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Marie E Robert

Publications and source records attributed to Marie E Robert.

At least 19 recordsLinked to original sources
PubMed2006

Gastric siderosis: patterns and significance.

Recently, we encountered 2 cases of diffuse iron deposition in gastric antral and fundic glandular epithelium, which in 1 patient eventually led to the diagnosis of hemochromatosis. Gastric mucosal siderosis (GS) has previously been described in hemochromatosis patients, alcoholics, and in association with iron medications. However, the prevalence of various patterns of iron deposition in the gastric mucosa and their clinical significance have not been studied in detail. The 2 index cases mentioned above and 500 additional consecutive gastric biopsies examined over a period of 8 months at our institution were stained for iron by the Prussian blue method. In addition, all patients with genetic hemochromatosis diagnosed by liver biopsy in our department between 1998 and 2003 who also had gastric biopsies were identified from the surgical pathology files and included in the study (n = 3). The location of iron deposition [stromal cells (endothelium, fibroblasts, macrophages), glandular epithelium, or extracellular] was recorded and subjectively graded as 1+ to 3+ according to the severity of deposition within the mucosa. Relevant histologic changes (inflammation, presence of H. pylori, ulceration) and clinical features were reviewed. Three patterns of GS were identified: A) "nonspecific GS" with predominant iron deposition in the stromal cells including macrophages, and focally in epithelium; B) "iron-pill gastritis" with often mild gastritis and reactive gastropathy type changes, and mostly extracellular deposition with focal stromal cells and epithelial deposition; and C) predominant deposition in antral and fundic glandular epithelium. Of the 500 cases studied, a total of 18 (3.6%) cases were found to have GS. Of these 18 cases, 11 (2.2%) showed pattern A, 4 (0.8%) showed pattern B, and 3 (0.6%) showed pattern C. The GS in patterns A and B was always focal or patchy (1+ to 2+), whereas in pattern C it was generally diffuse and strong (2+ to 3+). A history of oral iron medication was present in 2 (n = 11, 0.4%) patients with pattern A, in all patients with pattern B (n = 4, 100%), and in none of patients with pattern C (n=3, 0%). Varying degrees of mucosal inflammation were noted in patients with pattern A cases, and 2 had evidence of active Helicobacter pylori infection. Of the 3 cases with known hemochromatosis, only one gastric biopsy showed pattern C GS (1+). In conclusion, gastric mucosal siderosis is relatively uncommon (3%) but is important to look for as it may lead to a diagnosis of hemochromatosis in some cases. Three patterns are recognized: A) a "nonspecific" stromal cell predominant pattern, which may be associated with gastric inflammation, possibly prior mucosal hemorrhages or iron medications; B) extracellular coarse clumps of crystalline iron deposition associated with oral iron medications, mild gastritis, and reactive gastropathy type changes ("Iron-pill gastritis"); and C) gastric glandular siderosis, which may be associated with systemic iron overload/hemochromatosis.

Biopsy↗
PubMed2005

The anti-apoptotic protein Mcl-1 inhibits mitochondrial Ca2+ signals.

Apoptosis contributes to the regulation of cell growth and regeneration and to the development of neoplasia. Mcl-1 is an anti-apoptotic protein that is particularly important for the development of hematological and biliary malignancies, but the mechanism of action of Mcl-1 is unknown. A number of pro- and anti-apoptotic proteins exhibit their effects by modulating Ca2+ signals, so we examined the effects of Mcl-1 on components of the Ca2+ signaling pathway that are known to regulate apoptosis. Expression of Mcl-1 did not affect expression of the inositol 1,4,5-trisphosphate receptor or the size of endoplasmic reticulum Ca2+ stores. However, mitochondrial Ca2+ signals induced by either Ca2+ agonists or apoptotic stimuli were decreased in cells overexpressing Mcl-1 and increased in cells in which Mcl-1 expression was inhibited. These findings provide evidence that Mcl-1 directly inhibits Ca2+ signals within mitochondria, which may provide a novel mechanism to inhibit apoptosis and thereby promote neoplasia.

Adenocarcinoma↗
PubMed2005

Gluten sensitive enteropathy and other causes of small intestinal lymphocytosis.

Recent studies on gluten sensitive enteropathy (GSE) have heightened the pathologist's awareness of intraepithelial lymphocytes in duodenal biopsies. Mild histologic forms of GSE are now recognized with increased IELs as the only histologic change. In this review, both the classic morphology and "minimal deviation" GSE are discussed in detail, with special emphasis on the differential diagnosis and how to avoid overdiagnosing this condition. The Marsh-Oberhuber classification is described and contrasted with a more practical diagnostic terminology that is recommended for use in pathology reports. Other important conditions associated with duodenal lymphocytosis, such as refractory sprue, autoimmune enteropathy, and Helicobacter pylori-associated duodenitis, are also presented.

Biopsy↗
PubMed2005

Painful cystic duct remnant diagnosed by endoscopic ultrasound.

Postcholecystectomy pain may remain unexplained and difficult to treat. This report describes three patients with constant postcholecystectomy abdominal pain that may have arisen from the cystic duct remnant or a neuroma of the cystic duct stump. In each case pain was exacerbated by pushing on cystic duct surgical clips with an EUS-guided needle, and temporarily abolished by an EUS-guided injection of bupivicaine and triamcinolone. Two patients underwent surgical resection of the cystic duct remnant and the third did not require further treatment. Two of the three patients had long-term improvement. EUS is a novel modality for assessing the cystic duct remnant and performing a therapeutic trial.

Abdominal Pain↗
PubMed2005

Rab11a immunohistochemical analysis does not distinguish indefinite, low-, and high-grade dysplasia in Barrett esophagus.

Our aim was to determine whether p53 and Rab11a immunoreactivity enhance diagnostic assessment of esophageal dysplasia. Histologic sections from 68 cases of Barrett esophagus obtained as part of a 12-institution study were stained with antibodies to p53 and Rab11a, randomized, and coded. The mucosal surface layer and deeper glands were scored blindly on a semiquantitative scale. The correlations between p53 and Rab11a scoring with the consensus diagnosis of dysplasia were analyzed. The histologic scale was as follows: no dysplasia, indefinite, low-grade dysplasia, high-grade dysplasia, intramucosal carcinoma, and invasive carcinoma. Rab11a staining was most prominent in epithelia negative for dysplasia but with regenerative features. There was an inverse relationship between Rab11a staining and findings of surface dysplasia (P < .02, chi(2)). However, statistical significance largely reflected loss of Rab11a immunoreactivity in intramucosal and invasive carcinoma, which was not a diagnostic dilemma. There was a strong positive correlation of p53 immunoreactivity with an increasing degree of epithelial dysplasia and carcinoma (P < .03, chi(2)). Rab11a immunoreactivity did not enhance the diagnostic assessment of dysplasia in Barrett esophagus. The previously reported positive correlation of p53 immunoreactivity with the presence of dysplasia in Barrett esophagus was confirmed.

Adenocarcinoma↗
PubMed2004

Benign fibroblastic polyps of the colon: a histologic, immunohistochemical, and ultrastructural study.

Mesenchymal proliferations presenting as mucosal polyps are relatively uncommon and are represented by gastrointestinal stromal tumors, smooth muscle and neural tumors, and inflammatory fibroid polyps. In this report, we describe the clinicopathologic features of a distinctive type of mucosal polyp composed of cytologically bland spindled cells with fibroblastic features. Fourteen cases with histologic features of"fibroblastic polyps" were identified from our case files from January 2000 to December 2003. The clinical and endoscopic findings were reviewed. Immunohistochemistry using a panel of antibodies (vimentin, smooth muscle actin, desmin, CD31, CD34, Bcl-2, c-Kit, S-100, and epithelial membrane antigen) was performed in all cases, and electron microscopy was performed in two cases. The lesions were solitary in all cases and not associated with an identifiable polyposis syndrome. Associated adenomata and/or hyperplastic polyps at different sites were present in 10 cases and hyperplastic polyps were seen in close association in 3 cases. These polyps were characterized by a monomorphic spindle cell proliferation in the lamina propria, without necrosis or mitotic activity. The lesions were intimately associated with the muscularis mucosae and resulted in wide separation and disorganization of the colonic crypts. Immunohistochemical analysis revealed strong and diffuse positivity for vimentin only. Weak and focal reactivity was noted in 2 cases for CD34 and smooth muscle actin, while staining for other antibodies was negative. Electron microscopy revealed sparse cytoplasmic organelles and many intermediate filaments. The histology and ultrastructural and immunohistochemical findings are suggestive of fibroblastic differentiation of these spindle cells. In summary, these lesions represent a distinctive type of colonic mucosal polyp that should be distinguished from other stromal polyps of the gastrointestinal tract.

Actins↗
PubMed2004

Inhibin expression in ovarian-type stroma in mucinous cystic neoplasms of the pancreas.

Mucinous cystic neoplasms (MCNs) of the pancreas are typically found in middle-aged to elderly women and contain ovarian-type stroma in the cyst wall. Whether the resemblance of this stroma to ovarian stroma is only morphologic or has more functional similarity is still unclear. Estrogen receptors (ER) and progesterone receptors (PR) have been shown to be expressed in a wide variety of tissues and tumors, including the ovarian-type stroma of MCN. Inhibin, on the other hand, has been shown to have a more restricted expression, limited to ovarian sex cord-stromal components and placental cells, and has recently been shown to be expressed in pancreatic MCNs. However, it is still unclear whether this expression is limited to MCNs of the pancreas and whether it has any diagnostic role. Seven cases of MCN (4 mucinous cystadenoma, 2 borderline MCN, and 1 mucinous cystadenocarcinoma with microinvasion), 6 cases of intraductal papillary mucinous tumor, 1 of mucinous cystic tumor of uncertain classification, 2 of mucinous noncystic adenocarcinoma, 4 of serous cystadenoma, and 4 solid pseudopapillary neoplasms were selected for this study. Five cases with normal pancreatic tissue were included as controls. Immunohistochemical stains for alpha-inhibin, ER, and PR were performed on a representative section from each case on formalin-fixed, paraffin-embedded tissue sections using a standard indirect immunoperoxidase method. All cases of MCN were in female patients with an average age of 55.3 years, showing ovarian-type stroma and clusters of alpha-inhibin-positive luteinized theca-like cells. In all these cases, moderate to strong PR positivity was also noted in the ovarian-type stroma, including many of the alpha-inhibin-positive luteinized theca-like cells. ER was expressed in 2 cases. The epithelial cells of MCNs were all negative for ER, PR, and alpha-inhibin staining. Of the other tumors, 4 solid pseudopapillary neoplasms showed positivity for only PR in the tumor cells. The remaining tumors were negative for all markers. In conclusion, the finding of alpha-inhibin positivity in MCN with ovarian-type stroma further supports its similarity to true ovarian stromal tissue and may suggest a role of complex hormonal interaction in the pathogenesis. In addition, its limited expression in MCNs of the pancreas may be diagnostically useful in difficult cases.

Adult↗
PubMed2004

Patterns of colonic involvement at initial presentation in ulcerative colitis: a retrospective study of 46 newly diagnosed cases.

Studies have shown that rectal sparing and patchiness develop in treated and longstanding ulcerative colitis (UC), making the distinction from Crohn colitis increasingly difficult after treatment is initiated. However, no histologic studies of the incidence of rectal sparing in adults at UC onset have been performed. Colectomy specimens from 46 patients with classic UC histologic features and no Crohn disease features were identified. Biopsy specimens obtained before medical therapy were retrieved and examined blindly by 2 pathologists, along with appropriate control samples. Slides were scored for chronicity (crypt branching, subcryptal plasma cells, lamina propria plasma cells) and activity (cryptitis, crypt abscesses, epithelial injury). In 28 cases, only rectal biopsy specimens were taken; for 16, rectal and at least 1 proximal biopsy specimen were taken. All cases showed rectal involvement; none had rectal sparing at initial biopsy. Of 16 cases with rectal and more proximal biopsy specimens, 5 (31%) showed relative rectal sparing (lower scores in rectum than in more proximal sites). In 16 cases with rectal and more proximal biopsy specimens, chronicity and activity scores were higher in the rectum than in more proximal sites (P = .01; chronicity and activity). The mean overall chronicity score decreased in a linear manner from rectum to cecum. The rectum is involved and shows evidence of chronicity and activity at disease onset in UC, using colectomy as the gold standard for diagnosis. Because rectal sparing at UC onset has been reported, a prospective study using uniform biopsy protocols is needed to establish the true incidence of rectal sparing at presentation.

Adolescent↗
PubMed2004

Total fibrous obliteration of main portal vein and portal foam cell venopathy in chronic hepatic allograft rejection.

CONTEXT: Chronic hepatic allograft rejection is characterized by arteriopathy and bile duct loss. Pathology of the portal vein or its branches is not considered to play a major role in chronic rejection. OBJECTIVE: A recent case of chronic rejection with total fibrous obliteration of the portal vein at the hilum and graft loss prompted us to retrospectively analyze cases of failed allografts for portal vein changes. DESIGN: Six cases of failed hepatic allograft recorded in our files from 1994 to 1998 were selected for the study. For comparison, 4 cases of hepatitis C cirrhosis were included. Clinical features, including arteriograms or Doppler studies, were reviewed whenever available. Sections taken from the hilum and random parenchyma stained with routine hematoxylin-eosin, elastic van Gieson, and Masson trichrome were examined by 3 experienced liver pathologists in a randomized, blinded fashion. RESULTS: Significant hepatic artery occlusion with foam cell change and bile duct loss was seen in all cases of chronic rejection (3/3), but not in the other cases. Foam cell change in the portal vein at the hilum (3/3) and occasionally into the distal branches (2/3) with variable occlusion of the lumen was seen only in cases of chronic hepatic allograft rejection. Mild luminal narrowing was observed in all the cases of cirrhosis (4/4) as a result of phlebosclerosis, most likely representing a change secondary to portal hypertension. Total obliteration of the portal vein at the hilum was seen in the index case (case 1) only. CONCLUSION: Portal venopathy can be a significant finding in chronic hepatic allograft rejection and may contribute to graft dysfunction or failure. Two-vessel disease must be considered in cases of chronic hepatic allograft rejection, and pathologists should thoroughly examine the hilum in explanted hepatic allografts.

Adult↗
PubMed2004

Isolated gastric malakoplakia: a case report and review of the literature.

A 62-year-old African American woman presented with weight loss and dyspepsia. She did not have any clinical evidence of immunodeficiency. Upper gastrointestinal endoscopy revealed multiple small polypoid lesions in the gastric body and fundus that appeared larger and more erythematous than usual fundic gland polyps. Examination of biopsy specimens revealed an infiltrate of large histiocytes with eosinophilic granular cytoplasm located in the lamina propria and containing Michaelis-Gutmann bodies. These histologic findings were diagnostic of gastric malakoplakia. Gastrointestinal malakoplakia is uncommon, and exclusive gastric involvement is extremely rare. Because occult bacterial infection has been postulated as the underlying cause of malakoplakia, the presence of Helicobacter pylori infection was investigated using immunohistochemical and serologic techniques, and the presence of Yersinia enterocolitica or Yersinia pseudotuberculosis infection was investigated by polymerase chain reaction assay. There was no evidence of H pylori, Y enterocolitica, or Y pseudotuberculosis in these biopsy specimens, and there was no evidence of malakoplakia or concurrent malignancy at any other site. Follow-up examination 12 months later revealed no endoscopic or histologic improvement.

Black or African American↗
PubMed2003

Loss of inositol 1,4,5-trisphosphate receptors from bile duct epithelia is a common event in cholestasis.

BACKGROUND AND AIMS: Cholestasis is one of the principal manifestations of liver disease and often results from disorders involving bile duct epithelia rather than hepatocytes. A range of disorders affects biliary epithelia, and no unifying pathophysiologic event in these cells has been identified as the cause of cholestasis. Here we examined the role of the inositol 1,4,5-trisphosphate receptor (InsP3R)/Ca(2+) release channel in Ca(2+) signaling and ductular secretion in animal models of cholestasis and in patients with cholestatic disorders. METHODS: The expression and distribution of the InsP3R and related proteins were examined in rat cholangiocytes before and after bile duct ligation or treatment with endotoxin. Ca(2+) signaling was examined in isolated bile ducts from these animals, whereas ductular bicarbonate secretion was examined in isolated perfused livers. Confocal immunofluorescence was used to examine cholangiocyte InsP3R expression in human liver biopsy specimens. RESULTS: Expression of the InsP3R was selectively lost from biliary epithelia after bile duct ligation or endotoxin treatment. As a result, Ca(2+) signaling and Ca(2+)-mediated bicarbonate secretion were lost as well, although other components of the Ca(2+) signaling pathway and adenosine 3',5'-cyclic monophosphate (cAMP)-mediated bicarbonate secretion both were preserved. Examination of human liver biopsy specimens showed that InsP3Rs also were lost from bile duct epithelia in a range of human cholestatic disorders, although InsP3R expression was intact in noncholestatic liver disease. CONCLUSIONS: InsP3-mediated Ca(2+) signaling in bile duct epithelia appears to be important for normal bile secretion in the liver, and loss of InsP3Rs may be a final common pathway for cholestasis.

Animals↗
PubMed2003

Sampling error in the standard evaluation of endoscopic colonic biopsies.

It is assumed that the diagnostic information in small gastrointestinal mucosal biopsies is obtained regardless of which side of the biopsy is sectioned. Based on this assumption, mucosal biopsies of the colon are embedded randomly with respect to the side of the biopsy that faces the microtome blade. Our hypothesis is that reorienting ("flipping") the biopsy specimen 180 degrees and sectioning the opposite side might provide new diagnostic information in cases with no specific histopathologic diagnosis. Sixty-one consecutive cases with a clinical impression of a polyp and no histologic abnormality on three hematoxylin and eosin-stained slides (6-15 levels) were selected. Formalin-fixed, paraffin-embedded tissue was reoriented, and three additional hematoxylin and eosin-stained slides (6-15 levels) were evaluated. The side of the specimen initially sectioned was arbitrarily designated "A," and the side of the specimen sectioned after reembedding was designated "B." The slides were sequentially numbered 1-3, and the first slide on which the new diagnosis was evident was recorded. New diagnoses were made for 19 of 61 (31.1%) specimens from a total of 51 patients and included tubular adenomas (12 of 61; 19.7%) and hyperplastic polyps (7 of 61; 11.5%). In 17 of 19 specimens (89.5%), the new diagnosis was evident on the first slide. Reembedding endoscopic colonic biopsies facilitates rendering a definitive diagnosis in cases of discordance between the clinical impression and the histologic impression. Routine examination of at least two sides of randomly oriented biopsy material could provide additional diagnostic, and sometimes critical, information.

Biopsy↗
PubMed2002

IL-10 regulates murine lupus.

MRL/MpJ-Tnfrsf6(lpr) (MRL/MpJ-Fas(lpr); MRL-Fas(lpr)) mice develop a spontaneous lupus syndrome closely resembling human systemic lupus erythematosus. To define the role of IL-10 in the regulation of murine lupus, IL-10 gene-deficient (IL-10(-/-)) MRL-Fas(lpr) (MRL-Fas(lpr) IL-10(-/-)) mice were generated and their disease phenotype was compared with littermates with one or two copies of an intact IL-10 locus (MRL-Fas(lpr) IL-10(+/-) and MRL-Fas(lpr) IL-10(+/+) mice, respectively). MRL-Fas(lpr) IL-10(-/-) mice developed severe lupus, with earlier appearance of skin lesions, increased lymphadenopathy, more severe glomerulonephritis, and higher mortality than their IL-10-intact littermate controls. The increased severity of lupus in MRL-Fas(lpr) IL-10(-/-) mice was closely associated with enhanced IFN-gamma production by both CD4(+) and CD8(+) cells and increased serum concentration of IgG2a anti-dsDNA autoantibodies. The protective effect of IL-10 in this lupus model was further supported by the observation that administration of rIL-10 reduced IgG2a anti-dsDNA autoantibody production in wild-type MRL-Fas(lpr) animals. In summary, our results provide evidence that IL-10 can down-modulate murine lupus through inhibition of pathogenic Th1 cytokine responses. Modulation of the level of IL-10 may be of potential therapeutic benefit for human lupus.

Animals↗
PubMed2002

Utilization of acidophil bodies in the diagnosis of recurrent hepatitis C infection after orthotopic liver transplantation.

BACKGROUND: The distinction between acute rejection and early recurrent hepatitis C infection (RHCV) in the setting of orthotopic liver transplantation is often difficult. In liver biopsies acidophil bodies and lobular hepatitis are used to suggest a diagnosis of RHCV over rejection, however, the reliability of this practice has not been established. Because portal tract changes in RHCV and rejection often overlap, we sought to determine whether the degree of hepatocyte acidophil body formation seen on liver biopsies could be used to distinguish between these two conditions. METHODS: Quantification of acidophil bodies was performed on liver biopsies in orthotopic liver transplant patients with RHCV (n = 10), non-hepatitis C orthotopic liver transplant patients with uncomplicated rejection episodes (n = 10) and non-transplant patients with chronic hepatitis C infection (n = 10). Hematoxylin and Eosin stained slides from all three groups were randomized and tissue segments 1.0 cm in length and of variable width (0.04-0.13 cm) were examined at 200x magnification in a blinded fashion by two pathologists in order to quantify the number of acidophil bodies/cm(2). Lobular chronic inflammation was also graded on a 0-3+ scale. RESULTS: Liver biopsies taken at the onset of RHCV exhibited 606 +/- 101 acidophil bodies/cm(2) (mean +/- standard error of mean, range 200-1390). These counts were significantly greater (P =.0061, paired 2-tailed t-test) than the 241 +/- 53 acidophil bodies/cm(2) (range 80-514) for acute rejection, and the 194 +/- 21 acidophil bodies/cm(2) (range 100-333) for non-liver transplant chronic hepatitis C infection (P =.0013). No difference in lobular inflammation between index RHCV and rejection biopsies was detected. CONCLUSIONS: Although there is overlap, on average there are twice as many acidophil bodies in the initial stage of RHCV when compared with acute rejection (average of 55 per linear cm in RHCV versus 21 per linear cm for rejection). Lobular inflammation was not a reliable indicator of the initial onset of RHCV.

Adolescent↗
PubMed2002

Are ulcers a marker for invasive carcinoma in Barrett's esophagus? Data from a diagnostic variability study with clinical follow-up.

OBJECTIVES: We correlated follow-up information from 138 patients with Barrett's esophagus and varying degrees of dysplasia with the presence of ulcers. METHODS: A group of pathologist participants were asked to contribute patients' initial biopsy slides showing Barrett's esophagus (BE) without dysplasia and with epithelial changes indefinite for dysplasia, low grade dysplasia (LGD), high grade dysplasia (HGD), and adenocarcinoma. From the initial 250 cases used for a diagnostic reproducibility study, follow-up information was available for 138 patients. RESULTS: There were 44 cases submitted as BE, 22 as BE with epithelial changes indefinite for dysplasia, 26 as BE with LGD, 33 as BE with HGD, and 13 as BE with adenocarcinoma. Ulcers were present in 35/138 cases (25%), including 3/44 cases of BE without dysplasia (7%), 2/22 cases of BE with epithelial changes indefinite for dysplasia (9%), 0/26 cases of BE with LGD (0%), 10/33 cases of BE with HGD (30%), and 7/13 cases of BE with adenocarcinoma (54%). On follow-up, there were no invasive carcinomas detected among the BE without dysplasia group (median follow-up = 38.5 months). Adenocarcinomas were detected in 4/22 cases (18%) submitted as BE with epithelial changes indefinite for dysplasia at 19, 55, 60, and 62 months and in 4/26 cases (15%) of BE with LGD at 9, 9, 11, and 60 months. None of these carcinomas occurred in cases in which an ulcer was present in the initial biopsy specimen. Among the 33 HGD cases, 20 (60%) were found to have adenocarcinoma on subsequent resection specimens. The presence of an ulcer with HGD increased the likelihood of finding carcinoma in the resection specimen, as 8/10 biopsies (80%) of HGD patients with ulcers had carcinoma, compared to 12/23 biopsies (52%) of HGD patients without ulcers. All of the cases interpreted as adenocarcinomas on biopsy were found either to have invasive carcinoma on esophageal resection or to have metastases that were demonstrated in unresectable patients. CONCLUSION: If an ulcer accompanies HGD in a biopsy specimen from a patient with BE, it is likely that invasive carcinoma is also present at that time.

Adenocarcinoma↗
PubMedDate not supplied

Defining dysplasia in Barrett esophagus.

Histologic grading of esophageal biopsies remains the cornerstone of management in patients with Barrett esophagus. This remains true despite ongoing research into the genetic abnormalities that occur in the setting of intestinal metaplasia, dysplasia, and adenocarcinoma of the esophagus. As of this writing, there are no objective tests that can replace the pathologist's eyes in predicting prognosis in this setting. However, pathologists and clinicians are well aware that the histologic interpretation of biopsies is an inherently subjective practice. The validity of this exercise depends entirely on the experience of the pathologist. Having said that, two interobserver studies on the grading of dysplasia in Barrett esophagus suggest that, if published criteria are adhered to, the histologic grading of dysplasia is a useful tool in patient management. In this review, the updated pathologic criteria for each category of dysplasia are presented, and the results of two large interobserver variability studies are reviewed.

Adenocarcinoma↗