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T T Wu

Publications and source records attributed to T T Wu.

At least 19 recordsLinked to original sources
PubMed2006

Gender-based analysis of esophageal cancer patients undergoing preoperative chemoradiation: differences in presentation and therapy outcome.

The purpose of this study was to identify gender-dependent differences in presentation at baseline and therapy outcome in esophageal carcinoma patients treated with preoperative chemoradiotherapy (CTRT). We stratified patients according to gender and statistically compared pretreatment clinical stage, post-CTRT effect on carcinoma in the resected specimen, overall survival (OS), and patterns of failure. Of the 235 patients who underwent preoperative CTRT, 203 were men and 32 were women. Carcinomas in women correlated significantly with clinical stage II classification (78%vs. 55%) while cancers in men correlated significantly with clinical stage III classification (39%vs. 16%; P = 0.02). Carcinomas in women also correlated significantly with lower clinical N classification; more women had cN0 (52%) compared to men (28%; P = 0.01). Similarly, in the surgical specimens, more women had pN0 (78%) compared to men (64%; P = 0.06). At a median follow-up of 37 months, 10% more women than men remain alive (63%vs. 53%; P = 0.3). Distant metastases-free survival time was longer for women than men. Our results suggest that localized esophageal carcinoma is diagnosed in more advanced stages in men than in women. The reasons for these differences remain unclear and further expansion of these observations and study of biologic differences that might exist are warranted.

Chemotherapy, Adjuvant↗
PubMed2005

Paclitaxel-based chemoradiotherapy in localized gastric carcinoma: degree of pathologic response and not clinical parameters dictated patient outcome.

PURPOSE: Preoperative chemoradiotherapy may increase the R0 (curative) resection rate, overall survival (OS) duration, and disease-free survival (DFS) duration. We evaluated paclitaxel-based induction chemotherapy and chemoradiotherapy in patients with localized gastric or gastroesophageal adenocarcinoma to determine its feasibility, impact on the R0 resection rate, type of pathologic response, OS, and DFS. PATIENTS AND METHODS: Patients with operable, localized gastric, or gastroesophageal adenocarcinoma were eligible. Staging included endoscopic ultrasonography (EUS) and laparoscopy. Patients received two 28-day cycles of induction chemotherapy of fluorouracil, paclitaxel, and cisplatin followed by 45 Gy of radiation and concurrent fluorouracil plus paclitaxel. The cancer was restaged and surgery was attempted. Postsurgery pathologic findings and R0 resection were correlated with OS and DFS. RESULTS: Forty-one patients were enrolled. Most carcinomas were proximal (83%) and pretreatment stage EUST3 (85%). Forty patients (98%) underwent surgery, and 78% had an R0 resection. We observed a pathologic complete response (pathCR) rate of 20% and a pathologic partial response (pathPR) rate of 15% (< 10% residual cancer cells in the resected specimen). No pretreatment parameter (sex, cancer location, baseline T stage, or baseline N stage) predicted the type of postsurgery pathologic response, OS, or DFS. However, pathCR (P = .02), pathCR + pathPR (P = .006), R0 resection (P < .001), and postsurgery T and N stages (P = .01 and P < .001, respectively) were associated with OS. Same parameters were significantly correlated with DFS. Toxicity was manageable. CONCLUSION: The type of pathologic response but not pretreatment parameters was associated with OS and DFS. Efforts to increase the rate of pathologic response and better systemic cancer control are warranted.

Adenocarcinoma↗
PubMed2003

Barrett's esophagus with high grade dysplasia: surgical results and long-term outcome--an update.

We updated our surgical results and long-term outcome for prophylactic esophagectomy in patients with Barrett's esophagus and high-grade dysplasia (HGD) and determined the incidence of occult adenocarcinoma. Sixty consecutive patients with HGD who underwent esophagectomy had pre- and postoperative pathology examined at our institution from 1982 to 2001. We reviewed medical records to determine patient characteristics, surgical approach, operative morbidity and mortality, pathology, and length of stay. Patients and/or referring physicians were contacted to determine long-term outcome. Fifty-three men (88%) and 7 women (12%) were followed up for a median of 4.6 years. Transhiatal esophagectomy was performed in the majority of patients (82%). There was one operative death (1.7%) and 15 complications (29%). Median length of stay was 9 days. In 18 patients (30%), invasive adenocarcinoma was detected in the resected specimen. When examined by time periods, 43% (13/30) of patients were diagnosed with occult cancer from 1982-1994, whereas 17% (5/30) harbored occult malignancy from 1994-2001. All patients with adenocarcinoma in the recent interval had stage I disease, as opposed to only 61.5% of patients from the earlier study. Operative mortality declined from 3.3% to 0% over the two intervals as did mean length of stay from 14 days to 10 days. Five-year survival was excellent at 88%. Age and amount of preoperative weight loss were preoperative predictors of survival, whereas major postoperative complications and stage were postoperative predictors of outcome. Barrett's esophagus with high-grade dysplasia continues to be an indication for prophylactic esophagectomy. Overall prevalence of occult adenocarcinoma remains high. We have demonstrated a declining incidence of occult cancer and treatment of earlier stage adenocarcinoma when found in this population of patients treated with esophagectomy.

Adenocarcinoma↗
PubMed2003

What to learn about sildenafil in the treatment of erectile dysfunction from 3-year clinical experience.

We retrospectively assessed the clinical uses and results of sildenafil in the treatment of erectile dysfunction (ED) in daily clinical practice from a cohort of 1658 subjects at a multispecialty medical center from 1999 to 2001 through a chart review, mailed questionnaire and telephone interview. The overall follow-up rate was 77.8% (1290/1658). The mean age was 63.8 y and ED duration was 3.4 y, and 44.6% of them had one or more concomitant conditions. The mean score of the International Index of Erectile Function erectile function domain was 12.7 in 314 nonselective subjects, and 75% of them had moderate to severe ED. The average number of purchase-visits and tablets of sildenafil purchased was 2.27 and 10.8 per person, respectively, and the prescription refill rate was 58.6%. Urology accounts for 91.4% of the specialties of prescribers. The response rate was 72.0%, which was significantly lower in subjects with diabetes, ischemic heart disease and following radical pelvic surgery than those without. Subjects with psychogenic etiology had the highest response rate, while those following radical pelvic surgery the lowest. Of the nonresponders, 67% did not try the maximum dose of 100 mg and 71.1% bought no more than four tablets. Adverse events were reported in 20.1% of the subjects. No one discontinued the treatment because of the adverse events. Mortality occurred in 17 subjects and none was considered related to sildenafil use. In conclusion, sildenafil was effective and safe in the treatment of ED in clinical practice. Compared with clinical trials or prospective clinical practice based studies, lack of dose titration, less follow-up visits and inadequate attempts before giving up were the main shortfalls in daily practice.

Adult↗
PubMed2002

Endoscopic findings predict the histologic diagnosis in gastrointestinal graft-versus-host disease.

BACKGROUND AND STUDY AIMS: Graft-versus-host disease (GvHD) of the gastrointestinal tract is a major cause of morbidity and mortality after allogeneic bone marrow transplantation (BMT). Whether endoscopic findings predict the histologic diagnosis of GvHD in the gastrointestinal tract remains controversial. We performed a study to determine the diagnostic accuracy of macroscopic endoscopy findings in the diagnosis of acute and chronic histologically proven gastrointestinal GvHD (GI-GvHD). PATIENTS AND METHODS: Endoscopic images from the intestinal mucosa of post-BMT patients were blindly graded as positive or negative for GI-GvHD and compared with corresponding histological findings, which were used as the gold standard. RESULTS: 44 BMT patients were referred for 96 endoscopic evaluations. Using 162 endoscopy-biopsy pairs, a positive association between endoscopic grading and histologic grading of GI-GvHD (odds ratio [OR] = 11.97, 95% CI 3.86, 37.16) was observed. Endoscopic diagnosis correctly predicted histologic diagnosis in both acute and chronic GI-GvHD (OR = 9.3 vs. 23.1, P = 0.31). CONCLUSIONS: The diagnostic accuracy of endoscopy was high in both acute and chronic histologically proven GI-GvHD. Accurate diagnosis of GI-GvHD might be obtained with mucosal biopsies from either the upper or lower gastrointestinal tract. Endoscopy may play a significant role in establishing early diagnosis and treatment for GI-GvHD in patients following BMT, but histologic evaluation of the gastrointestinal mucosa is needed to confirm the final diagnosis.

Adult↗
PubMed2002

Application of narrow band laser ultrasonics to the nondestructive evaluation of thin bonding layers.

In this paper, a modified laser induced grating technique (LIG) has been utilized to generate narrow band surface waves in an epoxy-bonded copper-aluminum layered structure. A high performance optical interferometer system was utilized to detect the laser-generated surface waves. The dispersion of surface wave in an epoxy-bonded copper-aluminum specimen was measured and compared with the theoretical solution. An inverse algorithm based on the simplex method was then introduced to determine the bonding thickness as well as the elastic properties of the bonding layer. The inversion results demonstrated that the thickness in the microm range or the elastic properties of the bonding layer could be successfully determined.

Journal Article↗
PubMed2001

Molecular predictors of survival after adjuvant chemotherapy for colon cancer.

BACKGROUND: Adjuvant chemotherapy improves survival among patients with stage III colon cancer, but no reliable molecular predictors of outcome have been identified. METHODS: We evaluated loss of chromosomal material (also called loss of heterozygosity or allelic loss) from chromosomes 18q, 17p, and 8p; cellular levels of p53 and p21(WAF1/CIP1) proteins; and microsatellite instability as molecular markers. We analyzed tumor tissue from 460 patients with stage III and high-risk stage II colon cancer who had been treated with various combinations of adjuvant fluorouracil, leucovorin, and levamisole to determine the ability of these markers to predict survival. RESULTS: Loss of heterozygosity at 18q was present in 155 of 319 cancers (49 percent). High levels of microsatellite instability were found in 62 of 298 tumors (21 percent), and 38 of these 62 tumors (61 percent) had a mutation of the gene for the type II receptor for transforming growth factor beta1 (TGF-beta1). Among patients with microsatellite-stable stage III cancer, five-year overall survival after fluorouracil-based chemotherapy was 74 percent in those whose cancer retained 18q alleles and 50 percent in those with loss of 18q alleles (relative risk of death with loss at 18q, 2.75; 95 percent confidence interval, 1.34 to 5.65; P=0.006). The five-year survival rate among patients whose cancer had high levels of microsatellite instability was 74 percent in the presence of a mutated gene for the type II receptor for TGF-beta1 and 46 percent if the tumor did not have this mutation (relative risk of death, 2.90; 95 percent confidence interval, 1.14 to 7.35; P=0.03). CONCLUSIONS: Retention of 18q alleles in microsatellite-stable cancers and mutation of the gene for the type II receptor for TGF-beta1 in cancers with high levels of microsatellite instability point to a favorable outcome after adjuvant chemotherapy with fluorouracil-based regimens for stage III colon cancer.

Aged↗
PubMed2001

Kabat Database and its applications: future directions.

The Kabat Database was initially started in 1970 to determine the combining site of antibodies based on the available amino acid sequences. The precise delineation of complementarity determining regions (CDR) of both light and heavy chains provides the first example of how properly aligned sequences can be used to derive structural and functional information of biological macromolecules. This knowledge has subsequently been applied to the construction of artificial antibodies with prescribed specificities, and to many other studies. The Kabat database now includes nucleotide sequences, sequences of T cell receptors for antigens (TCR), major histocompatibility complex (MHC) class I and II molecules, and other proteins of immunological interest. While new sequences are continually added into this database, we have undertaken the task of developing more analytical methods to study the information content of this collection of aligned sequences. New examples of analysis will be illustrated on a yearly basis. The Kabat Database and its applications are freely available at http://immuno.bme.nwu.edu.

Animals↗
PubMed2001

Distinctive molecular genetic alterations in sporadic and familial adenomatous polyposis-associated pancreatoblastomas : frequent alterations in the APC/beta-catenin pathway and chromosome 11p.

Pancreatoblastomas are unusual malignant neoplasms of the pediatric pancreas that may also rarely affect adults. The molecular pathogenesis of pancreatoblastomas is unknown. They are clinicopathologically distinct from adult pancreatic ductal adenocarcinomas, but their occasional occurrence in patients with Beckwith-Wiedemann syndrome and the case presented here of a pancreatoblastoma in an adult patient with familial adenomatous polyposis (FAP) suggests that they might bear a genetic similarity to other infantile embryonal tumors such as hepatoblastomas. We analyzed a series of nine pancreatoblastomas for mutations common to other embryonal malignancies including somatic alterations in the adenomatous polyposis coli (APC)/beta-catenin pathway and chromosome 11p, using immunohistochemistry for beta-catenin, 5q and 11p allelic loss assays, and direct DNA sequencing of exon 3 of the beta-catenin gene and the mutation cluster region of the APC gene. In addition, we analyzed the pancreatoblastomas for alterations found in adult-type pancreatic ductal adenocarcinomas including mutations in the K-ras oncogene and the p53 and DPC4 tumor suppressor genes, using direct DNA sequencing of exon 1 of K-ras and immunohistochemistry for p53 and Dpc4. Allelic loss on chromosome 11p was the most common genetic alteration in pancreatoblastomas, present in 86% (six of seven informative cases). Molecular alterations in the APC/beta-catenin pathway were detected in 67% (six of nine), including five neoplasms with activating mutations of the beta-catenin oncogene and the one FAP-associated tumor with biallelic APC inactivation (germline truncating mutation combined with loss of the wild-type allele); seven neoplasms showed abnormal nuclear accumulation of beta-catenin protein. In contrast, loss of Dpc4 protein expression was present in only two cases (one diffuse and one focal), and no alterations in the K-ras gene or p53 expression were detected. Our findings indicate that pancreatoblastomas are genetically distinct from the more common pancreatic ductal adenocarcinomas, but bear a close molecular pathogenesis to hepatoblastomas. In addition, pancreatoblastoma may represent an extracolonic manifestation of FAP.

Adenomatous Polyposis Coli↗
PubMed2001

Histopathological identification of colon cancer with microsatellite instability.

Cancer with high levels of microsatellite instability (MSI-H) is the hallmark of hereditary nonpolyposis colorectal cancer syndrome, and MSI-H occurs in approximately 15% of sporadic colorectal carcinomas that have improved prognosis. We examined the utility of histopathology for the identification of MSI-H cancers by evaluating the features of 323 sporadic carcinomas using specified criteria and comparing the results to MSI-H status. Coded hematoxylin and eosin sections were evaluated for tumor features (signet ring cells; mucinous histology; cribriforming, poor differentiation, and medullary-type pattern; sponge-like mucinous growth; pushing invasive margin) and features of host immune response (Crohn's-like lymphoid reaction, intratumoral lymphocytic infiltrate, and intraepithelial T cells by immunohistochemistry for CD3 with morphometry). Interobserver variation among five pathologists was determined. Subjective interpretation of histopathology as an indication for MSI testing was recorded. We found that medullary carcinoma, intraepithelial lymphocytosis, and poor differentiation were the best discriminators between MSI-H and microsatellite-stable cancers (odds ratio: 37.8, 9.8, and 4.0, respectively; P = 0.000003 to < 0.000001) with high specificity (99 to 87%). The sensitivities, however, were very low (14 to 38%), and interobserver agreement was good only for evaluation of poor differentiation (kappa, 0.69). Mucinous histopathological type and presence of signet ring cells had low odds ratios of 3.3 and 2.7 (P = 0.005 and P = 0.02) with specificities of 95% but sensitivities of only 15 and 13%. Subjective interpretation of the overall histopathology as suggesting MSI-H performed better than any individual feature; the odds ratio was 7.5 (P < 0.000001) with sensitivity of 49%, specificity of 89%, and moderate interobserver agreement (kappa, 0.52). Forty intraepithelial CD3-positive lymphocytes/0.94 mm2, as established by receiver operating characteristic curve analysis, resulted in an odds ratio of 6.0 (P < 0.000001) with sensitivity of 75% and specificity of 67%. Our findings indicate that histopathological evaluation can be used to prioritize sporadic colon cancers for MSI studies, but morphological prediction of MSI-H has low sensitivity, requiring molecular analysis for therapeutic decisions.

CD3 Complex↗
PubMed2001

Sporadic fundic gland polyps: common gastric polyps arising through activating mutations in the beta-catenin gene.

Fundic gland polyps (FGPs) are the most common gastric polyps. FGPs traditionally have been regarded as nondysplastic hamartomatous or hyperplastic lesions, but their pathogenesis remains unclear. We have recently shown that somatic adenomatous polyposis coli (APC) gene alterations are frequently present in FGPs associated with familial adenomatous polyposis (FAP), raising the possibility that mutations of the beta-catenin gene affecting the APC/beta-catenin pathway might be involved in the pathogenesis of sporadic FGPs. We analyzed somatic beta-catenin gene mutations in 57 sporadic FGPs from 40 patients without FAP and in 19 FGPs from 13 FAP patients. Direct DNA sequencing of exon 3 encompassing the glycogen synthase kinase-3beta phosphorylation region for beta-catenin was used with confirmation by HIN:fI restriction endonuclease digestion. The foveolar epithelium and dilated fundic glands of the polyps were separately microdissected and analyzed in 22 of 57 sporadic FGPs. Activating beta-catenin gene mutations were present in 91% (52 of 57) of sporadic FGPs. Both the foveolar epithelium and the dilated fundic gland epithelium comprising the polyps were shown to have the same somatic beta-catenin mutation in 21 of 22 (95%) sporadic FGPs. In contrast, beta-catenin gene mutations were not present in any of the 19 FAP-associated FGPs (P: < 0.000001). The high frequency of beta-catenin mutations in sporadic FGPs indicates that these lesions arise through activating mutations of the beta-catenin gene. Beta-catenin mutations in gastrointestinal tract polyps have previously only been demonstrated in a subset of adenomatous (dysplastic) or neoplastic polyps. Sporadic FGPs are therefore the only lesions of the gastrointestinal tract to demonstrate beta-catenin mutations while lacking dysplastic morphology.

Cytoskeletal Proteins↗
PubMed2001

Frequent beta-catenin mutations in juvenile nasopharyngeal angiofibromas.

Juvenile nasopharyngeal angiofibromas (JNAs) are locally aggressive vascular tumors occurring predominantly in adolescent males. The pathogenesis of JNAs is unknown. Recently, JNAs have been reported to occur at increased frequency among patients with familial adenomatous polyposis, suggesting that alterations of the adenomatous polyposis coli (APC)/beta-catenin pathway might also be involved in the pathogenesis of sporadic JNAs. We analyzed somatic beta-catenin and APC gene mutations in 16 sporadic JNAs from nonfamilial adenomatous polyposis patients using immunohistochemistry for beta-catenin, and direct DNA sequencing for exon 3 of the beta-catenin gene and the mutation cluster region of the APC gene. Nuclear accumulation of beta-catenin was diffusely present in the stromal cells but not in the endothelial cells of all 16 JNAs. Activating beta-catenin gene mutations were present in 75% (12 of 16) of JNAs. Six JNA patients also had recurrent tumors after surgery, and in all cases the beta-catenin gene status of the recurrent JNA was identical to the initial tumor. No mutations in the mutation cluster region of the APC gene were detected in the four JNAs without beta-catenin mutations. The high frequency of beta-catenin mutations in sporadic JNAs and the presence of identical beta-catenin gene mutations in recurrent tumors indicates that activating beta-catenin gene mutations are important in the pathogenesis of JNAs. The immunohistochemical localization of beta-catenin only to the nuclei of stromal cells further suggests that the stromal cells, rather than endothelial cells, are the neoplastic cells of JNAs.

Adolescent↗
PubMed2001

Superficial fibromatoses are genetically distinct from deep fibromatoses.

Whereas deep fibromatoses (abdominal, extra-abdominal, mesenteric) display locally aggressive behavior, superficial fibromatoses typically remain small and less likely to recur despite essentially identical morphology. Somatic beta-catenin or APC gene mutations have been reported in < or =74% of sporadic deep fibromatoses and in virtually 100% of Gardner syndrome-associated fibromatoses, whereas genetic events in superficial fibromatoses remain less well characterized. We performed immunohistochemical staining for beta-catenin on 29 superficial fibromatoses (22 palmar, 5 plantar, 1 penile, and 1 infantile digital fibromatosis) and 5 deep fibromatoses. Mutations of beta-catenin and APC genes were analyzed in cases of superficial fibromatoses by direct DNA sequencing of the beta-catenin gene on Exon 3 encompassing the GSK-3 36 phosphorylation region and of the APC gene on the mutation cluster region. Nuclear accumulation of beta-catenin was present in 86% (25/29) of superficial fibromatosis cases ranging from 5 to 100% of nuclei (mean, 13%; median, 10%), though in a minority of nuclei in most examples. Deep fibromatoses had 60 to 100% nuclear staining in all five cases. No somatic mutations of beta-catenin or APC genes were identified in any of the superficial fibromatoses. In contrast to deep fibromatoses, superficial fibromatoses lack beta-catenin and APC gene mutations; the significance of focal nuclear beta-catenin accumulation is unclear. This difference may account inpart for their divergent clinical manifestations despite their morphologic resemblance to deep fibromatoses.

Adult↗
PubMed2001

Annual changes in the clinical features of prostatic adenocarcinoma in Taiwan.

OBJECTIVE: To determine, using a clinical and pathological database, the annual changes in the characteristics of adenocarcinoma of the prostate diagnosed in consecutive men in Taiwan. PATIENTS AND METHODS: All prostatic adenocarcinomas newly diagnosed between 1991 and 1999 in our institution were analysed. Using logistic regression for dichotomous variables, the annual trends were assessed for changes in the percentage of T1c disease, incidental carcinoma, clinically localized disease and Gleason grade 4/5 cancers. The annual trends for changes in the pathological features of disease in patients treated by radical prostatectomy were also analysed. RESULTS: The study included 694 patients; the median age at diagnosis increased significantly (P = 0.004) and there was a significant increase in clinical T1c disease (relative risk, RR, 1.142, P = 0.022). There were also significant decreases in incidental carcinomas (RR 0.789, P < 0.001), patients with a serum prostate-specific antigen (PSA) level of > 20 ng/mL (RR 0.848, P < 0.001) and with Gleason grade 4/5 tumours (RR 0.919, P = 0.005). There was no significant change in the percentage of clinically localized disease. Radical prostatectomy was undertaken in 179 men; the annual incidence of lymph node metastases decreased significantly (P = 0.035) and there was a significant 19% increase in the RR of having organ-confined disease (pT1-2N0M0) and a 19% decrease in Gleason grade 4/5 tumours. CONCLUSIONS: These results may reflect the annual trends of prostate cancer in Taiwan in the period for which the PSA assay became available. The increasing application of PSA testing was associated with a significant increase in clinical T1c disease and decrease in incidental carcinoma. There was also a significant trend towards less aggressive cancers. Despite the dramatic increase in the annual detection rate, tumours were not detected at an earlier stage. However, for patients treated with radical prostatectomy, there was a significant change to earlier stage disease and fewer de-differentiated cancers.

Adenocarcinoma↗
PubMed2001

Clinicopathologic and molecular analysis of high-grade dysplasia and early adenocarcinoma in short- versus long-segment Barrett esophagus.

Barrett esophagus, especially dysplastic Barrett mucosa, has been regarded as a preneoplastic lesion for esophageal adenocarcinoma. However, the etiology and pathogenesis of dysplasia and early adenocarcinoma in short- (SSBE) and long- (LSBE) segment Barrett esophagus have not been studied in detail. The aims of this study were to clarify clinicopathologic and genetic differences between high-grade dysplasia (HGD) and early adenocarcinoma in SSBE versus LSBE. We analyzed the clinicopathologic features from 47 patients (19 SSBE [<3 cm] and 28 LSBE [> or =3 cm]) with esophagectomy for HGD/T1 adenocarcinoma. Allelic losses on chromosomes 3p (FIHT), 5q (APC), 9p (p16), and 17p (p53) were compared in 12 HGD and 9 T1 tumors from 19 cases of SSBE and in 23 HGD and 15 T1 tumors from 28 cases of LSBE. Patients with SSBE were more likely to be smokers than were patients with LSBE (94.7% v 57.1%; P =.004). HGD or T1 tumors arising from SSBE were less likely to show adjoining nondysplastic Barrett mucosa than those from LSBE (73.6% v 100%; P =.02). LSBE more frequently showed a circumferential pattern of Barrett mucosa than did SSBE (96.4% v 47.3%; P =.0002). Chromosomal allelic losses on 3p, 5q, 9p, and 17p were detected in 19% (4 of 21), 43% (15 of 35), 40% (14 of 35), and 48% (16 of 33) of HGD, respectively, and 26% (5 of 19), 35% (8 of 23), 35% (8 of 23), and 57% (13 of 23) of T1 tumor, respectively. There were no significant differences in allelic loss of 3p, 5q, 9p, or 17p in HGD or T1 tumors from SSBE versus LSBE. These results suggest that both HGD and early adenocarcinoma in SSBE and LSBE may occur through similar genetic alterations, whereas there are some clinicopathologic differences between SSBE and LSBE. HUM PATHOL

Aged↗
PubMed2001

Hyperplastic polyps of the stomach: associations with histologic patterns of gastritis and gastric atrophy.

Hyperplastic polyps are common gastric lesions characterized by hyperplastic foveolae with variable amounts of inflamed stroma. Their pathogenesis is unknown, but they have been reported to occur in association with various forms of chronic gastritis, particularly autoimmune gastritis and Helicobacter pylori gastritis. Comprehensive histologic evaluation of the background mucosal pathology in patients with hyperplastic polyps has not been previously performed. We studied 160 patients with gastric hyperplastic polyps and characterized endoscopic and histologic features of the polyps (i.e., location, multiplicity, and presence of dysplasia and adenocarcinoma) and the background gastric mucosa (i.e., intestinal metaplasia, dysplasia, carcinoma, and presence and classification of gastritis). Hyperplastic polyps were most common in the antrum (60%) and were multiple in 20% of patients. Focal intestinal metaplasia of the polyp was present in 16% and dysplasia in 4% of patients. Only one patient (0.6%) had adenocarcinoma within the polyp. Evaluation of the surrounding gastric mucosa showed at least focal intestinal metaplasia in 37% of patients, adenoma or low-grade flat epithelial dysplasia in 2%, and synchronous or metachronous adenocarcinoma in 6%. Eighty-five percent of patients had inflammatory mucosal pathology, most commonly active chronic H. pylori gastritis (25%), reactive or chemical gastropathy (21%), and metaplastic atrophic gastritis of the autoimmune (12%) or environmental (8%) type. These results indicate a strong association between various forms of gastritis and the development of hyperplastic polyps and further emphasize the importance of biopsy of the nonpolypoid gastric mucosa during endoscopic examination.

Adenocarcinoma↗
PubMed2001

Upper gastrointestinal tract injury in patients receiving kayexalate (sodium polystyrene sulfonate) in sorbitol: clinical, endoscopic, and histopathologic findings.

Kayexalate (sodium polystyrene sulfonate) in sorbitol has been demonstrated to cause colonic necrosis in a subset of uremic patients who are administered the cation exchange resin for treatment of hyperkalemia. Upper gastrointestinal damage associated with Kayexalate in sorbitol is reported far less frequently, and the clinicopathologic spectrum of disease in cases with upper gastrointestinal damage has not been investigated previously. The authors studied the clinical, endoscopic, and histologic features of 11 patients with Kayexalate crystals in biopsies from the esophagus (n = 7), stomach (n = 6), and duodenum (n = 2). The endoscopic appearance was markedly abnormal in all 11 patients. The effects of the medication closely mimicked other endoscopic and radiologic diagnoses in three cases, including esophageal carcinoma, Candidal esophagitis, and gastric bezoar. Histologic and/or endoscopic evidence of mucosal injury in the form of an ulcer or erosion was present in nine patients (82%). In four patients with mucosal injury, no other etiology apart from Kayexalate in sorbitol could be identified. In comparison with a cohort of patients with Kayexalate crystals in lower gastrointestinal specimens identified during the same period (11 patients) the frequency of associated mucosal damage was not significantly different (55%, p = 0.19), but no patient with upper gastrointestinal Kayexalate required surgical resection or died as a result of Kayexalate-induced mucosal injury. The results of this study provide evidence that Kayexalate in sorbitol can induce damage to the upper gastrointestinal tract. Recognition of Kayexalate crystals in histologic sections as a marker for sorbitol-induced mucosal damage may aid in establishing the correct diagnosis for clinically or endoscopically misleading lesions.

Aged↗