Journal of Gastrointestinal & Digestive System最新文献

Background: There is increasing evidence that endoscopic mucosal healing (EMH) is a key target in inflammatory bowel disease (IBD) therapy. However, there is limited evidence of EMH rates with conventional IBD therapy outside of Western population groups.

Ai̇m: To evaluate the role of azathioprine (AZA) in inducing EMH in IBD patients.

Methods: Patients with inflammatory bowel disease were evaluated in terms of endoscopic mucosal healing and the incidence of surgical interventions during the azathioprine treatment between 1995 to 2014.

Results: A total of 120 inflammatory bowel disease patients were enrolled. Endoscopic mucosal healing was found in 37% patients with inflammatory bowel disease (42% in chronic ulcerative colitis and 33% in Crohn's disease). Male gender had a negative impact on the efficacy of azathioprine (P<0.05). Responder inflammatory bowel disease patients were older (age at the IBD diagnose) than the nonresponder (P<0.05). Azathioprine therapy reduced the number of the surgical interventions (P<0.05).

Conclusi̇on: We showed that azathioprine therapy significantly induced endoscopic mucosal healing in biologic naïve patients with active inflammatory bowel disease as well as decreasing the surgical interventions, with negative predictive factors identified by a younger age at IBD presentation and male gender.

The present report describes a 50-year-old female recently diagnosed with multiple myeloma who presented with hepatosplenomegaly, miliary-type hyper enhancing liver tumors, and esophageal varices. We performed a transjugular liver biopsy when liver biopsy was requested to evaluate the miliary-type liver lesions. This was done to lower the risk of bleeding given the patient's anemia and probable portal hypertension. This approach was successful in safely providing diagnostic samples for surgical pathology and flow cytometry to assess the nature of focal miliary liver lesions. It also proved portal hypertension.

Introduction: The aim of this study was to investigate and analyze the incidence of early-onset colorectal cancer in Arizona, using the Arizona Cancer Registry.

Methods: We performed a retrospective analysis of patients with colorectal cancer reported in the Arizona Cancer Registry from 1995-2010. Outcome measure: incidence of CRC in patients younger than 50 years.

Results: 39,623 cases of colorectal cancer were reported to the Arizona Cancer Registry during a period of 15 years. Overall, there was a 17% decrease in the incidence of CRC. However, there was a 23% increase in incidence among patients in the age group 10-50. During the same time period, 15% and 41% increase in the incidence of colon and rectal cancer was observed, respectively. The most significant increase (102%) in overall CRC incidence was seen in the age group 10-29. The highest increase (110%) in incidence of colon cancer was observed in the same age group, while the most significant increase in incidence rates (225%) of rectal cancer was seen in the age group 30-34.

Conclusion: Although there is an overall decrease in incidence of colorectal cancer in Arizona, alarming increase in incidence of early-onset CRC was observed; mirroring the national trends.

Background: Despite the decreasing incidence of colorectal cancer (CRC) over the past three decades disparities remain in its incidence, stage at presentation, and efficiency of staging and treatment between different communities, particularly when comparing urban and rural areas. The aim of the study was to assess disparities that exist in CRC outcomes among urban, international border counties, and non-border counties in Arizona.

Methods: A retrospective analysis of CRC data from the Arizona Cancer Registry was performed. Data obtained included age, sex, ethnicity, tumor grade, and tumor stage. The data was then categorized into three sections: international border counties, urban counties, and rural counties. The outcome measure was stage of CRC at diagnosis.

Results: There were a total of 39, 958 reported incident cases of colorectal cancer from 1995-2010. Of the total incident cases, 53.1% were male and the average age at diagnosis was 69.5. 86.6% were white non-Hispanic, 8.37% Hispanic, 2.4% African American, 1.7% Native American and 1% Asian. There was a significant decrease in the incidence of CRC in all counties, 24.08% in border, 22.5% in urban, and 12.3% in rural. Rural counties showed a higher number of observed cases than expected cases of stage 4 CRC and more unknown diagnosis of grade, stage and lymph node assessment as determined by the adjusted residual.

Conclusion: Patients in rural counties are more likely to present with a higher stage of CRC and are less likely to have their cancer adequately staged. This is likely due to lack of better access to healthcare, lack of awareness and poor education and also inadequate specialists.

Phytobezoars are a rare cause of small bowel obstruction. Such cases are most commonly associated with previous abdominal surgery or poor dentition or psychiatric conditions. A 40 year old man with a virgin abdomen and excellent dentition and no underlying psychiatric condition presented with an acute abdomen. CT scan revealed a transition point between dilated proximal loops of small bowel and collapsed distal loops. Exploratory laparotomy revealed a phytobezoar unable to be milked into the cecum and an enterectomy with primary anastamosis was performed without complication. A detailed history revealing several less common predisposing factors for phytobezoars should increase clinical suspicion of a phytobezoarinduced small bowel obstruction in the setting of an acute abdomen. Vigilance in presentations of an acute abdomen improves the usefulness of medical imaging, such as a CT, to detect phytobezoars. Understanding mechanisms of phytobezoar formation helps guide management and may prevent surgery.

Patients with celiac disease (CD) are increasingly interconnected through social media, exchanging patient experiences and health-tracking information between individuals through various web-based platforms. Social media represents potentially unique communication interface between gastroenterologists and active social media users - especially young adults and adolescents with celiac disease-regarding adherence to the strict gluten-free diet, gastrointestinal symptoms, and meaningful discussion about disease management. Yet, various social media platforms may be underutilized for research purposes to collect patient-reported outcomes data. In this commentary, we summarize the scientific rationale and potential for future growth of social media in patient-reported outcomes research, focusing on college freshmen with celiac disease as a case study and provide overview of the methodological approach. Finally, we discuss how social media may impact patient care in the future through increasing mobile technology use.

Asbestos-related diseases, such as malignancies and asbestosis, remain a significant occupational and public health concern. Asbestos is still widely used in many developing countries despite being a recognized carcinogen that has been banned over 50 countries. The prevalence and mortality from asbestos-related diseases continue to pose challenges worldwide. Many countries are now experiencing an epidemic of asbestos-related disease that is the legacy of occupational exposure during the 20th century because of the long latency period (up to 40 years) between initial asbestos exposure and exhibition of disease. However, the gastrointestinal (GI) cancers resulting from asbestos exposure are not as clearly defined. In this review, we summarize some of the recent epidemiology of asbestos-related diseases and then focus on the evidence implicating asbestos in causing GI malignancies. We also briefly review the important new pathogenic information that has emerged over the past several years that may account for asbestos-related gastrointestinal cancers. All types of asbestos fibers have been implicated in the mortality and morbidity from GI malignancies but the collective evidence to date is mixed. Although the molecular basis of GI cancers arising from asbestos exposure is unclear, there have been significant advances in our understanding of mesothelioma and asbestosis that may contribute to the pathophysiology underlying asbestos-induced GI cancers. The emerging new evidence into the pathogenesis of asbestos toxicity is providing insights into the molecular basis for developing novel therapeutic strategies for asbestos-related diseases in future management.

Mucins are high-molecular-weight glycoproteins expressed throughout the gastrointestinal tract, with a key role in mucosal protection and function. In gastric cancer expression of MUC5AC and MUC1 is reduced and denovo expression of MUC2 occurs. With progressive loss of tumor differentiation and increased tumor stage, expression of MUC5AC and MUC1 is further reduced, and MUC2 decreases. Isolated MUC2 expression (the intestinal phenotype) correlates with metastatic spread and poor survival. There is emerging evidence that MUC1 acts as an oncoprotein when overexpressed. The cytoplasmic tail of MUC1 interacts with the H. pylori virulence factor cagA and is a major effector of the wnt-β catenin intracellular signalling cascade. Polymorphism in the MUC1 gene has been identified in gastric cancer patients and may have a prospective role in the stratification of high-risk subjects. The MUC1 gene also mediates resistance to the recombinant HER2/neu antibody trastuzumab. Future research efforts will examine targeting MUC1 for therapeutic purposes.

We used a database of 4139 Taiwanese HCC patients to take a new approach (Network Phenotyping Strategy) to HCC subset identification. Individual parameters for liver function tests, complete blood count, portal vein thrombosis, AFP levels and clinical demographics of age, gender, hepatitis or alcohol consumption, were considered within the whole context of complete relationships, being networked with all other parameter levels in the entire cohort. We identified 4 multi-parameter patterns for one tumor phenotype of patients and a separate 5 multi-parameter patterns to characterize another tumor phenotype of patterns. The 2 subgroups were quite different in their clinical profiles. The means of the tumor mass distributions in these phenotype subgroups were significantly different, one being associated with larger (L) and the other with smaller (S) tumor masses. These significant differences were seen systematically throughout the tumor mass distributions. Essential and common clinical components of L-phenotype patterns included simultaneously high blood levels of AFP and platelets plus presence of portal vein thrombosis. S included higher levels of liver inflammatory parameters. The 2 different parameter patterns of L and S subgroups suggest different mechanisms; L, possibly involving tumor-driven processes and S more associated with liver inflammatory processes.

The epithelium of gastrointestinal (GI) mucosa has the most rapid turnover rate of any tissue in the body and its integrity is preserved through the dynamic balance between cell migration, proliferation, growth arrest and apoptosis. To maintain tissue homeostasis of the GI mucosa, the rates of epithelial cell division and apoptosis must be highly regulated by various extracellular and intracellular factors including cellular polyamines. Natural polyamines spermidine, spermine and their precursor putrescine, are organic cations in eukaryotic cells and are implicated in the control of multiple signaling pathways and distinct cellular functions. Normal intestinal epithelial growth depends on the available supply of polyamines to the dividing cells in the crypts, and polyamines also regulate intestinal epithelial cell (IEC) apoptosis. Although the specific molecular processes controlled by polyamines remains to be fully defined, increasing evidence indicates that polyamines regulate intestinal epithelial integrity by modulating the expression of various growth-related genes. In this review, we will extrapolate the current state of scientific knowledge regarding the roles of polyamines in gut mucosal homeostasis and highlight progress in cellular and molecular mechanisms of polyamines and their potential clinical applications.