-
Golden Celik posted an update 7 days ago
Endoscopic resections (ERs) are both diagnostic and curative and should be performed by clinicians who are skilled with advanced endoscopic techniques. Proper preparation and handling of ERs are essential to assess histological parameters that dictate the curative nature of the procedure. Those parameters are adequacy of resection and risk of lymph node metastasis. The risk of lymph node metastasis is determined by depth invasion and presence of poor differentiation and lymphovascular invasion. Those adenocarcinomas with invasion up to muscularis mucosae (pT1a) and those with superficial submucosal invasion (pT1b) up to 500 µ with no poor differentiation and lymphovascular invasion and negative margins may be considered cured by endoscopic resections.Since the description of Helicobacter pylori (HP) as the most common cause of gastritis and its neoplastic complications, numerous articles have been written about the epidemiology, clinical features, diagnostic methods, histopathology, pathogenesis, molecular biology and treatment of this infection. This review focuses on those aspects of the infection that challenge the universality of the medical implications through the lens of evolutionary science applied to medicine. The divergent epidemiological and clinical outcomes observed in different populations and the possible beneficial aspects of the infection are discussed. Also reviewed are Correa’s seminal contributions to our understanding of gastric cancer in particular and postinflammatory tumours in general, and the renewed interest in intestinal metaplasia and its clinical implications.Despite the relative rarity of hereditary gastric cancer syndromes, the prompt recognition of their specific clinical features and histopathological characteristics is pivotal in offering patients the most appropriate treatment. In this article, we address the three major inherited syndromes that primarily affect the stomach hereditary diffuse gastric cancer (HDGC), caused by germline variants in CDH1 and CTNNA1; gastric adenocarcinoma and proximal polyposis of the stomach, caused by germline mutations in promoter 1B of APC; and familial intestinal gastric cancer, which has a poorly defined genetic cause. The main focus will be on HDGC, in light of the recent publication of updated clinical practice guidelines and emerging concepts regarding HDGC histopathology. In particular, we describe the broad morphological spectrum of HDGC lesions, stressing the importance of recognising indolent and aggressive phenotypes. Moreover, we discuss the increased risk of gastric (pre)malignancies developing in patients with other well-defined hereditary cancer syndromes, such as familial adenomatous polyposis, Lynch syndrome, Peutz-Jeghers syndrome, juvenile polyposis, Li-Fraumeni syndrome, and hereditary breast and ovarian cancer syndrome.Neuroendocrine neoplasms (NENs) of the gastrointestinal tract (GIT) comprise neuroendocrine tumours (NETs) and neuroendocrine carcinomas (NECs). During the last decade the classification and grading of GIT NENs has undergone significant changes, culminating in the World Health Organisation (WHO) 2019 classification. These changes, some of which are attributable to an only partially successful attempt to achieve uniform nomenclature among different organs, include slight changes to the cut-off used for the Ki-67 proliferative index to distinguish grade 1 from grade 2 NETs; an emphasis on the distinction between grade 3 NETs (low-grade NETs with a high proliferative rate) and NECs which, by definition, are all high grade; classification of tumours with mixed non-neuroendocrine and neuroendocrine differentiation as MiNENs; and replacement of the term ‘goblet cell carcinoid’ with ‘goblet cell adenocarcinoma’. While some of these changes seem minor, even semantic, each was made for very specific reasons which reflect an improved understanding of neuroendocrine neoplasia. The changes have definite implications for pathologists in clinical practice, not all of which may be readily apparent. This review is an attempt to explain the background behind each of the recent changes to the classification of neuroendocrine neoplasms of the gastrointestinal tract and summarise their impact on surgical pathologists – including a guide on how to approach certain recurrent difficulties encountered with the WHO 2019 system in routine clinical practice.The liberal use of upper endoscopy has led to an increased detection of gastric and duodenal polyps, which are identified in as many as 6 and 4.6% of patient examinations, respectively. PF-07220060 supplier Gastroduodenal polyps are a heterogeneous group of lesions that can be neoplastic or non-neoplastic (e.g. hyperplastic or heterotopical). Most polyps present characteristic topographical features, as well as endoscopic appearance and size. Evaluation of the surrounding mucosa is essential in assessing the underlying pathology (e.g. Helicobacter pylori, autoimmune gastritis or inherited polyposis syndromes). Phylogenetically, gastric and duodenal polyps can be classified according to the epithelial compartment from which they derive. Polyps that arise from the surface epithelium can either be of foveolar or intestinal type, and they can develop from either the native mucosa or the metaplastic epithelium (gastric intestinal metaplasia or duodenal foveolar metaplasia). Other polyps develop from the deeper glandular component, such as pyloric/oxyntic gland derived subtypes. In this review we focus upon epithelial polyps, with an emphasis on the most common and clinically relevant lesions, and present recently described entities.This review describes the indications and contraindications for endoscopic biopsy, in routine practice, of the upper gastrointestinal (GI) tract. We accept that this review provides grounds for controversy, as our stance in certain situations is counter to some national guidelines. Nevertheless, we provide evidence to support our viewpoints, especially on efficiency and economic grounds. We describe the particular controversies concerning the biopsy assessment of Barrett’s oesophagus, chronic gastritis and the duodenum in the investigation of coeliac disease. We accept that there are indications for more extensive upper GI biopsy protocols in children than in adults; the latter constitute our main focus in this article. We would encourage detailed discussion between pathologists and their endoscopy colleagues about the indications, or lack of them, for routine upper GI endoscopic biopsy, as studies have shown that adherence to agreed guidelines has resulted in a very considerable diminution in the biopsy workload without compromising patient management.