Résection endoscopique des tumeurs digestives: indications, critères de qualité et resultats

Endoscopic resection of digestive tumors: indications, quality criteria and results In the past decade, two developments have changed the approach to superficial digestive tumors: 1) new endoscopic techniques allow "en bloc" resection of superficial tumors with almost no limit in tumor diameter and 2) the risk of lymph node metastases is better stratified (e.g., in the colon, the risk of lymph node metastasis is negligible for superficial malignant invasion of the submucosa). Endoscopic submucosal dissection (ESD) allows "en bloc" resection of large laterally-spreading tumors, in contrast with prior resection techniques (endoscopic mucosal resection - EMR) that required piecemeal resection for large tumors. As a result, relapse rate is lower with ESD compared to EMR. Pathological examination is also more reliable with "en bloc" specimens; it must precisely assess resection margins and the depth of malignant invasion

Do eosinophil numbers differentiate eosinophilic esophagitis from gastroesophageal reflux disease?

CONTEXT: Although the healthy esophageal mucosa contains no eosinophils, eosinophilic infiltration is observed in 2 major clinicopathologic settings: gastroesophageal reflux disease (GERD) and eosinophilic esophagitis (EE). The prevalence of EE is increasing in many countries, and this increase seems only partly to be due to a better awareness of the pathology, following the relatively recent description of EE. Gastroesophageal reflux disease and EE represent 2 entities that do not respond to the same treatment modalities and, thus, need to be distinguished. However, diagnostic criteria of EE have been defined arbitrarily, and the more recent articles tend to prove that the overlap with GERD is probably greater than initially believed, leading the authors to advise strict exclusion of GERD before considering the diagnosis of EE. OBJECTIVES: To provide pathologists with the currently proposed histologic criteria of GERD and EE, to stress the need to combine these criteria with clinical data and endoscopic findings, and to outline the remaining controversies. DATA SOURCES: This review is based on selected articles identified by a PubMed (US National Library of Medicine, Bethesda, Maryland) search of the literature in English for GERD and EE, a recent review by the American Gastroenterological Association (Bethesda), the Proceedings of the First International Gastrointestinal Eosinophil Research Symposium, and the authors' experience. CONCLUSION: Proper identification of the etiology of eosinophilic infiltration of the esophagus allows accurate medical or surgical treatment and follow-up. Eosinophilic esophagitis and GERD diagnoses require integration of the histologic findings with the clinical and endoscopic data

Le syndrome de Lynch: pathologiste et praticien peuvent ensemble réduire le risque de cancer

Lynch syndrome is an autosomal dominant disease associated with an important risk of cancer, mainly endometrial and colorectal-cancer. This risk can be efficiently lessen by an appropriate screening as far as the mutations carriers are identified. As current clinicopathological recommendations lack sensitivity, a systematic pre-screening of every patient with a colorectal or endometrial cancer can be proposed. Oncogenetic units of the HUG in Geneva and ICHV in Valais have set up a population-based study to evaluate the efficacy of such a strategy. Whatever the approach, the pathologist is directly implicated as Lynch syndrome harbors specific histological aspects that can help to its identification, but also as pre-screening tests are directly realized on tumor-tissue

Atteintes médicamenteuses du tractus gastro-intestinal: une revue clinico-pathologique

Many drugs are known to have adverse effects on the gastrointestinal tract. The consequences can range from asymptomatic histological lesions in the gastrointestinal mucosa to fatal complications such as haemorrhage or perforation. On the biopsies (or on surgical specimens), there is a limited number of injury pattern that should suggest drug-induced pathology. They are mostly non specific (ex: ulcer). However, some drugs may induce pathognomonic histological lesions. For this reason, the diagnosis of a drug-induced gastrointestinal pathology depends on a clinicopathological correlation and implies a good communication between the pathologist and the clinician. In this review, we focus on the most common and well-described drug-related clinico-pathological conditions of the gastrointestinal tract using an organ and lesion based approach

Recurrence of type 1 diabetes after simultaneous pancreas-kidney transplantation in the absence of GAD and IA-2 autoantibodies

We report herein the patterns of type 1 diabetes recurrence in a simultaneous pancreas-kidney transplant (SPK) recipient, in the absence of rejection. A 38-year-old female underwent SPK for end-stage nephropathy secondary to type 1 diabetes. Fasting blood glucose, HbA1c, fructosamine, C-peptide and autoantibodies (GAD-65, IA-2) were monitored throughout follow-up. At 3.5 years post-SPK, HbA1c and fructosamine increased sharply, indicating loss of perfect metabolic control, despite C-peptide levels in the normal-high range. Exogenous insulin was restarted 4 months later. C-peptide levels abruptly fell and became undetectable at 5.5 years. Autoantibody levels, which were undetectable at the time of SPK, never converted to positivity. Pancreas retranspantation was performed at 6 years. The failed pancreas graft had a normal macroscopic appearance. On histology, there were no signs of cellular or humoral rejection in the kidney or pancreas. A selective peri-islet lymphocytic infiltrate was observed, together with near-total destruction of β cells. At 2.5 years post retransplantation, pancreatic graft function is perfect. This observation indicates unequivocally that pancreas graft can be lost to recurrence of type 1 diabetes in the absence of rejection. GAD-65 and IA-2 autoantibodies are not reliable markers of autoimmunity recurrence

Grading epithelial atypia in endoscopic ultrasound-guided fine-needle aspiration of intraductal papillary mucinous neoplasms: an international interobserver concordance study

Preoperative cytological analysis of cyst fluid from intraductal papillary mucinous neoplasms (IPMN) contributes to risk stratification for malignancy. To the authors' knowledge, agreement among pathologists in grading epithelial atypia in IPMN cyst fluids has not been studied to date

Acinar cell carcinoma: a possible diagnosis in patients without intrapancreatic tumour

BACKGROUND: Acinar cell carcinomas of the pancreas are rare neoplasms. Usually diagnosed at an advanced stage, in general they are large solid pancreatic tumours with an average size of more than 10 cm. AIMS AND RESULTS: We report 3 cases of acinar cell carcinomas involving the peripancreatic lymph nodes, the liver hilum and the colon respectively, without clinical or pathological evidence of pancreatic tumours. These highly cellular neoplasms showed a predominantly acinar cell differentiation intermingled with a ductal component, with intracellular or extracellular mucin production by at least 25% of tumour cells. In addition, one case showed endocrine differentiation. Diffuse immunoreactivity for acinar enzymes trypsin and chymotrypsin was present in all cases. CONCLUSION: The occurrence of acinar cell carcinomas outside the pancreas underlines the notion that acinar cell carcinomas may originate in extrapancreatic sites and probably develop from heterotopic or metaplastic pancreatic foci present along the biliary tract

Extensive biliary intraepithelial neoplasia (BilIN) and multifocal early intrahepatic cholangiocarcinoma in non-biliary cirrhosis

Biliary intraepithelial neoplasia (BilIN), a preneoplastic condition that may precede invasive intrahepatic cholangiocarcinoma (ICC), has been compared to pancreatic intraepithelial neoplasia (PanIN), a precursor lesion of pancreatic carcinoma. Biliary tract carcinoma development and progression is associated with several gene alterations, but BilIN lesions have yet to be studied in detail by molecular techniques. We describe a case of extensive intrahepatic biliary dysplasia, with lesions ranging from BilIN-1 to BilIN-3 lesions, and multifocal microscopic ICC in hepatitis C virus (HCV)- and alcohol-related cirrhosis. The small ICC foci had remained undetected prior to transplantation. Fluorescence in situ hybridization (FISH) analysis was performed on three foci of BilIN-3 lesions and on three microinvasive ICC foci with a combination of three FISH probes directed against genes frequently altered in pancreatic and biliary tract carcinomas. FISH analysis revealed a CDKNA2 heterozygous deletion in one BilIN-3 focus, and in one non-contiguous ICC focus, although the deletion was just above the chosen threshold. No deletions were detected in the genomic regions encoding TP53 and SMAD4. This report documents for the first time the development of multifocal ICC in the setting of extensive biliary dysplasia in a patient with three risk factors, HCV infection, alcohol abuse, and cirrhosis, and suggests heterogeneous carcinogenesis in ICC and possible involvement of the CDKNA2 gene