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Adenocarcinoma in Barrett’s Esophagus
To the Editor: In their population-based cohort study, Hvid-Jensen et al. (Oct. 13 issue)1 report an annual risk of esophageal adenocarcinoma of 0.12% among patients with Barrett’s esophagus. This annual risk increased to 0.26% when high-grade dysplasia was taken into account. Since these rates are about three times lower than the annual incidence rates usually reported,2 we question the current surveillance guidelines for patients with Barrett’s esophagus, which rely on these epidemiologic data.
Moreover, several studies have reported a re-lationship between the length of the segment of Barrett’s esophagus and adenocarcinoma risk.2-4 Weston et al. reported that the prevalence of dysplasia or adenocarcinoma and the incidence of dysplasia in patients with traditional Barrett’s esophagus are significantly higher than in pa-tients with a segment of Barrett’s esophagus that is shorter than 3 cm.5 For instance, a pre-diction of progression to esophageal adenocarci-noma has been reported to be 1.53 times as high in patients with a segment of Barrett’s esopha-gus that is 3 cm or longer as in patients with a segment of Barrett’s esophagus that is shorter than 3 cm (odds ratio, 1.53; 95% confidence interval, 1.34 to 1.74).4 Thus, we would appreci-ate knowing whether, in the cohort in the study by Hvid-Jensen et al., the incidence rate of cancer among patients with a segment of Barrett’s esophagus that is long (≥3 cm) was higher, war-ranting endoscopic surveillance.
Maximilien Barret, M.D. Stanislas Chaussade, M.D., Ph.D. Romain Coriat, M.D. Université Paris Descartes Paris, France
No potential conflict of interest relevant to this letter was re-ported.
1. Hvid-Jensen F, Pedersen L, Drewes AM, Sorensen HT, Funch-Jensen P. Incidence of adenocarcinoma among patients with Barrett’s esophagus. N Engl J Med 2011;365:1375-83.2. Yousef F, Cardwell C, Cantwell MM, Galway K, Johnston BT, Murray L. The incidence of esophageal cancer and high-grade dysplasia in Barrett’s esophagus: a systematic review and meta-analysis. Am J Epidemiol 2008;168:237-49.3. Gatenby PA, Caygill CP, Ramus JR, Charlett A, Fitzgerald RC, Watson A. Short segment columnar-lined oesophagus: an un-derestimated cancer risk? A large cohort study of the relation-ship between Barrett’s columnar-lined oesophagus segment length and adenocarcinoma risk. Eur J Gastroenterol Hepatol 2007;19:969-75.4. Weston AP, Sharma P, Mathur S, et al. Risk stratification of Barrett’s esophagus: updated prospective multivariate analysis. Am J Gastroenterol 2004;99:1657-66.5. Weston AP, Krmpotich PT, Cherian R, Dixon A, Topalosvki M. Prospective long-term endoscopic and histological follow-up of short segment Barrett’s esophagus: comparison with tradi-tional long segment Barrett’s esophagus. Am J Gastroenterol 1997;92:407-13.
The Authors Reply: Barret et al. address an important issue. Looking at the risk among subgroups in the population with Barrett’s esophagus (thereby identifying patients with a need for special surveillance) is an important part of future research. The presence of dyspla-sia, as shown in our study, and the influence of the length of Barrett’s segments in estimating the risk of adenocarcinoma of the esophagus are im-portant factors.
However, we are not able to shed light on the risk related to the length of segments of Bar-rett’s esophagus, since a reliable classification system that includes the length of the segment
this week’s letters2539 AdenocarcinomainBarrett’sEsophagus
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of Barrett’s esophagus was not implemented in Danish practice during the first part of our study. Furthermore, the C and M classification (based on the circumference and maximum ex-tent of a lesion) is not registered in our nation-wide database, and this information would need to be extracted from every single patient’s endo-scopic description.
We do agree that the question raised, as well
as other possible subclassifications (such as bio-markers), are of importance in future studies.
Frederik Hvid-Jensen, M.D. Peter Funch-Jensen, M.D., Dr.Med.Sci.Aarhus University Hospital Aarhus, Denmark [email protected]
Since publication of their article, the authors report no fur-ther potential conflict of interest.
Change in FEV1 over Time in COPD
To the Editor: Vestbo and colleagues (Sept. 29 issue)1 reported on the variability in the rate of the decline in forced expiratory volume in 1 second (FEV1) in patients with chronic obstructive pul-monary disease (COPD) from the cohort in the Evaluation of COPD Longitudinally to Identify Predictive Surrogate Endpoints study (ECLIPSE) (ClinicalTrials.gov number, NCT00292552) and stress the importance of smoking cessation to attenuate this decline. Although large drug trials have provided evidence for some attenuation of lung-function decline,2,3 we do not agree with the authors’ interpretation that intensive phar-macologic treatment resulted in the rather mild decline seen in the ECLIPSE cohort. Although the mild — or even reversed — decline could be due to regression to the mean in these patients with relatively severe COPD (i.e., the mean FEV1 was 48% of predicted), we think it reflects the 64% of participants who did not smoke or did not con-tinue to smoke. Since smoking is known to be the main determinant of a decline in lung func-tion, and smoking cessation is by far the most effective intervention to prevent both the devel-opment and the progression of COPD,3-5 the dis-tribution of the rate of decline within the sub-groups of smokers and nonsmokers would be of interest.
Wouter D. van Dijk, M.D. Tjard R. Schermer, Ph.D.Radboud University Nijmegen Medical Center Nijmegen, the Netherlands [email protected]
No potential conflict of interest relevant to this letter was re-ported.
1. Vestbo J, Edwards LD, Scanlon PD, et al. Changes in forced expiratory volume in 1 second over time in COPD. N Engl J Med 2011;365:1184-92.2. Tashkin DP, Celli B, Senn S, et al. A 4-year trial of tiotropium
in chronic obstructive pulmonary disease. N Engl J Med 2008;359: 1543-54.3. Celli BR, Thomas NE, Anderson JA, et al. Effect of pharma-cotherapy on rate of decline of lung function in chronic obstruc-tive pulmonary disease: results from the TORCH study. Am J Respir Crit Care Med 2008;178:332-8.4. Anthonisen NR, Connett JE, Kiley JP, et al. Effects of smok-ing intervention and the use of an inhaled anticholinergic bron-chodilator on the rate of decline of FEV1. JAMA 1994;272:1497-505.5. Kuller LH, Ockene JK, Meilahn E, Wentworth DN, Svendsen KH, Neaton JD. Cigarette smoking and mortality. Prev Med 1991; 20:638-54.
To the Editor: Vestbo et al. found a mean de-cline in FEV1 of 33±2 ml per year in patients with COPD, which is substantially less than the 64 ml per year observed by Fletcher and Peto in 1977.1 We would like information about the effect on the decline in the ECLIPSE cohort of pulmonary rehabilitation, which is recognized as an effec-tive treatment for COPD.2 Some studies report that the decline in FEV1 in patients with COPD who undergo such rehabilitation is significantly lower than that achieved with standard drug treatment.3,4
Gian Galeazzo Riario Sforza, M.D. Cristoforo Incorvaia, M.D.Istituti Clinici di Perfezionamento Milan, Italy [email protected]
No potential conflict of interest relevant to this letter was re-ported.
1. Fletcher C, Peto R. The natural history of chronic airflow obstruction. Br Med J 1977;1:1645-8.2. Nici L, Donner C, Wouters E, et al. American Thoracic Soci-ety/European Respiratory Society statement on pulmonary reha-bilitation. Am J Respir Crit Care Med 2006;173:1390-413.3. Cote CG, Celli BR. Pulmonary rehabilitation and the BODE index in COPD. Eur Respir J 2005;26:630-6.4. Stav D, Raz M, Shpirer I. Three years of pulmonary rehabili-tation inhibit the decline in airflow obstruction, improves exer-cise endurance time, and body-mass index, in chronic obstruc-tive pulmonary disease. BMC Pulm Med 2009;9:26-30.
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