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Barrett’s oesophagus in systemic sclerosis: author’s reply
Article first published online: 26 JAN 2007
Alimentary Pharmacology & Therapeutics
Volume 25, Issue 7, pages 858–859, April 2007
How to Cite
Marie, I. (2007), Barrett’s oesophagus in systemic sclerosis: author’s reply. Alimentary Pharmacology & Therapeutics, 25: 858–859. doi: 10.1111/j.1365-2036.2007.03264.x
- Issue published online: 26 JAN 2007
- Article first published online: 26 JAN 2007
Oesophageal involvement is still recognized to be associated with significant morbidity in patients with systemic sclerosis (SSc), leading to erosive oesophagitis, ulcerations, as well as peptic stricture formation and Barrett’s oesophagus (BE) with its potential for adenocarcinoma degeneration.1 Oesophageal mucosal abnormalities are favoured by both low-pressure in the lower oesophageal sphincter (LES) and abnormal motility, leading to decreased acid clearance and prolonged acid-mucosal contact time.1
In our prospective study of 133 SSc patients, who underwent systematic endoscopy, we have observed oesophagitis in 43 patients (32%) and BE in nine patients (6.8%).1 From a practical point of view, the knowledge of predictive factors of oesophagitis/BE is essential in patients with SSc, as it may result in effective management at an early stage. Interestingly, we have clearly observed that patients with severe oesophageal motor disorders on manometry (defined, according to Hurwitz’s classification2 as: both aperistalsis and decreased LES pressure) had more frequently endoscopic oesophagitis/BE when compared with those without (65% vs. 37%; P = 0.001).1 Our data indicate that these SSc patients with severe oesophageal motor disorders on manometry should undergo systematically endoscopy, to detect oesophageal mucosal involvement. In this instance, because of the small number of patients with BE (n = 9), we did not compare oesophageal manometric characteristics between SSc patients with BE and those without1. In their smaller series of SSc, Wipff et al.3 reported that 13% of patients had BE; in the same way, because of the small sample of patients with BE, a comparison of characteristics between patients with BE and those without cannot reasonably be made by these authors.
Finally, in their letter to Alimentary Pharmacology & Therapeutics, Wipff et al. claim that SSc patients at risk of BE remain a crucial challenge, in regard with the recently described high risk of oesophageal adenocarcinoma.4 In essence, in a series of 769 SSc patients, Derk et al.4 have reported recently that the standardized incidence ratio for: (i) all cancers was 1.55 [1.16–1.93]; (ii) oropharyngeal cancer was 9.63 (2.97–16.29); and (iii) oesophageal cancer was 15.9 (4.2–27.6). However, Derk et al.4 did not mention the histological characteristics of oesophageal cancer in their seven SSc patients; in turn, the readers do not know whether these seven latter SSc patients had either: (i) epidermoid oesophageal cancer; or (ii) oesophageal adenocarcinoma (related to BE or not). In our present series, no SSc patient with BE had oesophageal adenocarcinoma.1 Our data confirm those of Segel et al.’s,5 who found that none of their 680 SSc patients exhibited oesophageal adenocarcinoma related to BE.
Nevertheless, because an increased risk of adenocarcinoma has been found in non-SSc patients with BE, SSc patients with BE should also be screened similarly by endoscopy: (i) every 2–3 years if no dysplasia is found; (ii) yearly if low-grade dysplasia occurs; and (iii) every 3 months in the case of high-grade dysplasia.1