Local recurrence risk of esophageal squamous cell carcinoma due to intralesional damage during endoscopic submucosal dissection.


Journal

Journal of gastroenterology and hepatology
ISSN: 1440-1746
Titre abrégé: J Gastroenterol Hepatol
Pays: Australia
ID NLM: 8607909

Informations de publication

Date de publication:
Oct 2023
Historique:
revised: 26 06 2023
received: 19 04 2023
accepted: 10 07 2023
medline: 23 10 2023
pubmed: 31 7 2023
entrez: 31 7 2023
Statut: ppublish

Résumé

It is unclear whether additional treatment should be considered given the recurrence risk after endoscopic submucosal dissection (ESD) for esophageal squamous cell carcinoma (ESCC) when the vertical margin is positive or unclear (VM1/VMX) due to intralesional damage. This study aimed to elucidate the local recurrence risk of ESCC caused by intralesional damage during ESD. Among consecutive patients with pT1a ESCCs initially treated by ESD at our institution between January 2006 and December 2018, ESCCs diagnosed as VM1/VMX were retrospectively reviewed. Exclusion criteria were piecemeal resection and any additional treatment after ESD. Intralesional damage included the following three types: a macroscopic hole inside the lesion, an incision from the lateral margin of the specimen into the lesion, and crushing injury or burn effect into the deepest area of the lesion without an obvious hole. The local recurrence rate after ESD was primarily analyzed. Of 1174 pT1a ESCCs initially treated using ESD, 22 lesions were histopathologically diagnosed as VM1/VMX due to intralesional damage (1.9%; 95% confidence interval [CI], 1.2-2.8%). At a median follow-up period of 60.0 (interquartile range, 15.0-84.0) months, no local recurrence was observed (0.0%; 95% CI, 0.0-13.3%) among 21 lesions finally evaluated. The impact of intralesional damage during ESD for ESCC on local recurrence might be negligible. Follow-up without additional treatment may be acceptable even if intralesional damage occurs and results in VM1/VMX after ESD for pT1a ESCCs.

Sections du résumé

BACKGROUND AND AIM OBJECTIVE
It is unclear whether additional treatment should be considered given the recurrence risk after endoscopic submucosal dissection (ESD) for esophageal squamous cell carcinoma (ESCC) when the vertical margin is positive or unclear (VM1/VMX) due to intralesional damage. This study aimed to elucidate the local recurrence risk of ESCC caused by intralesional damage during ESD.
METHODS METHODS
Among consecutive patients with pT1a ESCCs initially treated by ESD at our institution between January 2006 and December 2018, ESCCs diagnosed as VM1/VMX were retrospectively reviewed. Exclusion criteria were piecemeal resection and any additional treatment after ESD. Intralesional damage included the following three types: a macroscopic hole inside the lesion, an incision from the lateral margin of the specimen into the lesion, and crushing injury or burn effect into the deepest area of the lesion without an obvious hole. The local recurrence rate after ESD was primarily analyzed.
RESULTS RESULTS
Of 1174 pT1a ESCCs initially treated using ESD, 22 lesions were histopathologically diagnosed as VM1/VMX due to intralesional damage (1.9%; 95% confidence interval [CI], 1.2-2.8%). At a median follow-up period of 60.0 (interquartile range, 15.0-84.0) months, no local recurrence was observed (0.0%; 95% CI, 0.0-13.3%) among 21 lesions finally evaluated.
CONCLUSIONS CONCLUSIONS
The impact of intralesional damage during ESD for ESCC on local recurrence might be negligible. Follow-up without additional treatment may be acceptable even if intralesional damage occurs and results in VM1/VMX after ESD for pT1a ESCCs.

Identifiants

pubmed: 37519057
doi: 10.1111/jgh.16307
doi:

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

1802-1807

Informations de copyright

© 2023 Journal of Gastroenterology and Hepatology Foundation and John Wiley & Sons Australia, Ltd.

Références

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Auteurs

Tatsunori Minamide (T)

Division of Endoscopy, Shizuoka Cancer Center, Shizuoka, Japan.

Noboru Kawata (N)

Division of Endoscopy, Shizuoka Cancer Center, Shizuoka, Japan.

Yuki Maeda (Y)

Division of Endoscopy, Shizuoka Cancer Center, Shizuoka, Japan.

Masao Yoshida (M)

Division of Endoscopy, Shizuoka Cancer Center, Shizuoka, Japan.

Yoichi Yamamoto (Y)

Division of Endoscopy, Shizuoka Cancer Center, Shizuoka, Japan.

Hiroshi Ashizawa (H)

Division of Endoscopy, Shizuoka Cancer Center, Shizuoka, Japan.

Kazunori Takada (K)

Division of Endoscopy, Shizuoka Cancer Center, Shizuoka, Japan.

Yoshihiro Kishida (Y)

Division of Endoscopy, Shizuoka Cancer Center, Shizuoka, Japan.

Sayo Ito (S)

Division of Endoscopy, Shizuoka Cancer Center, Shizuoka, Japan.

Kenichiro Imai (K)

Division of Endoscopy, Shizuoka Cancer Center, Shizuoka, Japan.

Kinichi Hotta (K)

Division of Endoscopy, Shizuoka Cancer Center, Shizuoka, Japan.

Junya Sato (J)

Division of Endoscopy, Shizuoka Cancer Center, Shizuoka, Japan.

Hirotoshi Ishiwatari (H)

Division of Endoscopy, Shizuoka Cancer Center, Shizuoka, Japan.

Hiroyuki Matsubayashi (H)

Division of Endoscopy, Shizuoka Cancer Center, Shizuoka, Japan.

Takashi Sugino (T)

Division of Pathology, Shizuoka Cancer Center, Shizuoka, Japan.

Hiroyuki Ono (H)

Division of Endoscopy, Shizuoka Cancer Center, Shizuoka, Japan.

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