Endoscopy 2009; 41(12): 1102-1103
DOI: 10.1055/s-0029-1215348
Letters to the editor

© Georg Thieme Verlag KG Stuttgart · New York

Reply to Abe et al.

S.  Coda, I.  Oda, T.  Gotoda
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Publication History

Publication Date:
04 December 2009 (online)

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We thank Dr. S. Abe and colleagues for their interest in our study and greatly appreciate their comments.

The first aim of our study was to assess the risk factors for cardiac and pyloric stenosis after endoscopic submucosal dissection (ESD) for early gastric cancer (EGC), but early in our experience we realized that in these cases, especially for pyloric resections, the development of a suitable treatment also deserved investigation.

We were naturally aware of the patients’ clinical status during the treatment, and our main concern was always whether resection should be avoided for mucosal defects of more than 3/4 circumferential extent or more than 5 cm longitudinal extent and the patient instead referred to surgery (especially distal gastrectomy), or, conversely, whether resection could be considered acceptable.

However, in our study there were no complications following any of the balloon dilations and the overall outcome was excellent despite the severity of stenosis, though admittedly the relevant number of patients was limited.

In planning the treatment of lesions at high risk of post-ESD stenosis, it is important to focus on how to prevent the development of stenosis in the first place. In this regard, we wonder whether endoscopy might not still play a decisive role. In the absence of comparison studies, and although we have not conducted a prospective study, our impression is that the overall outcome would be improved by carrying out a prophylactic dilation before ESD or by placing a biodegradable stent immediately after.

Concerning the efficacy and safety of endoscopic balloon dilation, if we assumed the post-ESD pyloric stenosis to be sustained by a physiopathologic mechanism in some way similar to peptic ulcer-induced outlet obstruction, then many papers might be invoked in favor of endoscopic treatment rather than surgery [1] [2] [3] [4] [5].

Unfortunately, there are still few reports regarding the outcome of balloon dilation in strictures caused by ESD of gastric neoplasms. In the series described by Dr. S. Abe and colleagues, post-ESD stenosis occurred in five of 185 pyloric resections, and there was one case of perforation during the first balloon dilation.

Tsunada et al. reported a high incidence of perforation (50 %) induced by endoscopic balloon dilation in four cases of stricture caused by circumferential resection of the gastric antrum by ESD. For treatment using the balloon procedure, they recommended starting dilation in the early stage of the healing process after ESD [6]. By contrast, a study from Germany on a series of 71 cases reported two post-ESD pyloric stenoses, which were successfully treated with endoscopy [7].

Various combinations of factors may have been involved in the development of stenosis and the abovementioned complications. We cannot elaborate these in further detail here. It is, however, interesting to note that pyloric stenosis was decisively resolved with frequent balloon dilations in the majority of cases.

We agree that balloon dilation is not always a safe treatment, but no treatment is risk-free. Although we recognise there is a risk of perforation during balloon dilation, it is significantly less than 100 %, and there remains the possibility of coping with a perforation by means of an emergency operation.

We therefore think that endoscopic balloon dilation can be regarded as a first-choice treatment option, in place of laparoscopic distal gastrectomy with lymph node dissection, for early gastric cancers with a high risk of post-ESD pyloric stenosis.

We understand that the frequency of procedures needed means that patients’ quality of life is not good during such periods. However, patients can preserve all gastric function and their quality of life is completely restored after resolution of pyloric stenosis. In addition, we believe that the quality of life following the resolution of residual stenosis is much better than that of patients who have undergone laparoscopic distal gastrectomy. Surgery is not only associated with significant postoperative morbidity but also with long-term sequelae, such as anemia and malabsorption, dumping syndrome, and weight loss [8] [9].

More surprisingly, a significant proportion of patients have been reported to remain symptomatic even after surgery [10] [11].

Moreover, one should consider that, from the patient’s perspective, the judgment of which is the best treatment available is strictly connected to their quality of life in the long term.

With reference to the patient in our series with pyloric post-ESD stenosis, who underwent an additional gastrectomy with lymph node dissection following endoscopic balloon dilation, surgery was mandatory because the resected specimen was subsequently shown to have deep submucosal invasion (sm2) with the possible risk of lymph node metastasis. If histology had not revealed this, gastrectomy would have been unnecessary. In terms of less invasive treatment and the potential risk of lymph node metastasis, i. e. to avoid unnecessary surgery, Abe N. et al. introduced a combination of ESD with laparoscopic lymph node dissection after ESD, to enable the complete resection of the primary tumor and the histologic assessment of lymph node status [12].

In conclusion, we agree that ESD of EGC for those at high risk for pyloric stenosis requires precise resection planning, possibly involving prophylactic and/or immediate follow-up endoscopic balloon dilation. Laparoscopic distal gastrectomy, including lymph node dissection, should be reserved for endoscopic treatment failures or complications.

Competing interests: None

References

S. CodaMD 

Department of Histopathology, Gastroenterology and Photonics
Division of Investigative Science, Hammersmith Hospital
Faculty of Medicine, Imperial College London
Room 729, Blackett Laboratory, South Kensington Campus

Prince Consort Road
London SW7 2AZ, UK

Fax: +44-20-75947714

Email: s.coda@imperial.ac.uk