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Robert D Odze - One of the best experts on this subject based on the ideXlab platform.

  • muc2 is a highly specific marker of goblet cell metaplasia in the distal esophagus and gastroesophageal junction
    The American Journal of Surgical Pathology, 2011
    Co-Authors: Maria Mcintire, Genevieve Soucy, Thomas L Vaughan, Aliakbar Shahsafaei, Robert D Odze
    Abstract:

    Currently, the American College of Gastroenterology requires identification of goblet cells in mucosal biopsies from the esophagus to diagnose Barrett esophagus (BE). Identification of goblet cells in mucosal biopsies is fraught with limitations such as sampling and interpretation error. One previous study by our group suggested that MUC2 expression in esophageal nongoblet Columnar cells represents a late biochemical reaction in the conversion of mucinous Columnar cells to goblet cells in BE. We conducted this study to evaluate the prevalence, sensitivity, and specificity of MUC2 positivity in nongoblet Columnar Epithelium for detection of goblet cells in the distal esophagus and gastroesophageal junction (GEJ) region. We also sought to identify associations between MUC2 positivity and clinical and endoscopic risk factors for BE. This analysis utilized mucosal biopsies of the distal esophagus or GEJ from 100 patients who participated in a community clinic-based study of patients with chronic gastroesophageal reflux disease evaluated prospectively in the western part of Washington state. We randomly selected 50 patients who had Columnar Epithelium with goblet cells, representing the study group and 50 patients without goblet cells, representing the comparison group. Immunohistochemistry for MUC2 was performed on samples in a blinded manner without knowledge of the clinical or endoscopic features of the patients. The presence of staining was noted in both goblet and nongoblet Epithelium, both close to and distant from the mucosa with goblet cells, when the latter were present. All study patients showed MUC2 positivity in goblet cells. MUC2 was present in nongoblet Columnar Epithelium in 78% of study patients with goblet cells, but in only 4% of controls without goblet cells (P<0.0001) (sensitivity, 78%; specificity, 96% for goblet cell metaplasia). MUC2 was significantly more common in nongoblet Columnar cells close to, rather than distant from, the mucosa with goblet cells (P<0.00001). Finally, MUC2 was significantly associated with endoscopic evidence of Columnar metaplasia in the distal esophagus, and with known risk factors for BE, such as older age, white race, frequent heartburn, and elevated body mass index. We conclude that goblet cells likely develop from a field of MUC2-positive mucinous Columnar cells, and as such, MUC2 represents a late event in the development of goblet cells. MUC2 staining in nongoblet Columnar cells is a reasonably sensitive and highly specific marker for goblet cells in the distal esophagus and GEJ, and its presence is predictive of endoscopic Columnar metaplasia of the esophagus, even in patients without goblet cells.

  • intestinal differentiation in metaplastic nongoblet Columnar Epithelium in the esophagus
    The American Journal of Surgical Pathology, 2009
    Co-Authors: Hejin P Hahn, Stuart J Spechler, Patricia L Blount, Kamrun Ayub, Kiron M Das, Rhonda F Souza, Robert D Odze
    Abstract:

    Barrett esophagus (BE) is defined by the presence of metaplastic esophageal Columnar Epithelium with goblet cells within endoscopically recognizable areas of the esophagus. However, some carcinomas in BE, or from the gastroesophageal junction region, develop within mucosa devoid of goblet cells. However, the biologic properties, pathogenesis, and risk of malignancy of metaplastic, esophageal nongoblet Columnar Epithelium, is, essentially, unknown. In this study, 89 patients with metaplastic esophageal Columnar Epithelium were evaluated immunohistochemically for markers of intestinal differentiation, such as MUC2, DAS-1, Villin, and CDX2, a marker of gastric differentiation (MUC5AC), and Ki67, a marker of cell proliferation. Of the 89 patients, 59 had Columnar metaplasia with goblet cells (BE), which were further separated into low-density goblet cell and high-density goblet cell groups based on the percentage of crypts with goblet cells, and 30 patients had Columnar metaplasia of the esophagus without goblet cells. As controls, gastric biopsies from 19 age and sex matched patients without esophageal or gastric pathology were used. The rate of positivity of the markers and the location of Ki67 staining was evaluated only in non-goblet Columnar Epithelium from all patient groups. Patients with metaplastic esophageal Columnar Epithelium without goblet cells showed positivity for MUC5AC, MUC2, DAS-1, Villin, and CDX2 in 100%, 0%, 30%, 17%, and 43% of cases, respectively. 17% of cases showed aberrant surface Ki67 positivity. These values were significantly higher than gastric controls, which showed absence of staining for all markers except MUC5AC (100%). In patients with metaplastic esophageal Columnar Epithelium with goblet cells (BE) a significant increased rate of staining was observed for all markers, except MUC5AC. In addition, both MUC2 and surface Ki67 staining were significantly increased in BE patients with high-density goblet cells versus those with low-density goblet cells. In a separate analysis in which metaplastic esophageal nongoblet Epithelium was evaluated in areas of mucosa devoid of goblet cells compared with areas of mucosa with goblet cells, from patients who had goblet cells elsewhere in the mucosa (N=59), no significant differences were observed with regard to the percentage of cases that stained with any of the markers in the nongoblet Epithelium in areas devoid of goblet cells, similar to the patient group with metaplastic esophageal Epithelium without goblet cells (N=30). Similar to above, in all cases, expression of intestinal markers increased in areas of mucosa adjacent to goblet cells. This study provides evidence that metaplastic esophageal Columnar Epithelium without goblet cells shows phenotypic evidence of intestinal differentiation and supports the theory that squamous Epithelium converts initially to nongoblet Columnar Epithelium before goblet cell metaplasia. Further prospective studies are needed to evaluate the pathogenetic sequence, natural history, and risk of malignancy of metaplastic esophageal nongoblet Epithelium.

  • metaplastic esophageal Columnar Epithelium without goblet cells shows dna content abnormalities similar to goblet cell containing Epithelium
    The American Journal of Gastroenterology, 2009
    Co-Authors: Weitian Liu, Hejin Hahn, Robert D Odze, Raj K Goyal
    Abstract:

    Metaplastic Esophageal Columnar Epithelium Without Goblet Cells Shows DNA Content Abnormalities Similar to Goblet Cell–Containing Epithelium

  • biologic properties of Columnar Epithelium underneath reepithelialized squamous mucosa in barrett s esophagus
    The American Journal of Surgical Pathology, 2005
    Co-Authors: Jason L Hornick, Patricia L Blount, Carissa A Sanchez, David S Cowan, Kamran Ayub, Carlo C Maley, Brian J Reid, Robert D Odze
    Abstract:

    : Chronic proton pump inhibitor (PPI) therapy may lead to partial regression of Barrett's esophagus (BE), resulting in the development of reepithelialized islands of squamous mucosa that may cover the underlying BE. The purpose of this study was to evaluate the clinical, histologic, and biologic characteristics of BE that is situated underneath squamous islands (BUSI). A total of 97 mucosal biopsies from 44 BE patients with BUSI were evaluated for a variety of histologic features (eg, type of Epithelium, anatomic relationship of the underlying glands to the luminal surface, presence of adjacent mucosal glands or ducts, and the presence and degree of dysplasia), and immunostained for Ki-67, cyclin D1, and p53. BUSI was compared with adjacent areas of BE for all parameters. A clinical control group consisting of 50 BE patients without microscopic evidence of BUSI was selected for comparison of clinical and endoscopic features. The study group (34 males, 10 females; mean age, 67 years; mean length of BE, 5.5 cm) consisted of 27 (61%) and 12 (27%) patients on low- and high-dose PPI, respectively. On endoscopy, visible islands of squamous mucosa were noted in only 43% of study group patients (despite the presence of BUSI microscopically in all cases); one island was noted in 2%, multiple islands in 27%, and extensive islands in 14% of patients. The extent of squamous islands was unrelated to PPI dose. The study group was significantly more likely to have endoscopic evidence of extensive squamous islands compared with the control group (P = 0.009). Histologically, 89% of biopsies with BUSI showed intestinal-type, and 11% showed cardia-type, Epithelium. Low- and high-grade dysplasia was noted in 4 (4%) and 5 (5%) biopsies, respectively. All patients with dysplasia in BUSI also showed dysplasia in other areas of the esophagus as well. Interestingly, BUSI reached the mucosal surface either by penetrating directly through, or by wrapping around, islands of squamous Epithelium, in 68% of biopsies. Twenty-one percent of biopsies showed BUSI adjacent to submucosal glands or ducts. BUSI showed a significantly lower Ki-67 proliferation rate (29% vs. 49%, P < 0.001), and a lower, albeit nonsignificant, degree of cyclin D1 (16% vs. 29%) and p53 (4% vs. 17%) positivity in comparison to adjacent areas of BE. Furthermore, significantly lower proliferation rates were observed in BUSI that did not reveal an opening to the mucosal surface in comparison to foci that did. BUSI is phenotypically similar to typical surface BE but shows less severe proliferative abnormalities, particularly in buried glands that have no detectable connection to the esophageal lumen. Reduced proliferation may be due either to decreased exposure to luminal contents or to disruption of sloughing of surface epithelial cells into the crypt lumen. Prospective studies of large numbers of patients with BUSI will be required to determine the magnitude of its risk of progression to cancer.

Roy C. Orlando - One of the best experts on this subject based on the ideXlab platform.

Nick Kralios - One of the best experts on this subject based on the ideXlab platform.

  • complete regression of barrett s esophagus with heat probe thermocoagulation mid term results
    Gastrointestinal Endoscopy, 1999
    Co-Authors: Spyros Michopoulos, P Tsibouris, Helias Bouzakis, Maria Sotiropoulou, Nick Kralios
    Abstract:

    Abstract Background: Barrett's esophagus is a premalignant condition. It has been reported that several methods of endoscopic ablation in combination with acid suppression result in replacement of specialized Columnar Epithelium by squamous Epithelium. The aim of this study was to assess whether ablation of Barrett's mucosa by means of heat probe and acid suppression restores normal esophageal mucosa. Methods: Thirteen patients with Barrett's Epithelium but not dysplasia were enrolled in the study. Helicobacter pylori was eradicated when discovered. Thermal energy was applied using a heat probe (pulses of 5 to 10 joules). Four-quadrant biopsies were obtained at 1 to 2 cm intervals 1 to 3 months after the last treatment session. All patients continuously took omeprazole, 40 mg/day. Results: Macroscopically, ablation of Barrett's mucosa was achieved in all patients after 1 to 5 sessions. Three of the 13 patients had residual specialized Columnar Epithelium beneath the restored mucosa but not overexpression of p53 and c-erbB-2. During follow-up (6 to 36 months) two patients in whom the length of Barrett's mucosa was greater than 2.5 cm relapsed after omeprazole discontinuation, whereas another two with length of less than 2.5 cm did not. One patient with residual Barrett's islands developed low-grade dysplasia. Conclusions: Heat probe is an effective and inexpensive method for Barrett's ablation. Islands of residual specialized Columnar Epithelium were found in 23% of patients. The length of Barrett's Epithelium determines relapse after omeprazole discontinuation. (Gastrointest Endosc 1999;50:165-72).

  • complete regression of barrett s esophagus with heat probe thermocoagulation mid term results
    United European Gastroenterology Week, 1999
    Co-Authors: Spyros Michopoulos, P Tsibouris, Helias Bouzakis, Maria Sotiropoulou, Nick Kralios
    Abstract:

    Background: Barrett's esophagus is a premalignant condition, it has been reported that several methods of endoscopic ablation in combination with acid suppression result in replacement of specialized Columnar Epithelium by squamous Epithelium. The aim of this study was to assess whether ablation of Barrett's mucosa by means of heat probe and acid suppression restores normal esophageal mucosa. Methods: Thirteen patients with Barrett's Epithelium but not dysplasia were enrolled in the study. Helicobacter pylori was eradicated when discovered. Thermal energy was applied using a heat probe (pulses of 5 to 10 joules). Four-quadrant biopsies were obtained at 1 to 2 cm intervals 1 to 3 months after the last treatment session. All patients continuously took omeprazole, 40 mg/day. Results: Macroscopically, ablation of Barrett's mucosa was achieved in all patients after 1 to 5 sessions. Three of the 13 patients had residual specialized Columnar Epithelium beneath the restored mucosa but not overexpression of p53 and c-erbB-2. During follow-up (6 to 36 months) two patients in whom the length of Barrett's mucosa was greater than 2.5 cm relapsed after omeprazole discontinuation, whereas another two with length of less than 2.5 cm did not. One patient with residual Barrett's islands developed low-grade dysplasia. Conclusions: Heat probe is an effective and Inexpensive method for Barrett's ablation. Islands of residual specialized Columnar Epithelium were found in 23% of patients. The length of Barrett's Epithelium determines relapse after omeprazole discontinuation.

Stuart J Spechler - One of the best experts on this subject based on the ideXlab platform.

  • intestinal differentiation in metaplastic nongoblet Columnar Epithelium in the esophagus
    The American Journal of Surgical Pathology, 2009
    Co-Authors: Hejin P Hahn, Stuart J Spechler, Patricia L Blount, Kamrun Ayub, Kiron M Das, Rhonda F Souza, Robert D Odze
    Abstract:

    Barrett esophagus (BE) is defined by the presence of metaplastic esophageal Columnar Epithelium with goblet cells within endoscopically recognizable areas of the esophagus. However, some carcinomas in BE, or from the gastroesophageal junction region, develop within mucosa devoid of goblet cells. However, the biologic properties, pathogenesis, and risk of malignancy of metaplastic, esophageal nongoblet Columnar Epithelium, is, essentially, unknown. In this study, 89 patients with metaplastic esophageal Columnar Epithelium were evaluated immunohistochemically for markers of intestinal differentiation, such as MUC2, DAS-1, Villin, and CDX2, a marker of gastric differentiation (MUC5AC), and Ki67, a marker of cell proliferation. Of the 89 patients, 59 had Columnar metaplasia with goblet cells (BE), which were further separated into low-density goblet cell and high-density goblet cell groups based on the percentage of crypts with goblet cells, and 30 patients had Columnar metaplasia of the esophagus without goblet cells. As controls, gastric biopsies from 19 age and sex matched patients without esophageal or gastric pathology were used. The rate of positivity of the markers and the location of Ki67 staining was evaluated only in non-goblet Columnar Epithelium from all patient groups. Patients with metaplastic esophageal Columnar Epithelium without goblet cells showed positivity for MUC5AC, MUC2, DAS-1, Villin, and CDX2 in 100%, 0%, 30%, 17%, and 43% of cases, respectively. 17% of cases showed aberrant surface Ki67 positivity. These values were significantly higher than gastric controls, which showed absence of staining for all markers except MUC5AC (100%). In patients with metaplastic esophageal Columnar Epithelium with goblet cells (BE) a significant increased rate of staining was observed for all markers, except MUC5AC. In addition, both MUC2 and surface Ki67 staining were significantly increased in BE patients with high-density goblet cells versus those with low-density goblet cells. In a separate analysis in which metaplastic esophageal nongoblet Epithelium was evaluated in areas of mucosa devoid of goblet cells compared with areas of mucosa with goblet cells, from patients who had goblet cells elsewhere in the mucosa (N=59), no significant differences were observed with regard to the percentage of cases that stained with any of the markers in the nongoblet Epithelium in areas devoid of goblet cells, similar to the patient group with metaplastic esophageal Epithelium without goblet cells (N=30). Similar to above, in all cases, expression of intestinal markers increased in areas of mucosa adjacent to goblet cells. This study provides evidence that metaplastic esophageal Columnar Epithelium without goblet cells shows phenotypic evidence of intestinal differentiation and supports the theory that squamous Epithelium converts initially to nongoblet Columnar Epithelium before goblet cell metaplasia. Further prospective studies are needed to evaluate the pathogenetic sequence, natural history, and risk of malignancy of metaplastic esophageal nongoblet Epithelium.

  • detection by scanning electron microscopy of a distinctive esophageal surface cell at the junction of squamous and barrett s Epithelium
    Digestive Diseases and Sciences, 1993
    Co-Authors: Helen M Shields, Felice R Zwas, Donald A Antonioli, Wilhelm G Doos, Stuart J Spechler
    Abstract:

    Metaplastic Columnar Epithelium replaces the normal squamous Epithelium in Barrett's esophagus. We characterized the surface epithelial cells of the junction between squamous and Barrett's Epithelium using scanning electron microscopy and light microscopy. In four biopsy specimens from the squamous-Barrett's junction in three patients, we found a distinctive cell type having features intermediate between those of squamous and Columnar Epithelium. Its distinguishing characteristic is the presence on its surface of two disparate structures not normally present on the same cell in the gastrointestinal tract: microvilli (a scanning electron microscopy feature of glandular Epithelium) and intercellular ridges (a scanning electron microscopy feature of squamous mucosa). The surface characteristics of this newly recognized cell were strikingly similar to those of cells found in the transformation zone of the uterine cervix, an area in which squamous Epithelium physiologically replaces Columnar Epithelium. We also examined 28 biopsies of the gastroesophageal junction area from 14 patients with and without a history of heartburn but with no evidence of Barrett's esophagus. None of these biosies showed the distinctive cell. We hypothesize that this distinctive cell represents an intermediate step in either the development or the healing of Barrett's Epithelium, during which surface characteristics of two different cell types, Columnar and squamous, coexist on the same cell.

Helen M Shields - One of the best experts on this subject based on the ideXlab platform.

  • detection by scanning electron microscopy of a distinctive esophageal surface cell at the junction of squamous and barrett s Epithelium
    Digestive Diseases and Sciences, 1993
    Co-Authors: Helen M Shields, Felice R Zwas, Donald A Antonioli, Wilhelm G Doos, Stuart J Spechler
    Abstract:

    Metaplastic Columnar Epithelium replaces the normal squamous Epithelium in Barrett's esophagus. We characterized the surface epithelial cells of the junction between squamous and Barrett's Epithelium using scanning electron microscopy and light microscopy. In four biopsy specimens from the squamous-Barrett's junction in three patients, we found a distinctive cell type having features intermediate between those of squamous and Columnar Epithelium. Its distinguishing characteristic is the presence on its surface of two disparate structures not normally present on the same cell in the gastrointestinal tract: microvilli (a scanning electron microscopy feature of glandular Epithelium) and intercellular ridges (a scanning electron microscopy feature of squamous mucosa). The surface characteristics of this newly recognized cell were strikingly similar to those of cells found in the transformation zone of the uterine cervix, an area in which squamous Epithelium physiologically replaces Columnar Epithelium. We also examined 28 biopsies of the gastroesophageal junction area from 14 patients with and without a history of heartburn but with no evidence of Barrett's esophagus. None of these biosies showed the distinctive cell. We hypothesize that this distinctive cell represents an intermediate step in either the development or the healing of Barrett's Epithelium, during which surface characteristics of two different cell types, Columnar and squamous, coexist on the same cell.