Treatment of Barrett's Esophagus by Endoscopic Laser Ablation and Antireflux Surgery

Salo, Jarmo A.; Salminen, Jukka; Kiviluoto, Tuula; Nemlander, Arto; Rämö, O. J.; Färkkilä, Martti; Kivilaakso, Eero; Mattila, S

doi:10.1097/00000658-199801000-00006

Cited by 115 publications

(53 citation statements)

References 38 publications

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“…The controversies surrounding the endoscopic, anatomic, and histologic definitions of short segment Barrett's esophagus versus a normal cardia with goblet cell metaplasia may disappear as additional follow-up studies are performed (35). The six patients with persistent CIM in this study have been placed in Barrett's esophagus type endoscopic surveillance programs (36). The true incidence of persistent or "reappearing" CIM is unknown given the uncontrolled nature (see below), and the short follow-up period of this study.…”

Section: Discussionmentioning

confidence: 98%

Gastric Cardia Intestinal Metaplasia: Biopsy Follow-Up of 85 Patients

Goldstein

2000

Modern Pathology

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Background: Gastric cardia intestinal metaplasia (CIM), denoted by goblet cells is common. The frequency of persistent CIM is unknown. Methods: 85 patients with CIM and follow-up endoscopies were prospectively identified during the time period of 10/6/94 -12/21/97. The presence of goblet cells was the defining feature of CIM, other metaplastic cell types were not evaluated. All 85 patients initially had biopsies that straddled the squamocolumnar junction (SCJ) showed CIM, an otherwise normal proximal stomach, lower esophagus, and squamocolumnar junction. The SCJ lay within the 2 cm of mucosa immediately proximal to the uppermost gastric fold and overlaid the junction of the tubular esophagus and the saccular dilatation of the stomach in all patients. The patients underwent endoscopy for many reasons. They were randomly identified based on the absence of a hiatal hernia and the presence of CIM. Results: Ten of the 85 patients had CIM on repeat biopsy. Among patients with no CIM in the first repeat endoscopy, the degree of cardia inflammation decreased between the initial and first repeat endoscopy, whereas there was no change in the amount of inflammation among patients who had CIM in the first repeat endoscopy. The changes in mean inflammation score was significantly different between the two groups (P ‫؍‬ .024). Twenty-two patients underwent a second repeat endoscopy and five had a third repeat endoscopy. Including all follow-up biopsies, six of the 85 patients (7%) had CIM. Four patients who did not have CIM on initial repeat endoscopy had CIM on their second repeat endoscopy, probably reflecting sampling issues. None of the biopsies had dysplasia. Conclusions: Cardia inflammation is a stimulus for cardia intestinal metaplasia, and a reduction in in-

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Section: Discussionmentioning

confidence: 98%

Gastric Cardia Intestinal Metaplasia: Biopsy Follow-Up of 85 Patients

Goldstein

2000

Modern Pathology

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“…Successful Similar data exist for other types of lasers including the argon laser and Nd:YAG laser [28][29][30][31]. For example, response was defined as residual CLE of =2 cm.…”

Section: Esophagectomymentioning

confidence: 90%

Therapeutic Options in Patients with Barrett’s Esophagus

Lim¹,

Waring²,

Saidi³

1999

Dig Dis

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The rising incidence of esophageal adenocarcinoma has focused attention on the only known risk factor: Barrett’s esophagus. Practice guidelines for the diagnosis, surveillance and management of Barrett’s esophagus were published recently. Although the ultimate goal in the management of this premalignant condition would be the permanent elimination of Barrett’s mucosa, current therapeutic options are limited or still in the investigational stages. This review summarizes current medical and surgical treatment options and introduces endoscopic ablative modalities currently under investigation.

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“…Legt man die spärlichen Informationen aus den Publikationen hierzu zugrunde, ist nach gegenwärtigen Erkenntnissen davon auszugehen, dass mindestens 5-10 Jahre eine pathologische Exposition der Speiseröhre mit entsprechend toxischem Refluat bestehen muss, bevor sich eine intestinale Metaplasie in der distalen Speiseröhre herausbildet [11]. Denkbare Gründe für eine Progression der intestinalen Metaplasie zur Entwicklung einer intraepithelialen Neoplasie und schließlich zum Karzinom könnten die aus dem Duodenum stammenden Refluatanteile wie Gallen-und Pankreassaftkomponenten sein, die beim duodenogastroösophagealen Reflux mit Säure vermischt in die Speiseröhre gelangen [14,16] [18] 1980 Nissen/Hill 4/10 Ransom et al [19] 1982 Nissen 4/6 Sprung et al [20] 1984 Fundoplicatio 4/15 Pollara et al [21] 1987 partielle Fundoplicatio Roux-Y 2/22 Wellinger et al [22] 1988 Antirefluxoperation 0/39 Ovaska et al [23] 1989 Nissen 3/10 Ollyo et al [24] 1990 Nissen 1/40 Williamson et al [25] 1990 Antirefluxoperation 4/37 DeMeester et al [26] 1990 Nissen 0/35 Attwood et al [27] 1992 Nissen 2/19 Pateron et al [28] 1992 transversale Antrektomie 7/31 Sagar et al [29] 1995 Nissen/Lind/Belsey 24/56 Ortiz et al [30] 1996 Nissen 8/32 Hölscher et al [31] 1997 Nissen 3/48 Salo et al [32] 1998 Antirefluxoperation + Lasertherapie 10/10 Tigges et al [33] 2001 EAPC + Nissen 20 /22 gewiesen wird [34][35][36][37][38]. Andere Untersuchungen können diesen Trend nicht bestätigen [6].…”

Section: Besondere Aspekte Beim Nicht Dysplastischen Barrett-ösophagusunclassified

Chirurgische Konzepte zu Prävention und Therapie von Präkanzerosen und Frühkarzinomen des Ösophagus

Fuchs¹,

Maroske²,

Tigges³

et al. 2002

Visc Med

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Surgical Concepts for Prevention and Therapy of Precanceroses and Early Carcinomas of the Esophagus Recently, precancerosis and early stage carcinoma of the esophagus and the cardia gained popularity. It is not only the epidemiology and diagnostic procedures which have changed, but also the therapeutic options and concepts. Meanwhile it is known that 5–10 years of pathologic exposition to toxic reflux are necessary to cause intestinal metaplasia. Basic thoughts for the development from intestinal metaplasia to carcinoma might be gall – and pancreatic juice refluxing into the esophagus. Gold treatment standard for the non-dysplastic Barrett’s esophagus is either medical by proton pump inhibitors or surgical by antireflux surgery. None of the named therapeutic concepts can prevent development from metaplasia into malignancy definitely. In the treatment of intraepithelial neoplasia, various alternatives, from modern endoscopic mucosa resection up to the radical subtotal esophageal resection followed by lymphadenectomy, are well described.

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Treatment of Barrett's Esophagus by Endoscopic Laser Ablation and Antireflux Surgery

Abstract: ObjectiveThe regeneration of intestinal metaplasia by squamous epithelium in 17 patients with Barrett's esophagus after endoscopic laser ablation in a reflux-free environment after successful antireflux surgery was prospectively examined.

Cited by 115 publications

References 38 publications

Gastric Cardia Intestinal Metaplasia: Biopsy Follow-Up of 85 Patients

Gastric Cardia Intestinal Metaplasia: Biopsy Follow-Up of 85 Patients

Therapeutic Options in Patients with Barrett’s Esophagus

Chirurgische Konzepte zu Prävention und Therapie von Präkanzerosen und Frühkarzinomen des Ösophagus

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