The Rationale for Esophagectomy as the Optimal Therapy for Barrett's Esophagus with High-Grade Dysplasia

Edwards, Michael J.; Gable, Dennis; Lentsch, Alex B.; Richardson, J. David

doi:10.1097/00000658-199605000-00014

Cited by 173 publications

(80 citation statements)

References 24 publications

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“…The patients who were recognized to have cancer after only a brief interval presumably had cancer present initially. Recently, the experience of prospective follow-up of high grade dysplasia has been greatly expanded, with 23 of 100 patients progressing from high grade dysplasia to cancer over 1-9 yr of follow-up (48,49).…”

Section: Ajg -July 1998mentioning

confidence: 99%

Practice guidelines on the diagnosis, surveillance, and therapy of Barrett's esophagus

Sampliner

1998

The American Journal of Gastroenterology

105

110

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Section: Ajg -July 1998mentioning

confidence: 99%

Practice guidelines on the diagnosis, surveillance, and therapy of Barrett's esophagus

Sampliner

1998

The American Journal of Gastroenterology

105

110

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“…5,7,8,[13][14][15][16][17][18][19] Esophagectomy is a very invasive intervention associated with a 1.8%-10% mortality rate. 5,7,8,[13][14][15][16][17][18][19][20] In this study, we aimed to compare the overall survival of a cohort of patients treated with photodynamic therapy (PDT) with a cohort treated with esophagectomy to define long-term outcomes, including risks and causes of death as well as rates of occurrence of esophageal cancer.…”

mentioning

confidence: 99%

Long-Term Survival Following Endoscopic and Surgical Treatment of High-Grade Dysplasia in Barrett’s Esophagus

et al. 2007

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Background & Aims-Photodynamic therapy (PDT) for high-grade dysplasia (HGD) in Barrett's esophagus is a Food and Drug Administration-approved alternative to esophagectomy. Critical information regarding overall survival of patients followed up long-term after these therapies is lacking. Our aim was to compare the long-term survival of patients treated with PDT with patients treated with esophagectomy.

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“…High-grade dysplasia is often regarded as an indication for oesophagectomy (Clark et al, 1996;Edwards et al, 1996;Cameron and Carpenter, 1997). A possible alternative, which is less mutilating and also applicable in patients with a high surgical risk, is 5-aminolaevulinic acid-induced photodynamic therapy (ALA-PDT).…”

mentioning

confidence: 99%

Porphyrin biosynthesis in human Barrett's oesophagus and adenocarcinoma after ingestion of 5-aminolaevulinic acid

et al. 2000

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Barrett's oesophagus (BE) is a pre-malignant condition in which progression from metaplasia to low-grade dysplasia and highgrade dysplasia could lead to invasive adenocarcinoma of the oesophagus (AC) (Hameeteman et al, 1989;van der Burgh et al, 1996;Drewitz et al, 1997). High-grade dysplasia is often regarded as an indication for oesophagectomy (Clark et al, 1996;Edwards et al, 1996;Cameron and Carpenter, 1997). A possible alternative, which is less mutilating and also applicable in patients with a high surgical risk, is 5-aminolaevulinic acid-induced photodynamic therapy (ALA-PDT).Two relevant clinical studies have been performed, in which patients with high-grade dysplasia or early cancer in BE received an oral dose of ALA (60 mg kg -1 ), followed by photoactivation 4-6 h later (Barr et al, 1996;Gossner et al, 1998). Both high-grade dysplasia and early cancer were eradicated allowing regeneration of squamous epithelium without scarring or stricture formation. However, the presence of islands of columnar cells remaining beneath regenerating squamous epithelium created the concern that superficial healing could mask underlying dysplasia. These results suggest that ALA-PDT needs to be improved.Haem biosynthesis, an essential process in every cell, is the basis of ALA-PDT ( Figure 1). ALA is the first intermediate, and two molecules of ALA are converted to porphobilinogen (PBG) which is metabolized to porphyrinogen intermediates by porphobilinogen deaminase (PBG-D). The last step of haem biosynthesis is the insertion of iron into PPIX by ferrochelatase (FC). Normally, haem synthesis is regulated by feedback inhibition of the enzyme ALA synthase. Exogenous ALA bypasses this feedback inhibition and the activities of PBG-D and FC and the intracellular iron pool become rate-limiting factors. As a result porphyrins, predominantly PPIX, will accumulate (Bishop and Desnick, 1982;Kennedy and Pottier, 1992). Previously, we observed an imbalance between the activities of PBG-D and FC in BE and AC (Hinnen et al, 1998). The ratio between PBG-D and FC activities, normalized for squamous epithelium, was found to be significantly higher in BE and AC. In that study, we suggested that this ratio, which we have called the PDT power index, might be a useful parameter for predicting the accumulation of PPIX in tissues after the administration of ALA.In this study, we examined the relation between the PDT power index and the intracellular concentration of PPIX in tissues of patients with BE and AC at approximately 6 h after ALA ingestion (60 mg kg -1 ) as this is the clinically most frequently used time interval. We determined the intracellular concentrations of ALA and other haem intermediates by biochemical extraction methods rather than fluorescence microscopy as used by others (Regula et al, 1995;Barr et al, 1996). In addition, plasma pharmacokinetics of ALA and porphyrins were studied and side-effects were monitored. MATERIALS AND METHODS PatientsIn total 10 patients (two women and eight men; age 44-81 years; mean 65 years) gave ...

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The Rationale for Esophagectomy as the Optimal Therapy for Barrett's Esophagus with High-Grade Dysplasia

Cited by 173 publications

References 24 publications

Practice guidelines on the diagnosis, surveillance, and therapy of Barrett's esophagus

Practice guidelines on the diagnosis, surveillance, and therapy of Barrett's esophagus

Long-Term Survival Following Endoscopic and Surgical Treatment of High-Grade Dysplasia in Barrett’s Esophagus

Porphyrin biosynthesis in human Barrett's oesophagus and adenocarcinoma after ingestion of 5-aminolaevulinic acid

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