Intestinal Dysplasia Research Articles

A435 - Remission of Barrett's Esophagus after Sleeve Gastrectomy, A Case Study

Background: Barrett's Esophagus (BE),common in individuals with gastroesophageal reflux disease (GERD), pre-disposes the affected individual to the potential development of intestinal metaplasia, dysplasia and esophageal adenocarcinoma. Due to physiologic changes incurred post Laparoscopic Sleeve Gastrectomy (LSG), there is an increased risk of BE development, or progression in patients with active GERD. Because of this, many surgeons consider a patient who has BE to be contraindicated for LSG surgery.

The Microbiota of Gastric Premalignant Lesions: 16S Sequencing Data in a Central American Population

Introduction: Gastric cancer develops through a cascade, from gastritis to atrophic gastritis and gastric intestinal metaplasia, to dysplasia and adenocarcinoma. Helicobacter pylori (Hp) plays a prominent role in this cascade, contributing to the high cancer incidence in regions such as Central America, but the role of other bacteria is less defined. We compared the gastric microbiota of patients with and without premalignant lesions (atrophic gastritis or intestinal metaplasia). Methods: We sequenced the V3—V4 region of the 16S ribosomal RNA gene extracted from gastric corpus biopsies obtained during routine clinical endoscopies at the national university hospital in Leon, Nicaragua. Using the Illumina MiSeq platform and QIIME processing pipeline, we obtained microbiota measures of alpha diversity, beta diversity, and individual taxa-both phyla and operational taxonomic units (OTUs). We compared these measures between groups using the Kruskal—Wallis test. Results: Of 81 subjects, 30 had premalignant lesions and 51 did not, with characteristics described in Table 1. Firmicutes was the dominant phylum in both groups, but only composed 43% of sequences in the premalignant group, compared to 68% of non—premalignant sequences (Figure 1). The difference was related to the Proteobacteria phylum (35% of OTUs in premalignant and 18% in non—premaligant), predominantly from Hp. No differences in alpha or beta diversity existed between groups however, whether calculated with Hp reads included or excluded (Figure 2). Alpha diversity was correlated with number of Hp counts (p<0.001). One OTU was found to be significantly less prevalent in premalignant than non—premalignant samples. The OTU belonged to the Bacillales order of the Firmicutes phylum (p=0.006).1216_A Figure 1 No Caption available.1216_B Figure 2. Summary of phyla detected in gastric biopsy specimens with gastric intestinal metaplasia (GIM), multifocal atrophic gastritis (MAG), non—atrophic gastritis (NAG), and “normal” histology, with H. pylori OTUs included.Conclusion: In this study of the gastric corpus microbiome, premalignant lesions were associated with increasing Hp density and a corresponding decrease in Firmicutes, but otherwise limited differences in microbiota compared to stomachs with minimal or non—atrophic gastritis on histology. Additional areas warranting study include the antrum microbiome and the microbiome in higher risk premalignant lesions (e.g., incomplete gastric intestinal metaplasia or dysplasia).1216_C Figure 3. Box plots of mean alpha diversity of corpus biopsies with and without premalignant lesions (gastric intestinal metaplasia or multifocal atrophic gastritis), according to A) Observed OTUs, B) chao1 index, C) phylogenetic diversity, D) Shannon index. Helicobacter pylori reads are excluded. No significant difference between—group difference was detected for any measure.

Should We Screen Gastric Cancer in an Intermediate Gastric Cancer Risk Country?: International Award

Introduction: Gastric cancer is the fifth most common cancer and the third most common cause of cancer—related death worldwide. In high risk gastric cancer countries, gastric cancer screening is implemented but in intermediate risk countries it is debatable. The aims of this study were to evaluate the prevalence of active infection of Helicobacter Pylori as well as the presence of gastric cancer and gastric cancer precursors in an asymptomatic population submitted to colon cancer screening. Methods: We made a prospective study in an intermediate risk country of gastric cancer of patients undergoing colorectal cancer screening colonoscopy with general anesthesia and performed at the same time the upper endoscopy with blind biopsies from the gastric body and antrum, according to Sydney protocol. Results: We included 1364 Caucasian patients, 54.4% female, with mean age of 57.1±11.1 years. There was gastric cancer family history in 1.7% of the patients. Helicobacter Pylori infection was present in 41% in the gastric body and in 41.1% in the antrum. We found an incidence of gastric atrophy in both locations (gastric body and antrum) in 5.1% and intestinal metaplasia in 13.3%. There were 4 cases of low grade dysplasia and we diagnosed 12 gastric cancers (0.9%). Conclusion: The prevalence of Helicobacter Pylori was 41% and we found 12 gastric cancer in an asymptomatic population (0.9% incidence). As an intermediate risk gastric cancer country, we would recommend gastric cancer screening at the same time of colon cancer screening, followed by a structured surveillance program in case of intestinal metaplasia, dysplasia or gastric cancer.

Gastric Sarcoidosis: A Rare Manifestation of the Disease

Sarcoidosis is a chronic systemic inflammatory disease of unclear etiology characterized by non-caseating granulomas. It can affect nearly every organ system. Alimentary tract sarcoidosis is atypical within which gastric sarcoidosis is the most common form. Involvement of the alimentary tract is usually as a part of systemic disease or rarely as an isolated finding. Symptomatic gastric sarcoidosis is further more distinct. We present a rare case of sarcoidosis initially presenting with gastrointestinal symptoms and without pulmonary symptoms. A 57 years old morbidly obese African American female with PMH of HTN and DM type II presented with epigastric abdominal pain, nausea, vomiting, and a six month history of unintentional 60lb weight loss secondary to early satiety and dysgeusia. She was found to have hypercalcemia of 13.4 mg/dL, AKI and lactic acidosis. A non-contrast CT and subsequent CTA of the abdomen and pelvis showed small bowel wall thickening, abdominal lymphadenopathy, patent celiac axis and mesenteric vessels, and numerous ˜1mm lung base nodules. EGD revealed erythematous mucosa of gastric antrum with erosions and shallow duodenal erosions (Image 1). Gastric biopsy revealed granulomatous inflammation. Duodenal biopsy showed mild villous blunting without granulomas. Stains for fungal elements and AFB was negative. No intestinal metaplasia, dysplasia or malignancy was noted. PTH, PTHrP, and TSH were normal. CT chest revealed centrilobular nodular interstitial opacities with extensive bilateral mediastinal and hilar lymphadenopathy (Image 2). FNA of right hilar lymphadenopathy under EBUS revealed epithelioid histiocytes and lymphocytes suggestive of granulomatous inflammation. No malignant cells were seen. Fungal and AFB stains and AFB culture were negative. PPD skin test was negative. Patient's GI symptoms improved with supportive care. Given the lack of pulmonary symptoms, corticosteroids were not started. Patient has continued to do well during subsequent clinic follow up. Gastric sarcoidosis is among the rarer subsets of the disease. Most cases have been described as posthumous discoveries on autopsy of known sarcoidosis patients as patients are usually asymptomatic. Biopsy proven pulmonary and gastric sarcoidosis presenting with GI symptoms and an anomalous lack of pulmonary symptoms is exceptionally rare and questions a broader understanding for consideration of sarcoidosis diagnosis.2704_A Figure 1. Erythematous mucosa of gastric antrum with erosions on EGD. H. pylori negative.2704_B Figure 2. CT Chest: Centrilobular nodular interstitial opacities throughout both lungs with moderate mediastinal, hilar, and upper abdominal lymphadenopathy

A Rare Cause of Anemia and Abdominal Pain in an HIV-Positive Patient

47 year old Hispanic male with HIV since 2000 on emtricitabine-tenofovir and dolutegravir with past history of Shigella sp enterocolitis and prostatitis, GERD on omeprazole. He was referred for endoscopy due to two 2 cm polypoid lesions in gastric fundus found through work up of chronic abdominal pain and bloating. Patient had intermittent compliance with anti-viral and CD4 counts fluctuated between 324 and 22. He had normocytic anemia (Hematocrit 31.1, MCV 86.9). Quantiferon TB, syphilis RPR, JC virus were negative. Two 20 mm pedunculated polyps with bleeding stigmata were found (gastric cardia and body) and removed via endoscopic mucosal resection. Histologically, they had lobular proliferation of cytologically bland capillaries with surface erosion and neutrophil infiltrate consistent with pyogenic granuloma. Additionally, Helicobacter pylori and CMV immune-stains were positive. There was no intestinal metaplasia, dysplasia or carcinoma. Pyogenic granuloma is a benign highly vascular tumor with friable surface which bleeds on contact. It is rarely found in the GI tract outside of the oral cavity. Proposed causes are reaction to chronic mucosal trauma or inflammation/ infection. Pyogenic granulomas of the GI tract are important cause of blood loss anemia. In HIV patients, they are known to occur in skin and oral mucosa and should be differentiated histologically from Kaposi's sarcoma. Treatment involves endoscopic mucosal resection and there is risk for post-procedural bleeding.2033_A Figure 1. A: Polyp in gastric cardia C: Neutrophilic infiltrate surrounds capillaries2033_B Figure 2. B: Lobular capillary proliferation

Gastric precancerous lesions: interdisciplinary view at the problem

The timely identification and effective treatment of gastric precancerous lesions is one of the strategic tasks of modern gastroenterology. The article presents the integral view of clinicians and endoscopists on precancerous changes in the stomach mucous: intestinal metaplasia and dysplasia. The considerations have been given for modern understanding of their classification, pathogenesis and morphological substrate.

Endoscopic therapy for Barrett's esophagus and early esophageal cancer: Where do we go from here?

Since Barrett’s esophagus is a precancerous condition, efforts have been made for its eradication by various ablative techniques. Initially, laser ablation was attempted in non-dysplastic Barrett’s esophagus and subsequently, endoscopic ablation using photodynamic therapy was used in Barrett’s patients with high-grade dysplasia who were poor surgical candidates. Since then, various ablative therapies have been developed with radiofrequency ablation having the best quality of evidence. Resection of dysplastic areas only without complete removal of entire Barrett’s segment is associated with high risk of developing metachronous neoplasia. Hence, the current standard of management for Barrett’s esophagus includes endoscopic mucosal resection of visible abnormalities followed by ablation to eradicate remaining Barrett’s epithelium. Although endoscopic therapy cannot address regional lymph node metastases, such nodal involvement is present in only 1% to 2% of patients with intramucosal adenocarcinoma in Barrett esophagus and therefore is useful in intramucosal cancers. Post ablation surveillance is recommended as recurrence of intestinal metaplasia and dysplasia have been reported. This review includes a discussion of the technique, efficacy and complication rate of currently available ablation techniques such as radiofrequency ablation, cryotherapy, argon plasma coagulation and photodynamic therapy as well as endoscopic mucosal resection. A brief discussion of the emerging technique, endoscopic submucosal dissection is also included.

&lt;em&gt;Helicobacter pylori&lt;/em&gt; promotes gastric epithelial cell survival through the PLK1/PI3K/Akt pathway

PurposeHelicobacter pylori (H. pylori) infection plays a critical role in the process of gastric carcinogenesis. However, the complicated pathogenic mechanism is still unclear. Polo-like kinase 1 (PLK1) is involved in the development of multiple human malignancies, including gastric cancer. Therefore, this study aimed to elucidate the role of PLK1 in H. pylori-induced gastric carcinogenesis and the underlying signaling mechanism.Materials and methodsWe detected the expression of PLK1 in 166 patients in different stages of gastric carcinogenesis as well as the established Mongolian gerbil model with H. pylori infection by immunohistochemistry. Cell Counting Kit-8 was used to estimate the survival of gastric cancer cells.ResultsWe found that PLK1 expression in gastric cancer tissues was significantly higher than that of paired adjacent mucosa. PLK1 expression was increased in intestinal metaplasia, dysplasia, and gastric cancer tissues compared to chronic non-atrophic gastritis tissues. Notably, PLK1 expression was much lower in H. pylori-negative tissues than in H. pylori-positive tissues at intestinal metaplasia stage. In addition, H. pylori infection increased PLK1 expression in the gastric epithelial cells of the Mongolian gerbil model, which was positively related to the duration of H. pylori infection. Inhibition of PLK1 significantly reduced H. pylori-induced cell proliferation. Furthermore, incubation of MKN-28 cells with H. pylori resulted in a significant increase in PLK1, p-PTEN, and the downstream PI3K/Akt pathway, and pretreatment with a PLK1 inhibitor reversed these molecular changes.ConclusionPLK1 is involved in H. pylori-induced gastric carcinogenesis at the early stage by activating the PI3K/Akt signaling pathway. These results may contribute to the development of new control strategies for H. pylori infection-related gastric cancer.

Grafting's Function in Patients with Liver Intestinal and Multivisceral Transplantation

Introduction There are few studies of the intestinal graft function in medium and long term. Objectives Assess the functional status of the graft in transplantation patients, once the immediate post-transplant has been overcome. Methodology Patients who received a liver-intestinal or multivisceral transplantation were prospectively evaluated through cross-sectional data collection during a review. Clinical, analytical and functional variables are analyzed. Unstable patients with intercurrent processes were excluded. Results Twenty-six patients were analyzed, 65.38% of them male. 21 with multivisceral graft (80.76%) and 5 liver-intestinal (19.23%). 7 multivisceral grafts were retransplantation (26.92%). The average age at transplantation was 1.73 + / 3.22 years (range: 7 months - 13 years). The average time post-transplant was 3.78 +/- 3.69 years (range 1.5 - 14 years). The indication for transplant was volvulus (19.23%), necrotizing enterocolitis (15.38%), gastroschisis (15.38%), pseudo-obstruction (11.53%), atresia (7.69%) intestinal ischemia (7.69%), epithelial dysplasia (7.69%), MartínezFrías syndrome (3.84%), mitochondrial disease (3.84%) and Hirschsprung's disease (3.84%). 96.15% of patients are autonomous oral-enteral. 1 (3.85%) maintains home parenteral nutrition. 15.38% receive enteral nocturnal nutrition. 3 patients (11.53%) maintain ostomy.Fecal alpha 1-antitrypsin was normal in 92.30% of patients. Fecal elastase was normal at 100%. Faecal fat excretion was normal in 84.61% of patients, only 4 (15.38%) with a moderate steatorrhea. Blood parameters were normal in 100% of patients, including serum citrulline levels with a mean of 37.16 μmol / L (range 21-74). Conclusion 1. Patients with liver-intestinal and multivisceral transplantation have good graft function in medium and long term. 2. Most maintain digestive autonomy. 3. Although in some patients steatorrhea is observed, pancreatic function is normal in 100% of patients with a multivisceral transplantation that includes a pancreatic graft.

Reversal of Intestinal Failure in Children With Tufting Enteropathy Supported With Parenteral Nutrition at Home.

The aim of the study was to review long-term outcome of intestinal epithelial dysplasia (IED)/tufting enteropathy (TE) patients treated with parenteral nutrition (PN) at home managed by an intestinal failure (IF) rehabilitation service. Infants presenting from 1986 to 2010 with IF, and TE histology were retrospectively reviewed for up to 30 years. Data collected included outcome, presentation, nutrition (parenteral/enteral), country of residence, race, EpCAM gene, growth, bone age, and occupation. Thirteen patients (6 boys) in Malta and the UK with TE histology were established on home PN. Survival was 100% for UK children and 92% overall (1 death aged 13 months). Six patients (50% of the surviving 12) weaned off PN. Overall PN requirements reduced with increasing age and <7 infusions/week were needed by 10/12, 83% by 10 years, 6/8, 75% who had reached 15 years, 5/7, 71% who had reached 20, and all 4, 100% >25 years. Two of 12 cases weaned from PN by 10 years, 1 of 8 by 15 years, 3 of 7 by 20 years, and 3 of 4 or 75% >25 years. Seven Maltese patients homozygous for the same EPCAM gene abnormality had a similar outcome to the other cases. Weight, height, bone mineralization, bone age, and insulin-like growth factor-1 (IGF-1) levels were low, but improved with age. Patients achieved educational levels of parents and were employed. IED cases should have >92% chance of long-term survival and >50% chance of enteral autonomy by/in early adult life and 75% by 25 years. Even if PN dependent s/he can gain employment. Patients with IED managed on PN at home by an IF rehabilitation service should avoid intestinal transplant.

Differentially localized survivin and STAT3 as markers of gastric cancer progression: Association with Helicobacter pylori.

Localization and differential expression of STAT3 and survivin in cancer cells are often related to distinct cellular functions. The involvement of survivin and STAT3 in gastric cancer has been reported in separate studies but without clear understanding of their kinetics in cancer progression. We examined intracellular distribution of STAT3 and survivin in gastric adenocarcinoma and compared it with normal and precancer tissues using immunoblotting and immunohistochemistry. Analysis of a total of 156 gastric samples comprising 61 histologically normal, 30 precancerous tissues (comprising intestinal metaplasia and dysplasia), and 65 adenocarcinomas, collected as endoscopic biopsies from treatment naïve study participants, revealed a significant (P<.001) increase in overall protein levels. Survivin expression was detectable in both cytoplasmic (90.8%) and nuclear (87.7%) compartments in gastric adenocarcinomas lesions. Precancerous dysplastic gastric lesions exhibited a moderate survivin expression (56.7%) localized in cytoplasmic compartment. Similarly, STAT3 and pSTAT3 expression was detected at high level in gastric cancer lesions. The levels of compartmentalized expression of survivin and STAT3/pSTAT3 correlated in precancerous and adenocarcinoma lesions. Although overexpression of these proteins was found associated with the tobacco use and alcohol consumption, their expression invariably and strongly correlated with concurrent Helicobacter pylori infection. Receiver operating characteristic analysis of nuclear survivin, STAT3, and pSTAT3 in different study groups showed acceptable positive and negative predictive values with area under the curve above 0.8 (P<.001). Overall, our results suggest that overall increase in survivin and STAT3 and their subcellular localization are key determinants of gastric cancer progression, which can be collectively used as potential disease biomarkers and therapeutic targets for gastric cancer.

The gastric mucosal protective effects of astragaloside IV in mnng-induced GPL rats

Gastric Cancer is one of the most common types of cancer. And the occurrence of gastric carcinoma is an evolutionary histopathological stage. As a result, further research of GPL, which is a borderline of gastric cancer, is indispensable for preventing the formation and development of gastric carcinoma. Several studies have demonstrated a correlation between the expression of autophagy, apoptosis and Gastric cancer (GC). However, the effects of autophagy and apoptosis on human gastric cancer progression, particularly on gastric precancerous lesions (GPL), have not totally been investigated. At present, Astragaloside IV(AS-IV) is a saponin purified from Astragalus membranaceous Bge, a traditional Chinese herb that has been widely used for more than 2000 y in the treatment of cancer, cardiovascular and immune disorders. This study was designed to investigate the mechanism of AS-IV protecting gastric mucosa in N-methyl-N’-nitro-N-nitrosoguanidine (MNNG)-induced GPL rats. The lesions of GIM and GED were significantly ameliorated compared with the model rats, especially crowded tubular glandular and back-to-back tubular structure, which were the dangerous borderline between GPL and GC. Western Blot analysis showed that the ratio of Bcl-2/Bax and the protein expression of Bcl-XL, p53, Beclin1, p62, ATG5 and ATG12 were decreased and the level of Caspase3 was increased in the group of AS-IV compared with the model group; RT-PCR analysis showed that the gene expression Ambra1, Beclin1, ATG5, LC3 and p62 were decreased in the group of AS-IV compared with the model group. This research manifested that the occurrence of gastric cancer was preceded by a prolonged precancerous stage, which could be ameliorated by the AS-IV. Meanwhile, the mild and moderate stage of precancerous lesions is similar with gastric adenocarcinoma in critical biological processes, including inflammation, cell proliferation, differentiation. But this lesion is very different from cancer, because it does not appear obvious invasion and malignant lesions in this pathologic stag. Further, AS-IV could regulate p53 expression to activate the Ambra1/Beclin1 complex in GPL, and it will protect the gastric mucosal injury, prevent and cure gastric mucosal atrophy, intestinal metaplasia and atypical hyperplastic lesions. It provided a potential therapeutic strategy in reversing intestinal metaplasia and dysplasia of gastric precancerous lesions and protecting the gastric mucosa in GPL rats.

Tu1138 - Presence of a Nodule Independently Decreases Likelihood of Achieving Complete Remission of Intestinal Metaplasia (CR-IM) and Dysplasia (CR-D) in Barrett's Esophagus Patients Treated with Radiofrequency Ablation (RFA)

Tu1138 - Presence of a Nodule Independently Decreases Likelihood of Achieving Complete Remission of Intestinal Metaplasia (CR-IM) and Dysplasia (CR-D) in Barrett's Esophagus Patients Treated with Radiofrequency Ablation (RFA)

Systematic review and meta-analysis of the effectiveness of radiofrequency ablation in low grade dysplastic Barrett's esophagus.

Barrett's esophagus (BE) is a premalignant condition characterized by replacement of the esophageal lining with metastatic columnar epithelium, and its management when complicated by low grade dysplasia (LGD) is controversial. This systematic review and meta-analysis aimed to determine the efficacy of radiofrequency ablation (RFA) in patients with LGD. MEDLINE, EMBASE, and Web of Science were searched for studies including patients with BE-associated LGD receiving RFA (January 1990 to May 2017). The outcome measures were complete eradication of intestinal metaplasia (CE-IM) and dysplasia (CE-D), rates of progression to high grade dysplasia (HGD) or cancer, and recurrence. Eight studies including 619 patients with LGD (RFA = 404, surveillance = 215) were analyzed. After a median follow-up of 26 months (range 12 - 44 months), the overall pooled rates of CE-IM and CE-D after RFA were 88.17 % (95 % confidence interval [CI] 88.13 % - 88.20 %; P < 0.001) and 96.69 % (95 %CI 96.67 % - 96.71 %; P < 0.001), respectively. When compared with surveillance, RFA resulted in significantly lower rates of progression to HGD or cancer (odds ratio [OR] 0.07, 95 %CI 0.02 - 0.22). The pooled recurrence rates of IM and dysplasia were 5.6 % (95 %CI 5.57 - 5.63; P < 0.001) and 9.66 % (95 %CI 9.61 - 9.71; P < 0.001), respectively. RFA safely eradicates IM and dysplasia and reduces the rates of progression from LGD to HGD or cancer in the short term.

Management and prognosis of intestinal epithelial dysplasia

Management and prognosis of intestinal epithelial dysplasia

Epigenetic Silencing of the MLH1 Promoter in Relation to the Development of Gastric Cancer and its use as a Biomarker for Patients with Microsatellite Instability: a Systematic Analysis

Background/Aims: Human mutL homolog 1 (MLH1) promoter methylation was reported in gastric cancer (GC). This study determined the clinicopathological, prognostic, and diagnostic effects of MLH1 promoter methylation in GC. Methods: The combined odds ratio (OR) or hazard ratio (HR) and their corresponding 95% confidence intervals (95% CI) were calculated. The pooled sensitivity, specificity, and area under the curve (AUC) were analyzed. Results: A total of 4654 GC patients and 3669 non-malignant controls were identified in this systematic analysis. MLH1 promoter methylation was significantly higher in GC samples than in gastric adenomas, chronic gastritis, adjacent tissues, normal gastric mucosa, and normal healthy blood samples, but it exhibited a similar frequency in GC vs. intestinal metaplasia and dysplasia samples. MLH1 promoter methylation correlated with age and microsatellite instability (MSI), but it was not associated with gender, H. pylori infection, smoking, drinking behaviors, pathological histology, tumor differentiation, clinical stage, lymph node status, distant metastasis, or overall survival of GC. MLH1 promoter methylation exhibited a poor sensitivity value (< 0.5) in patients with GC compared with adjacent tissues, gastric adenomas, chronic gastritis, normal gastric mucosa, and normal healthy blood samples. The pooled sensitivity, specificity, and AUC of MLH1 promoter methylation in GC with MSI vs. GC with microsatellite stability (MSS) samples were 0.64, 0.96, and 0.90, respectively. Conclusions: Our results suggest that the detection of MLH1 promoter methylation may be a potential prognostic biomarker for GC patients with MSI.

Concurrent radiofrequency ablation and Nissen fundoplication

Endoscopic radiofrequency ablation (RFA) today represents a well-established, safe and effective procedure for the treatment of Barrett’s esophagus (BE). Choice of additional treatment to RFA emerges as an important clinical issue, due to the fact that recurrence of BE after complete eradication (CE) of intestinal metaplasia (IM) or dysplasia may occur. Concerning the data available so far, recurrence may occur due to insufficient reflux control with standard PPI’s regimen, while those with large hiatal hernia and long segment BE represent the subgroup of patients at highest risk for recurrence. Due to the anatomical deviation in distal esophageal segment proper ablation may be difficult in such patients. These patients can be treated by employing concurrent ARS and RFA. Concurrent ARS and RFA was proven to be safe, not time consuming, and it can be performed in conjunction with the basic rules of RFA procedure. Early results, in term of enhanced healing of treated epithelium, and possible reduction in number of ablation sessions needed to achieve CE of IM or dysplasia, are promising. To conclude, antireflux surgery may have important role in some patients undergoing RFA, especially those with significant hiatal hernia and anatomical impairment in distal esophageal segment.

Assessment of Patients with Hirschsprung Disease and the Use of Laparoscopy.

Objectives:This study aims to evaluate patients who were diagnosed and treated due to Hirschsprung disease (HD) in our clinic.Methods:We retrospectively evaluated the demographic and clinical findings of the patients with HD, who were operated in our clinic between January 2010 and December 2015.Results:During study period, 28 patients (19 male 9 female) were found to be operated due to HD in our clinic. Mean age was 16.8 months (1-168). “Transanal Endorectal Pull–through (TERPT)” was performed to 20 of them, Duhamell procedure to five and Soave procedure to three of them. TERPT was applied as laparoscopy assisted in four of them and biopsies were taken laparoscopically preoperatively from one of the patients from each group. Soave procedure was performed in three patients; one had anal stenosis and history of recurrent enterocolitis after TERPT procedure and pathologic analysis revealed neuronal intestinal dysplasia and the other one had total colonic HD and performed Soave procedure with colonic patch. Seven (25%) patients had enterocolitis. Frequencies of enterocolitis were three in two patients, two in two patients and one in three patients. Broad spectrum anibiotics and rectal washouts were supplied to these patients. Five of the seven patients with enterocolitis were operated with TERPT; two patients were operated with Duhamell procedure. Only one of them had total colonic HD. Three patients had total colonic HD diagnosis. Two of them were operated with Duhamell-Martin procedure and one was with Soave procedure with colonic patch according to Kimura technique. Anal stenosis developed in two patients after TERPT and treated with dilatations. Soiling rate was 3% (1/28) and this single patient was treated with laxatives and toilet training. Mean duration of hospitalization was 8.75 (2-14) days. Mean length of the removed intestinal segment was 23.6 (5-38) cm. Mean follow-up was for 35.5 (2-56) months. Neither of the patients was followed in the intensive care unit postoperatively nor died.Conclusion:TERPT procedure win priority in HD, but other procedures keep importance. Recently, laparoscopy-assisted TERPT is preferred in our clinic in HD therapy due to easy biopsy, full exposure to the transitional zone, the advantage of meso preparation of colon and prevention of strained anastomosis.

Clinicopathologic and outcome study of sessile serrated adenomas/polyps with serrated versus intestinal dysplasia.

It is believed that sessile serrated adenomas/polyps lead to the development of microsatellite unstable cancer via a dysplasia-carcinoma sequence. Little is known regarding the morphologic and biologic features, and outcome of sessile serrated adenomas/polyps with dysplasia, or of its specific dysplasia subtypes (intestinal versus serrated). The aims of this study were to analyze and compare the clinical, pathologic, and outcome characteristics of sessile serrated adenomas/polyps with serrated versus intestinal dysplasia. The study included 86 patients with sessile serrated adenomas/polyps with dysplasia (50 serrated dysplasia, 22 intestinal dysplasia, 14 mixed serrated and intestinal dysplasia). The clinical and pathologic features, and the prevalence rate of prior, concurrent, and future neoplastic lesions, were compared between sessile serrated adenomas/polyps with intestinal versus serrated dysplasia and with matched control patients with ≥1 conventional adenoma. The mean age of the patients, polyp size, and prevalence of adenocarcinoma within the polyps were significantly higher in sessile serrated adenomas/polyps with high versus low-grade dysplasia. Sessile serrated adenomas/polyps with intestinal dysplasia showed a significantly higher rate of adenocarcinoma (23%) compared with those with serrated dysplasia (6%, P=0.05), and the high-grade lesions occurred at a significantly younger age in the former compared with the latter (65 versus 76 years, P=0.05). Compared with patients with conventional adenomas, patients with sessile serrated adenomas/polyps with dysplasia showed a significantly higher rate of invasive carcinoma within the polyps (12 versus 0%, P=0.01) and a significantly lower association with prior or future conventional adenomas. Sessile serrated adenomas/polyps with dysplasia should be considered high-risk neoplastic precursor lesions, particularly those with intestinal dysplasia. Cancer may develop from sessile serrated adenomas/polyps with either type of dysplasia.

Interleukin-12 and interferon-γ acting on damp-heat of spleen-stomach syndrome triggered by helicobacter pylori

ObjectiveTo investigate the expression of and interleukin-12 (IL-12) and interferon-γ (IFN-γ) in relation to the pathology of damp-heat of spleen-stomach syndrome (DHSS) induced by Helicobacter pylori (H. pylori) infection. MethodsIn total, 114 individual gastric mucosal specimens including 83 DHSS, 19 spleen-qi deficiency syndrome (SQD) and 12 from healthy volunteers (CON) were collected by gastroscopy. To explore the relationship between the two syndromes and H. pylori infection, individual samples were tested using rapid urease and methylene blue tests. Hematoxylin and eosin stained sections were examined to grade for the degree of inflammation and inflammatory activity, and expression of IL-12 and IFN-γ was investigated by immunohistochemistry. ResultsStatistically significant differences in the degree of inflammation and inflammatory activity were observed between the groups of specimens: DHSS, SQD and CON (P < 0.05). Additionally, greater intestinal metaplasia (IM) and dysplasia were observed in the DHSS group, especially those with H. pylori infection. Expression of both IFN-γ and IL-12 was higher in DHSS samples infected with H. pylori than in uninfected samples and in the CON (P < 0.05) but not in the SQD (P > 0.05) groups. Intriguingly, in gastric specimens exhibiting IM and dysplasia, IL-12 translocated from the nucleus into the cytoplasm. ConclusionOur findings suggest that IL-12 and IFN-γ are involved in DHSS pathology, but not in SQD, acting as healthy-Qi. DHSS is not just the consequence of those two cytokines but results from the cross-talk between a number of cytokines and/or other proteins, which may warrant further investigation in DHSS patients infected with H. pylori.