for cancers of the esophagus and gastric cardia adenocarcinoma versus squamous cell carcinoma.Cancer Epidemiol Biomarkers Prev. 1995; 4: 85-92PubMed Google Scholar 1995, n = 298 cases, n > 500 controls3.4 (1.4–8.0)1.8 (1.1–3.1)Menke-Pluymers et al,15Menke-Pluymers M.B. Hop W.C. Dees J. et al.The Rotterdam Esophageal Tumor Study GroupRisk factors for the development of an adenocarcinoma in columnar-lined (Barrett) esophagus.Cancer. 1993; 72: 1155-1158Crossref PubMed Scopus (215) Google Scholar 1993, n = 62 cases, n = 96 controls% smokers higher in AC vs Barrett's (P < .001)No associationAchkar et al,80Achkar J.P. Post A.B. Achkar E. et al.Risk of extraesophageal malignancy in patients with adenocarcinoma arising in Barrett's esophagus.Am J Gastroenterol. 1995; 90: 39-43PubMed Google Scholar 1995, n = 294 cases, n = 170 controlsP = .02 AC vs controlsP < .01 AC vs controlsGray et al,27Gray M.R. Donnelly R.J. Kingsnorth A.N. The role of smoking and alcohol in metaplasia and cancer risk in Barrett's columnar lined oesophagus.Gut. 1993; 34: 727-731Crossref PubMed Scopus (86) Google Scholar 1993, n = 23 cases, n = 82 controlsIncreased duration smoking in AC vs Barrett's (P < .01)AC greater alcohol intake than Barrett's (P < .02)Levi et al,81Levi F. Olloyo J. Vecchia C.L. et al.The consumption of tobacco and the risk of adenocarcinoma in Barrett's esophagus.Int J Cancer. 1990; 45: 852-854Crossref PubMed Scopus (75) Google Scholar 1990, n = 30 cases, n = 140 controlsOR 1.0 moderate smokersOR .7 moderateOR .9 heavy smokersOR 1.5 heavy drinkerLagergren et al,69Lagergren J. Bergstrom R. Adami H.O. et al.Association between medications that relax the lower esophageal sphincter and risk for esophageal adenocarcinoma.Ann Intern Med. 2000; 133: 165-175Crossref PubMed Scopus (161) Google Scholar 2000, n = 189 cases, n > 800 controlsNo associationNo associationAvidan et al,26Avidan B. Sonnenberg A. Schnell T.G. et al.Hiatal hernia size, Barrett's length, and severity of acid reflux are all risk factors for esophageal adenocarcinoma.Am J Gastroenterol. 2002; 97: 1930-1936Crossref PubMed Google Scholar 2002, n = 131 cases, n > 3000 controlsNo associationNo associationNOTE. Data are presented as the OR and 95% CI where available. Open table in a new tab In addition, there is evidence to suggest that there is little decrease in OR on stopping smoking such that the OR for current and ex-smokers was 2.0 times greater in the cancer cases even 30 years after cessation of smoking.29Gammon M. Schoenberg J. Ahsan H. Tobacco, alcohol and socioeconomic status and adenocarcinoma of the esophagus and gastric cardia.J Natl Cancer Inst. 1997; 89: 1277-1284Crossref PubMed Scopus (522) Google Scholar It has been suggested that the long lag-time before tumor risk is decreased in ex-smokers, which suggests that smoking may affect early-stage carcinogenesis. In addition, the increase in smoking prevalence during the first two thirds of this century may be reflected in the recent increasing incidence of these tumors among older individuals. The recent decrease in smoking may not yet have had an impact.Overall, the role of tobacco smoking in BE and associated AC are uncertain. There are more positive than negative studies suggesting an association, but its strength appears to be weak compared with squamous cell carcinoma of the esophagus.AlcoholThere are relatively few studies that examine the relationship between alcohol and BE. The UK BE registry has shown no association between alcohol consumption in patients with BE compared with patients found to have endoscopic reflux esophagitis.25Caygill C.P. Johnston D.A. Lopez M. et al.Lifestyle factors and Barrett's esophagus.Am J Gastroenterol. 2002; 97: 1328-1331Crossref PubMed Google Scholar More studies have examined the relationship between esophageal cancer and alcohol consumption and some of these studies have used patients with BE as a control group. One of the problems with interpreting these studies is that the definition of moderate and excessive alcohol consumption varies between studies and different types of alcohol may have variable effects.Six of 11 studies found some kind of association but the strength of the association generally was weak (Table 2). The strongest association was found by Kabat et al30Kabat G.C. Ng S.K. Wynder E.L. Tobacco, alcohol intake, and diet in relation to adenocarcinoma of the esophagus and gastric cardia.Cancer Causes Control. 1993; 4: 123-132Crossref PubMed Scopus (259) Google Scholar in a case-control study of 173 patients with AC compared with over 4000 hospitalized controls. They quantified the amount of alcohol consumption such that drinkers of 4 or more ounces of whiskey equivalents of alcohol per day were compared with those consuming less than 1 drink per week, resulting in an OR of 2.3 for AC (confidence interval [CI], 1.3–4.3). In the study by Brown et al,31Brown L.M. Silverman D.T. Pottern L.M. et al.Adenocarcinoma of the esophagus and esophagogastric junction in white men in the United States alcohol, tobacco, and socioeconomic factors.Cancer Causes Control. 1994; 5: 333-340Crossref PubMed Scopus (180) Google Scholar there also appeared to be a correlation between the magnitude of the risk and the amount of alcohol consumed.The Lagergren study (Table 2) was conducted using face-to-face interviews and they showed that the risk for these tumors was not related to beer (OR, .8; 95% CI, .6–1.1) or liquor consumption (OR, 1.1; 95% CI, .8–1.4), but it was decreased for drinking wine (OR, .6; 95% CI, .5–.8). Similar ORs were obtained for the development of distal gastric adenocarcinomas in relation to tobacco and alcohol use, but higher ORs were obtained for the development of esophageal squamous cell carcinomas.In summary, the evidence to date does not suggest a significant relationship between alcohol consumption and AC.Socioeconomic statusSocioeconomic status relates to the differences between groups of people caused mainly by their financial situation, which may in turn be a surrogate marker of such things as diet and exposure to infection. There are no published data on the impact of socioeconomic status associated with the presence of BE. The data for AC are summarized in Table 3. Some studies showed an increased risk in higher socioeconomic groups,29Gammon M. Schoenberg J. Ahsan H. Tobacco, alcohol and socioeconomic status and adenocarcinoma of the esophagus and gastric cardia.J Natl Cancer Inst. 1997; 89: 1277-1284Crossref PubMed Scopus (522) Google Scholar whereas others showed the reverse.31Brown L.M. Silverman D.T. Pottern L.M. et al.Adenocarcinoma of the esophagus and esophagogastric junction in white men in the United States alcohol, tobacco, and socioeconomic factors.Cancer Causes Control. 1994; 5: 333-340Crossref PubMed Scopus (180) Google Scholar In a case-control study examining the relationship between occupation and esophageal and gastric cardia cancer there seemed to be a small increased risk in persons employed in administrative support, finance, insurance, real estate, and health services (OR, 1.5–2.2).32Engel L.S. Vaughan T.L. Gammon M.D. et al.Occupation and risk of esophageal and gastric cardia adenocarcinoma.Am J Ind Med. 2002; 42: 11-22Crossref PubMed Scopus (35) Google Scholar However, some of these findings may be owing to chance in view of the multiple comparisons made in this study. Further studies are required to clarify the issue of occupation and socioeconomic status and cancer risk.Table 3Summary of Studies Examining the Relationship Between Socioeconomic (SE) Status and Risk for Esophageal AdenocarcinomaStudyORGammon et al,29Gammon M. Schoenberg J. Ahsan H. Tobacco, alcohol and socioeconomic status and adenocarcinoma of the esophagus and gastric cardia.J Natl Cancer Inst. 1997; 89: 1277-1284Crossref PubMed Scopus (522) Google Scholar 1997OR decreased from 1 to .5 for lowest SE groupsOR decreased from 1.3 to .7 for lowest educational groupsBrown et al,31Brown L.M. Silverman D.T. Pottern L.M. et al.Adenocarcinoma of the esophagus and esophagogastric junction in white men in the United States alcohol, tobacco, and socioeconomic factors.Cancer Causes Control. 1994; 5: 333-340Crossref PubMed Scopus (180) Google Scholar 1994OR = 3.4 highest risk in the lowest SE groupBrewster et al,82Brewster D.H. Fraser L.A. McKinney P.A. et al.Socioeconomic status and risk of adenocarcinoma of the oesophagus and cancer of the gastric cardia in Scotland.Br J Cancer. 2000; 83: 387-390Crossref PubMed Scopus (50) Google Scholar 2000No association Open table in a new tab Reflux symptomsIt is well accepted that GERD is an important part of the pathogenesis of BE as evidenced by human pH level, bilitec and motility studies,33Fitzgerald R. Traidafilopoulos G. Review article Barrett's oesophagus, dysplasia and pharmacologic acid suppression.Aliment Pharmacol Ther. 2001; 15: 269-276Crossref PubMed Scopus (51) Google Scholar, 34Sampliner R. Gastroenterology. atPPCotACo. Practice guidelines on the diagnosis, surveillance, and therapy of Barrett's esophagus.Am J Gastroenterol. 1998; 93: 1028-1032Crossref PubMed Scopus (633) Google Scholar, 35Stein H. Kauer W. Feussner H. et al.Bile reflux in benign and malignant Barrett's oesophagus effect of medical acid suppression and Nissen fundoplication.J Gastrointest Surg. 1998; 24: 333-341Crossref Google Scholar, 36Vaezi M. Richter J. Role of acid and duodenogastroesophageal reflux in gastro-oesophageal reflux disease.Gastroenterology. 1996; 111: 1192Abstract Full Text Full Text PDF PubMed Scopus (491) Google Scholar laboratory model systems,37Souza R. Shewmake K. Terada L. et al.Acid induces mitogen-activated protein kinase activation and decreases apoptosis in human esophageal adenocarcinoma cells.Gastroenterology. 2001; 120: A3588Google Scholar, 38Fitzgerald R.C. Omary M.B. Triadafilopoulos G. Dynamic effects of acid on Barrett's esophag
Referência(s)