Gastric pseudocarcinomatous regeneration

Gastric pseudocarcinomatous regeneration

S16 Pathology (2014), 46(S2) PATHOLOGY 2014 ABSTRACT SUPPLEMENT educational resources both for initial and on-going training, and the demonstration...

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Pathology (2014), 46(S2)


educational resources both for initial and on-going training, and the demonstration of attainment of competency in the key areas of medical knowledge, patient care, communication, system-based practice, professionalism, and practice-based learning.

Gastrointestinal Pathology: SY10-1

Frontier in Pathology: SY24-1

Chronic inflammatory bowel disease (CIBD) infers ulcerative colitis, Crohns disease and the pathological spectrum between, encompassing indeterminate colitis in resections and IBDU on biopsy. Histological assessment remains the gold standard for CIBD diagnosis and yet there are many conditions that show pathological mimicry of CIBD. It cannot be overemphasised that context is a critical determinant of the pathological diagnosis in inflamed colorectal biopsies. The lecture will focus on drug-induced colitis, diverticular colitis, focal active colitis, microscopic colitis and secondary colitis. All these conditions show pathological features similar to those seen in CIBD. There are also interesting parallels and associations between these conditions and CIBD. A small proportion of diverticular colitis cases will eventually re-present with classical ulcerative colitis, despite, initially, a normal rectal histology. In a similar proportion of cases, focal active colitis precedes the onset of classical Crohns disease. Drugs, especially NSAIDs, have an extraordinary relationship with CIBD. They cause (?), they mimic, they exacerbate, they induce and they treat CIBD. The diligent pathologist must be aware of the important mimics of CIBD and ensure that they are fully cognisant with the clinical, endoscopic, microbiological and radiological context before committing a patient to a definitive diagnosis of CIBD.

DIGITAL PATHOLOGY 101 (FRONTIERS OF PATHOLOGY) Lewis Allen Hassell1, Dirk Soenksen2, Curtis Stratman3, Elizabeth Chlipala4 and Liron Pantanowitz5 1University of Oklahoma Health Sciences Center, 2Ceresti Health, 3GE Healthcare, Omnyx, 4Premier Labs, and 5University of Pittsburgh Medical Center, USA This symposium will provide participants with a broad introductory overview of the field of digital pathology (DP), including: 1) Applications, benefits and limitations of DP. 2) DP technology issues (primarily whole slide imaging). 3) Regulatory, workflow and financial considerations. 4) Hands-on session focused on basic digital slide viewing using a variety of digital slides if possible. We will also cover the recently updated guidelines from the American Telemedicine Association on Telepathology, with particular reference to their impact on use of digital pathology.

MIMICS OF INFLAMMATORY BOWEL DISEASE Neil A. Shepherd Gloucestershire Cellular Pathology Laboratory, UK

Frontier in Pathology: SY24-4 TEACHING AND TESTING CRITICAL CLINICAL REASONING IN PATHOLOGY Shivayogi Bhusnurmath and Bharti Bhusnurmath Department of Pathology, St Georges University School of Medicine, Grenada, West Indies It is important for pathology residents to learn to critically evaluate the current information on various laboratory investigations as well as special tests used in the interpretation of biopsy and cytology slides and choose the most appropriate procedure in a given situation. They should be able to scientifically justify each step in their application and interpretation. Modified essay questions have been found to be a great tool to teach and test such critical reasoning. The usual teaching and testing tools like PowerPoint presentations, multiple choice questions or essay questions permit a fair amount of guess work and the learning outcome and scores do not necessarily reflect the accuracy of the judgements which a resident is capable of making. In generating modified essay questions, we give a brief description of the problem situation, e.g., a biopsy slide description of H&E stain from a given site along with any relevant clinical data like age, gender, main symptoms and signs. The last sentence is a question asking the resident to write in one word which immunocytochemistry stain would be most useful in confirming the diagnosis. No choices are mentioned. If the resident writes more than one choice, the score would be zero. Thus the residents are trained to critically evaluate the given data to come up with a specific laboratory solution. Multiple such situations will be illustrated. The modified essay questions are great tools for such teaching and evaluation for both residents and medical students.

Gastrointestinal Pathology: SY10-2 GASTRIC PSEUDOCARCINOMATOUS REGENERATION Michael Vieth Insitute of Pathology, Klinikum Bayreuth, Bayreuth, Germany Introduction: NSAID and ASA intake for various reasons is a widespread worldwide phenomenon. The first gastroscopic observation of ASA effects in the stomach dates back to 1938. Up till the beginning of the 1990 s before the era of Helicobacter eradication 70% of all gastric ulcers were connected to Helicobacter infection. From the beginning of the 21st century almost 70% of gastric ulcers are now believed to be based on NSAID/ASA intake. NSAID damages the epithelium in three ways: a) direct damage by inhibition of prostaglandin, b) inducing complications in preexisting ulcers, c) enhanced bleeding (due to inhibition of platelet aggregation). Besides these systemic effects, topical effects may play a role in ulcer etiogenesis with entrapment of Hþ ions within the cells by ion trapping. In conjunction with swelling of the cappilary endothelium these processes lead to the typical ischemic necrosis in NSAID ulcerations. It has been shown earlier that such typical necrosis may help to identify the etiology of gastric erosions and ulcerations. Regernating cells and ischemic damage may lead to hyperchromatic, pleomorphic cells that may sometimes be mixed up with carcinomatous changes. We aimed to answer the question how many gastric biopsies were erroneously assigned representing neoplastic changes instead of regenerative changes in cases that were sent in for second opinion. Patients and methods: Within ten years 738 gastric biopsy cases with suspicion for neoplasia were sent in for second opinion.

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Among these 228 cases were downstaged to pseudoneoplastic regeneration, 489 clear cut gastric carcinomas and 19 cases were diagnosed as tubular adenoma (LGD). Results: There were no gender differences in cases with regenerative changes (1.1:1) and adenomas (0.9:1) but carcinomas were more likely to be diagnosed in males (1.6:1). Patients with regernative changes significantly younger than carcinoma patients (62.8 vs 68.3 years). Regenerative lesions were found in 80% of the cases in the antrum whereas only 62% of the carcinomas occurred in the antrum. Following the time line from 2001 to 2011 it became evident that the overdiagnosis of regenerative changes as carcinomatous lesions decreased to 20% from the intial number in 2001. In parallel an increase in correct carcinoma diagnoses was observed. The gastritis status may help in a questionable situation since in regenerative changes less than 20% of the individuals had an active Helicobacter gastritis whereas this was in more than 70% the case in carcinoma patients. Discussion: The diagnosis of pseudocarcinomatous regeneration is an important differential diagnosis of neoplastic gastric lesions. In some cases it can be really hard to distinguish bizarre epithelial changes due to drug incuded lesions from carcinomatous foci. Without Helicobacter gastritis the diagnosis of carcinoma should be made even more carefully and the differential diagnosis of pseudocarcinomatous changes should be considered. Fortunatly with time the number of erroneously carcinoma diagnoses went down in 2011 to 20% compared to the year 2001. Nevertheless gastric ulcerations should always receive proper follow-up with biopsies until healed. In difficult cases a second opinion by an experienced GI-pathologist may be helpful to confirm pseudocarcinomatous changes vs carcinomatous lesions. References


microsatellite instability but p53 mutation and wnt pathway activation. In a study of 200 traditional serrated adenomas (TSAs), we demonstrated flat as well as protuberant growth, slit-like serrations as an important diagnostic feature and different clinicopathological associations of morphologically identical BRAF- and KRASmutated TSAs. Advanced TSAs showed abrupt transition to overt dysplasia with p53 mutation, wnt pathway activation and in BRAFmutated polyps, loss of p16. Morphologically similar serrated tubulovillous adenomas show some TSA-like features but not slit-like serrations. They demonstrate KRAS mutation, negligible CIMP and are the likely precursors of most microsatellite stable serrated adenocarcinomas.

Gynecologic Pathology: SS 12-1 INTERESTING CASES IN GYNECOLOGIC PATHOLOGY: CASE 5 Takako Kiyokawa Department of Pathology, Jikei University School of Medicine, Tokyo, Japan

Gastrointestinal Pathology: SY10-2

An 8.5-year-old girl presented with breast development, irregular uterine bleeding, and a spurt in height during the previous 9 months. She also complained of rapid increase of abdominal girth and body weight (4 kg). No remarkable past history or family history was noted. Her height (143 cm), breast development (Tanner stage 3), and pubic hair (Tanner stage 2) were compatible with precocious puberty. Laboratory examinations showed microcytic hypochromic anemia (Hb 9.2 g/dL), and serum estradiol was 138 pg/mL. LH and FSH were in the undetectable level even after a LH-RH (100 mg) injection. Ovarian tumor markers including CEA, CA19-9, CA125, a-fetoprotein, and hCG were within the normal range. Magnetic resonance imaging revealed a giant multilocular cystic tumor (25  14  10 cm) in the lower abdomen. Tumor resection was performed. The tumor originated from the right ovary and contained 3500  mL of yellowish serous fluid. The left ovary was grossly normal. The resected right ovarian tumor was multilocular cystic, measuring 16.0  cm in the greatest dimension, with occasional foci of whitish yellow elevated components in the cystic wall.


Gynecologic Pathology: SY12-3

1. Douthwaite AJ, Lintott GAM. Gastroscopic observation of the effect of aspirin and certain other substances on the stomach. Lancet 1938; 232: 1222. 2. Vieth M, Mu¨ller H, Stolte M. Can the diagnosis of NSAID-induced or Hpassociated gastric ulceration be predicted from histology? Z Gastroenterol 2002; 40: 783–8. 3. Vieth M, Go¨rgens D, Langner C. Pseudoneoplastic regneration of the stomach. Histopathology and differential diagnosis. Pathologe 2010; 31: 171–6. 4. Stolte M, Panayiotou S, Schmitz J. Can NSAID/ASA induced erosions of the gastric mucosa be identified at histology? Pathol Res Pract 1999; 195: 137–42.

Neal I. Walker1,2 and Mark Bettington1,2,3 1Envoi Specialist Pathologists, Brisbane, Australia, 2The School of Medicine, The University of Queensland, Brisbane, Australia, and 3The Conjoint Gastroenterology Laboratory, QIMR Berghofer Medical Research Institute, Brisbane, Australia An expert panel has recommended sessile serrated adenoma/polyp (SSA/P) be diagnosed if one crypt in a serrated polyp shows unequivocal architectural distortion, dilation and/or horizontal branching. In our practice, SSA/Ps represent 12.1% (WHO criteria) or 14.7% (expert panel criteria) of all polyps received, the highest levels yet reported. The expert panel defined SSA/Ps with cytological dysplasia (SSAD) as an advanced polyp with abrupt transition from typical SSA/P morphology to an area of cytological dysplasia. In our study, SSADs were no larger than SSA/Ps, represented 3.5% of SSA/Ps and 11% occurred in the left colon. Progression to SSAD involves not only MLH1 loss and

IMMUNOHISTOCHEMICAL AND MOLECULAR ADJUNCT TECHNIQUES IN DIFFERENTIAL DIAGNOSIS OF MOLAR LESIONS Annie N. Y. Cheung Department of Pathology, The University of Hong Kong, Queen Mary Hospital, Hong Kong Extensive use of ultrasound in early pregnancy has given rise to increased diagnostic dilemma, particularly the differential diagnosis of early complete mole, partial mole and abnormal nonmolar villous lesions. The rare entities of placental mesenchymal dysplasia, twin pregnancy with one complete mole further pose problems. Overdiagnosis of hydatidiform mole in ectopic pregnancy should also be avoided. Molecular cytogenetic studies, besides enhancing our understanding of pathogenesis, also facilitate diagnosis and management.

Copyright © Royal College of pathologists of Australasia. Unauthorized reproduction of this article is prohibited.