Scandinavian journal of gastroenterology. Supplement最新文献

{"title":"IBD and genetics: new developments.","authors":"L E Oostenbrug,&nbsp;H M van Dullemen,&nbsp;G J te Meerman,&nbsp;P L M Jansen","doi":"10.1080/00855920310002717","DOIUrl":"https://doi.org/10.1080/00855920310002717","url":null,"abstract":"<p><strong>Background: </strong>Inflammatory bowel disease (IBD) is a complex disorder with an aetiology that is only partly understood. Apart from environmental factors, inheritance contributes to IBD.</p><p><strong>Review: </strong>Family studies show an increased risk among family members of a patient with IBD, particularly among first-degree relatives. In twin studies, concordance for disease type and localization is observed. In genetically isolated groups there is a higher prevalence of IBD. For instance. Ashkenazi Jews carry the highest risk. Further evidence comes from animal species that spontaneously develop IBD. Unlike Mendelian inheritance, in complex genetic diseases like IBD, genes are expected to be low penetrant and therefore less prone to selection, which results in higher expected gene frequencies. NOD2/CARD15, the first gene associated with IBD, is a polymorphic gene involved in the innate immune system. The gene has over 60 variations. Three of these play a role in 27% of patients with CD, with a predilection for patients with ileal disease.</p><p><strong>Conclusion: </strong>Genetics plays an important role in unravelling the pathogenesis of IBD leading to possible new therapeutic approaches.</p>","PeriodicalId":21517,"journal":{"name":"Scandinavian journal of gastroenterology. Supplement","volume":" 239","pages":"63-8"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24182704","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Surveillance for familial pancreatic cancer.","authors":"W H de Vos tot Nederveen Cappel,&nbsp;M A C Lagendijk,&nbsp;C B H W Lamers,&nbsp;H Morreau,&nbsp;H F A Vasen","doi":"10.1080/00855920310002762","DOIUrl":"https://doi.org/10.1080/00855920310002762","url":null,"abstract":"<p><strong>Background: </strong>It is estimated that between 5% and 10% of pancreatic cancer (PC) cases are due to hereditary factors.</p><p><strong>Methods: </strong>Review of the literature.</p><p><strong>Results: </strong>In families with clustering of PC, germline mutations in specific genes might be responsible for the disease. It is suggested that PC progresses from precursor lesions, the pancreatic intraepithelial neoplasias (PanINs). Several key genetic alterations in oncogenes (K-ras, Her2/neu) and tumour suppressor genes (p16, p53, SMAD4) occur in the progression from PanIN lesions towards PC. PC is mostly diagnosed on clinical presentation at an advanced, no longer resectable, stage. The overall 5-year survival rate is extremely poor. Recent studies report a better survival rate of PC, providing surgery takes place at an early stage. Surveillance of family members at increased risk for PC might lead to detection of tumours at an early stage and improve overall survival.</p><p><strong>Conclusion: </strong>Clinicians should be aware of the tumour syndromes that are associated with an increased risk of PC. Efforts to improve PC survival must focus on identification of high-risk patients, detection of early stage disease and novel screening strategies.</p>","PeriodicalId":21517,"journal":{"name":"Scandinavian journal of gastroenterology. Supplement","volume":" 239","pages":"94-9"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24182709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hepatitis C 2002 guidelines: summary and annotations.","authors":"H Orlent,&nbsp;J M Vrolijk,&nbsp;B J Veldt,&nbsp;S W Schalm","doi":"10.1080/00855920310002780","DOIUrl":"https://doi.org/10.1080/00855920310002780","url":null,"abstract":"<p><strong>Background: </strong>The current NIH and French consensus provide physicians with clear guidelines on how to care best for patients with hepatitis C.</p><p><strong>Methods: </strong>Review and discussion.</p><p><strong>Results: </strong>Confirming the diagnosis and guiding the initial investigations have become straightforward. The standard treatment and its monitoring have been described in many publications. Recommending therapy to patients with moderate fibrosis has been the custom since the 1999 EASL guidelines. The 2002 guidelines have widened the spectrum of patients with chronic hepatitis C that should be considered for antiviral therapy. Patient categories not previously considered for therapy, such as alcoholics, intravenous drug users, prison inmates and social subgroups of society that lack adequate medical care, can now be offered therapy provided they are well supported in specific programmes. Liver physicians have learned throughout the years to manage side effects successfully and encourage patient adherence. This is reflected in the higher sustained viral response rates with standard interferon and ribavirin reported in the pegylated interferon registration trials compared with the interferon-ribavirin trials. Reducing the dose rather than stopping therapy is the key issue. Antidepressive agents have their place in the management of mood disorders prior to or during therapy.</p><p><strong>Conclusion: </strong>Every patient with chronic hepatitis C should be considered for antiviral therapy. It is probably best for a patient to be treated by a physician who has experience in managing possible side effects and in coaching a patient through his 6 or 12 months of treatment.</p>","PeriodicalId":21517,"journal":{"name":"Scandinavian journal of gastroenterology. Supplement","volume":" 239","pages":"105-10"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24182711","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Surgical management of acute necrotizing pancreatitis: a 13-year experience and a systematic review.","authors":"V B Nieuwenhuijs,&nbsp;M G H Besselink,&nbsp;L P van Minnen,&nbsp;H G Gooszen","doi":"10.1080/00855920310002799","DOIUrl":"https://doi.org/10.1080/00855920310002799","url":null,"abstract":"<p><strong>Background: </strong>The course of acute pancreatitis (AP) is unpredictable and can vary from mild to lethal. Mortality varies from low (<2%) in mild cases to high (20%-70%) in the case of infected pancreatic necrosis. Surgical management has not been investigated in well-designed trials. Based on literature review and retrospective results from our institution, recent insights are summarized and recommendations concerning surgical treatment of AP are given.</p><p><strong>Methods: </strong>Data of patients who underwent necrosectomy for AP in our hospital in the period 1988-2001 were reviewed. Surgical treatment strategy was divided into open abdomen strategy (OAS) and primary closure with continuous postoperative lavage (CPL). An extensive database literature search was performed to obtain articles on surgical management of AP. Level 5 evidence articles were excluded.</p><p><strong>Results: </strong>In our institution, 38 patients were treated with OAS and 21 with CPL. Mortality was high (47% in the OAS group and 33% in the CPL group). The primary cause of mortality was multiorgan failure. Only 50 manuscripts from the literature search contained useful data. Mortality of patients with OAS and CPL treatment was 27% and 15%. respectively. Fewer cases of gastro-intestinal fistulas. bleeding and re-interventions were reported with CPL. The majority of all survivors regained a good quality of life.</p><p><strong>Conclusion: </strong>Mortality of acute necrotizing pancreatitis remains high, despite optimal surgical and medical treatment. Current surgical practice is not based on well-designed clinical trails. Randomized studies are needed to define evidence-based surgery in acute necrotizing pancreatitis.</p>","PeriodicalId":21517,"journal":{"name":"Scandinavian journal of gastroenterology. Supplement","volume":" 239","pages":"111-6"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24181492","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Options for screening for colorectal cancer.","authors":"W Atkin","doi":"10.1080/00855910310001421","DOIUrl":"https://doi.org/10.1080/00855910310001421","url":null,"abstract":"<p><p>Unlike other types of cancer, there are several options for screening for colorectal cancer (CRC). The most extensively examined method, faecal occult blood testing (FOBT), has been shown, in three large randomized trials, to reduce mortality from CRC by up to 20% if offered biennally and possibly more if offered every year. Recently published data from the US trial suggest that CRC incidence rates are also reduced by up to 20%, but only after 18 years. In this study, the number of positive slides was associated with the positive predictive value both for CRC and adenomas larger than 1 cm, suggesting that the reduction in CRC incidence was caused by the identification and removal of large adenomas. In this respect, this study supports the concept that removing adenomas prevents CRC. More efficient methods of detecting adenomas include the use of colonoscopy or flexible sigmoidoscopy (FS). Considerable evidence exists from case-control and uncontrolled cohort studies to suggest that endoscopic screening by sigmoidoscopy reduces incidence of distal colorectal cancer. However, in the absence of evidence from a randomized trial, several countries have been reluctant to introduce endoscopic screening. Three trialsare currently in progress (in the UK, Italy and the US) to address this issue. Two of these trials are examining the hypothesis that a single FS screen at around age 55-64 might be a cost-effective and acceptable method for reducing CRC incidence rates. Recruitment and screening are now complete in both studies and the first analysis of results on incidence rates is expected in 2004. Colonoscopy screening at 10-year intervals has recently been endorsed in the US on the basis that the reductions in incidence observed with distal CRC screening can be extrapolated to the proximal colon. However, data are lacking and a pilot study for a trial of the acceptability and efficacy of colonoscopy screening is in progress in the US. It has also been suggested that FOBT testing should be used to detect proximal CRC missed by sigmoidoscopy screening, but the small amount of published data suggest that supplementing FS with FOBT offers very little advantage over FS alone. Other forms of CRC screening are under investigation and represent exciting options for the future. Extraction of DNA from stool is now feasible and a number of research groups have shown high sensitivity for CRC using a panel of DNA markers including mutations in k-ras, APC, p53 and BAT26. Data so far indicate that, with the exception of k-ras, these markers are highly specific and therefore represent a significant improvement over FOBT. Whether these tests will replace or supplement existing methods of screening has yet to be determined. It has been suggested that BAT26, which is a marker of microsatellite instability, a feature of proximal sporadic CRC, might be a useful adjunct to sigmoidoscopy screening. Others have suggested that a test for occult blood should be included with","PeriodicalId":21517,"journal":{"name":"Scandinavian journal of gastroenterology. Supplement","volume":" 237","pages":"13-6"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/00855910310001421","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22428940","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Management of Barrett's esophagus with and without dysplasia.","authors":"G Triadafilopoulos","doi":"10.1080/00855910310001494","DOIUrl":"https://doi.org/10.1080/00855910310001494","url":null,"abstract":"<p><p>Barrett's esophagus (BE), a premalignant lesion to esophageal adenocarcinoma is associated with long-standing, gastroesophageal reflux disease (GERD). BE is a multi-phase process: during the initiation phase, genetically predisposed individuals (mostly white men) suffering from clinical or occult reflux damage their distal esophagus and form a new cell phenotype (incomplete intestinal metaplasia). During the formation phase, this phenotype occupies an area of variable surface (short or long-segment BE). During the progression phase, the metaplastic epithelium either remains dormant or progresses to dysplasia and adenocarcinoma. We review the recent clinical and basic research literature that explores the interaction of the refluxate (acid, bile, etc.) with BE. Acid and bile reflux variably affect BE and may cause dysplasia or adenocarcinoma. Regardless of the underlying biology, a patient with BE may suffer from GERD symptoms or may remain asymptomatic. Acid may be synergistic to bile or it could be antagonistic and protective. Acid suppressive therapy, if profound and continuous enough to abolish symptoms and esophageal acid exposure, may decrease proliferation, increase differentiation and reduce BE surface. Overexpression of cyclooxygenase-2 (COX-2), not entirely independent of acid/bile reflux, may increase proliferation and increase the invasiveness and metastatic potential of Barrett's metaplasia and neoplasia. Clinically, both acid and bile reflux need to be inhibited, either with potent acid-suppressing drugs or anti-reflux surgery. Cyclooxygenase inhibition using aspirin, NSAIDs or the safer COX-2 inhibitors added to these anti-reflux therapies may enhance the therapeutic benefit. Many questions remain unanswered. We still do not know why only a fraction of patients with GERD develop BE, what factors of the refluxate (acid, bile, etc.) initiate metaplasia and/or promote carcinogenesis, which patients are at risk for malignancy, and what is the best chemopreventive strategy. Ablation therapies and endoscopic mucosal resection are still under study.</p>","PeriodicalId":21517,"journal":{"name":"Scandinavian journal of gastroenterology. Supplement","volume":" 237","pages":"40-6"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/00855910310001494","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22428238","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Resolution of liver cirrhosis and prevention of hepatocellular carcinoma by interferon therapy against chronic hepatitis C.","authors":"M Omata,&nbsp;H Yoshida","doi":"10.1080/00855910310001502","DOIUrl":"https://doi.org/10.1080/00855910310001502","url":null,"abstract":"<p><p>Hepatocellular carcinoma (HCC) is one of the most important medical problems facing the Asian-Pacific region, where the prevalence of chronic hepatitis B and C is so high. Every year, we have approximately 500 admissions to our department due to this malignancy. It is of utmost importance that we have efficient screening, diagnosis and treatment. Over the past several years, there has been steady improvement in elucidating the super-high risk group for HCC, and in the management of these patients. I discuss how effectively we can screen patients by using three tests, conventional AFP, AFP-L3 (lectin fraction) and DCP (des-gamma-carboxy-prothrombin). With these tests we can detect HCC as small as 10 mm. In addition, imaging technology including CT-angiography can effectively pick up small cancer nodules. However, they are not always readily available in all Asian countries. Thus, diagnostic procedures and treatment methods can be modified in each country depending on the situation. One such treatment modality is the percutaneous therapy. The recent introduction of radiofrequency ablation (RFA) has dramatically changed our daily clinical practice. The time needed to treat cancer nodules of 2 to 3 cm in size has been reduced from 1 month or longer with ethanol injection to less than a week with RFA. However, the most important issue is to prevent infection and progression from chronic hepatitis to HCC. The recent introduction of improved antiviral therapy makes us feel optimistically that we might eventually have a comprehensive strategy for HCC in the region where it is most needed.</p>","PeriodicalId":21517,"journal":{"name":"Scandinavian journal of gastroenterology. Supplement","volume":" 237","pages":"47-51"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/00855910310001502","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22428239","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Current concepts of the irritable bowel syndrome.","authors":"E M M Quigley","doi":"10.1080/00855910310001403","DOIUrl":"https://doi.org/10.1080/00855910310001403","url":null,"abstract":"<p><p>The irritable bowel syndrome is one of the most common clinical problems encountered by the generalist and gastroenterologist. The goal of this review is to critically evaluate, based on available peer-reviewed literature, the current status of our understanding of the pathophysiology of the irritable bowel syndrome. The epidemiology of this disorder, including the characteristics of its presentation, natural history and associated phenomena, have been clarified. Differences between those who seek specialist care ('the consulters') and those in the community are now recognized. While, in both, symptoms may be similar in nature and severity; 'the consulters' are differentiated by how they react to their complaints. In terms of pathophysiology, the focus has moved to visceral sensation and central perception and has led to the identification of visceral hypersensitivity, visceral hyperalgesia and abnormal central perception of visceral events. This is not to dismiss dysmotility; subtle abnormalities in gas transit may be closely associated with the induction of certain symptoms. On the psychological front, attention now focuses on such complex issues as somatosization, abuse and response to major life events. Interactions between enteric flora, mucosal inflammation, immune phenomena and the enteric neuro-muscular apparatus also attract interest; the entity of post-infectious irritable bowel is now clearly recognized and there is experimental evidence to suggest a role for inflammation. While the precise aetiology of irritable bowel syndrome remains uncertain, considerable progress has been made, with recent advances in pathophysiology offering hope for the development of new therapeutic approaches.</p>","PeriodicalId":21517,"journal":{"name":"Scandinavian journal of gastroenterology. Supplement","volume":" 237","pages":"1-8"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/00855910310001403","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"22428938","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sense and nonsense of lipids in artificial nutrition.","authors":"A H J Naber","doi":"10.1080/00855920310002636","DOIUrl":"https://doi.org/10.1080/00855920310002636","url":null,"abstract":"<p><p>Lipids are a component of artificial nutrition. For 20 years lipids covered only a limited percentage of the energy requirement of the patient, depending on parenteral nutrition. Ideas about dose, type and aims of lipids administration in artificial nutrition have changed during this period. The study is based on the discussion around lipids in artificial nutrition.</p>","PeriodicalId":21517,"journal":{"name":"Scandinavian journal of gastroenterology. Supplement","volume":" 239","pages":"11-4"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24181044","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pathophysiological characteristics of long- and short-segment Barrett's oesophagus.","authors":"P Zentilin,&nbsp;S Reglioni,&nbsp;V Savarino","doi":"10.1080/00855920310002681","DOIUrl":"https://doi.org/10.1080/00855920310002681","url":null,"abstract":"<p><strong>Background: </strong>Depending on the length of the segment of columnar epithelium in the distal oesophagus, Barrett's oesophagus can be divided into long-segment and short-segment Barrett's oesophagus. This article describes the pathophysiological characteristics of both forms of Barrett's oesophagus.</p><p><strong>Methods: </strong>Review of the literature.</p><p><strong>Results: </strong>Although there is some disagreement, ours and most other studies suggest that long-segment columnar-lined oesophagus is causally linked to chronic gastro-oesophageal reflux and that this from of Barrett's oesophagus is characterized by lower oesophageal sphincter tone, reduced oesophageal contractility and increased acid reflux. Short-segment Barrett's oesophagus is also associated with acid reflux, but the degree of oesophageal acid exposure and the level of other pathophysiological alterations seem to be lower.</p><p><strong>Conclusion: </strong>Pathophysiological abnormalities appear to be more prominent in long-segment Barrett's oesophagus than in short-segment Barrett's oesophagus.</p>","PeriodicalId":21517,"journal":{"name":"Scandinavian journal of gastroenterology. Supplement","volume":" 239","pages":"40-3"},"PeriodicalIF":0.0,"publicationDate":"2003-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"24181049","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}