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Barrett's Esophagus: Emerging Knowledge and Management Strategies.

Bhardwaj A, McGarrity TJ, Stairs DB, Mani H - Patholog Res Int (2012)

Bottom Line: Patients with BE have a greater than 40 folds higher risk of EAC compared with the general population.There is paucity of prospective data showing a survival benefit of screening or surveillance for BE.There is a need for identification of reliable clinical predictors or molecular biomarkers to risk-stratify patients who might benefit the most from screening or surveillance for BE.

View Article: PubMed Central - PubMed

Affiliation: Division of Gastroenterology and Hepatology, Penn State Milton S. Hershey Medical Center, 500 University Drive, P.O. Box 850, HU33, Hershey, PA 17033, USA.

ABSTRACT
The incidence of esophageal adenocarcinoma (EAC) has increased exponentially in the last 3 decades. Barrett's esophagus (BE) is the only known precursor of EAC. Patients with BE have a greater than 40 folds higher risk of EAC compared with the general population. Recent years have witnessed a revolution in the clinical and molecular research related to BE. However, several aspects of this condition remain controversial. Data regarding the true prevalence of BE have varied widely. Recent studies have suggested a lower incidence of EAC in nondysplastic BE (NDBE) than previously reported. There is paucity of prospective data showing a survival benefit of screening or surveillance for BE. Furthermore, the ever-increasing emphasis on healthcare cost containment has called for reexamination of the screening and surveillance strategies for BE. There is a need for identification of reliable clinical predictors or molecular biomarkers to risk-stratify patients who might benefit the most from screening or surveillance for BE. Finally, new therapies have emerged for the management of dysplastic BE. In this paper, we highlight the key areas of controversy and uncertainty surrounding BE. The paper discusses, in detail, the current literature about the molecular pathogenesis, biomarkers, histopathological diagnosis, and management strategies for BE.

No MeSH data available.


Related in: MedlinePlus

(a) Intestinal metaplasia is defined by the presence of goblet cells distended with mucin. In this photomicrograph there is no dysplasia, as evidenced by presence of surface maturation. Surface epithelial cells show uniform mucin caps and well-polarized nuclei. (b) Low-grade dysplasia of the intestinal type is characterized by hyperchromatic elongate nuclei that are seen in both the crypts and the surface epithelium (i.e., loss of surface maturation). (c) Presence of glandular crowding, nuclear stratification, and loss of nuclear polarity signifies high-grade dysplasia. (d) Glandular complexity, budding, and presence of incomplete glandular profiles are evidence of lamina propria invasion (intramucosal carcinoma).
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fig2: (a) Intestinal metaplasia is defined by the presence of goblet cells distended with mucin. In this photomicrograph there is no dysplasia, as evidenced by presence of surface maturation. Surface epithelial cells show uniform mucin caps and well-polarized nuclei. (b) Low-grade dysplasia of the intestinal type is characterized by hyperchromatic elongate nuclei that are seen in both the crypts and the surface epithelium (i.e., loss of surface maturation). (c) Presence of glandular crowding, nuclear stratification, and loss of nuclear polarity signifies high-grade dysplasia. (d) Glandular complexity, budding, and presence of incomplete glandular profiles are evidence of lamina propria invasion (intramucosal carcinoma).

Mentions: All biopsies for BE diagnosis and surveillance should include a qualifier regarding presence or absence of dysplasia. Dysplasia is assessed in columnar mucosa, preferably away from squamous mucosa, and where the surface lining is intact. Biopsies are categorized as being “negative for dysplasia” if the cells show maturation towards the surface in the form of decreasing nuclear size, decreasing nuclear hyperchromasia, increasing cytoplasmic volume and a mucus cap on surface cells (Figure 2(a)). In some cases, there may be some changes that are deemed insufficient to characterize as dysplasia, and these are categorized as “indefinite for dysplasia”. Cases that are classified as being indefinite for dysplasia are either those with minimal to mild cytologic atypia or those that have more than mild cytologic atypia but are accompanied by significant inflammation, raising a possibility of atypia reactive to the inflammatory response. These cases need rebiopsy after control of inflammation. Reactive changes tend to be more diffuse rather than abrupt, the latter being a feature of dysplasia. The category of “indefinite” should not be used to downgrade dysplasia, but rather to identify cases that may need followup biopsies.


Barrett's Esophagus: Emerging Knowledge and Management Strategies.

Bhardwaj A, McGarrity TJ, Stairs DB, Mani H - Patholog Res Int (2012)

(a) Intestinal metaplasia is defined by the presence of goblet cells distended with mucin. In this photomicrograph there is no dysplasia, as evidenced by presence of surface maturation. Surface epithelial cells show uniform mucin caps and well-polarized nuclei. (b) Low-grade dysplasia of the intestinal type is characterized by hyperchromatic elongate nuclei that are seen in both the crypts and the surface epithelium (i.e., loss of surface maturation). (c) Presence of glandular crowding, nuclear stratification, and loss of nuclear polarity signifies high-grade dysplasia. (d) Glandular complexity, budding, and presence of incomplete glandular profiles are evidence of lamina propria invasion (intramucosal carcinoma).
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC3369502&req=5

fig2: (a) Intestinal metaplasia is defined by the presence of goblet cells distended with mucin. In this photomicrograph there is no dysplasia, as evidenced by presence of surface maturation. Surface epithelial cells show uniform mucin caps and well-polarized nuclei. (b) Low-grade dysplasia of the intestinal type is characterized by hyperchromatic elongate nuclei that are seen in both the crypts and the surface epithelium (i.e., loss of surface maturation). (c) Presence of glandular crowding, nuclear stratification, and loss of nuclear polarity signifies high-grade dysplasia. (d) Glandular complexity, budding, and presence of incomplete glandular profiles are evidence of lamina propria invasion (intramucosal carcinoma).
Mentions: All biopsies for BE diagnosis and surveillance should include a qualifier regarding presence or absence of dysplasia. Dysplasia is assessed in columnar mucosa, preferably away from squamous mucosa, and where the surface lining is intact. Biopsies are categorized as being “negative for dysplasia” if the cells show maturation towards the surface in the form of decreasing nuclear size, decreasing nuclear hyperchromasia, increasing cytoplasmic volume and a mucus cap on surface cells (Figure 2(a)). In some cases, there may be some changes that are deemed insufficient to characterize as dysplasia, and these are categorized as “indefinite for dysplasia”. Cases that are classified as being indefinite for dysplasia are either those with minimal to mild cytologic atypia or those that have more than mild cytologic atypia but are accompanied by significant inflammation, raising a possibility of atypia reactive to the inflammatory response. These cases need rebiopsy after control of inflammation. Reactive changes tend to be more diffuse rather than abrupt, the latter being a feature of dysplasia. The category of “indefinite” should not be used to downgrade dysplasia, but rather to identify cases that may need followup biopsies.

Bottom Line: Patients with BE have a greater than 40 folds higher risk of EAC compared with the general population.There is paucity of prospective data showing a survival benefit of screening or surveillance for BE.There is a need for identification of reliable clinical predictors or molecular biomarkers to risk-stratify patients who might benefit the most from screening or surveillance for BE.

View Article: PubMed Central - PubMed

Affiliation: Division of Gastroenterology and Hepatology, Penn State Milton S. Hershey Medical Center, 500 University Drive, P.O. Box 850, HU33, Hershey, PA 17033, USA.

ABSTRACT
The incidence of esophageal adenocarcinoma (EAC) has increased exponentially in the last 3 decades. Barrett's esophagus (BE) is the only known precursor of EAC. Patients with BE have a greater than 40 folds higher risk of EAC compared with the general population. Recent years have witnessed a revolution in the clinical and molecular research related to BE. However, several aspects of this condition remain controversial. Data regarding the true prevalence of BE have varied widely. Recent studies have suggested a lower incidence of EAC in nondysplastic BE (NDBE) than previously reported. There is paucity of prospective data showing a survival benefit of screening or surveillance for BE. Furthermore, the ever-increasing emphasis on healthcare cost containment has called for reexamination of the screening and surveillance strategies for BE. There is a need for identification of reliable clinical predictors or molecular biomarkers to risk-stratify patients who might benefit the most from screening or surveillance for BE. Finally, new therapies have emerged for the management of dysplastic BE. In this paper, we highlight the key areas of controversy and uncertainty surrounding BE. The paper discusses, in detail, the current literature about the molecular pathogenesis, biomarkers, histopathological diagnosis, and management strategies for BE.

No MeSH data available.


Related in: MedlinePlus