2008 Summer Meeting - Leeds - The Pathological Society of Great ...

P45Evidence Supporting an Ischaemic Mechanism for NSAIDInjury to the Small BowelAAnthony 1 ,SKarim 1 .1 West Middlesex University Hospital, IsleworthBackground: Experimental studies have identified an early acute phase ofpre-ulcerative small intestinal injury induced by the non-steroidal antiinflammatorydrug (NSAID) indomethacin. This phase included villousshortening and buckling, capillary occlusion with congestion, smooth muscleand endothelial cell crowding all in the absence of significant inflammatory cellinfiltration. This phase, as well as the subsequent mucosal necrosis, wasconsidered to arise as a consequence of ischaemia induced by the drug.Aim: To report changes described above in histopathological specimens ofhuman small bowel reported as having ischaemic injury.Methods and results: Routine human surgical specimens with (i) acute smallbowel infarction or ischaemic enteritis (n=8) and (ii), ileum from right hemicolectomycolorectal cancer controls (n=10) were scored according to a gradingsystem defining progressive early NSAID damage in the rat. All eight of thehuman infarction cases, and only two of the controls, showed mucosal changesidentical to early experimental indomethacin injury (P=0.0011).Conclusions: A pattern of ischaemic change observed in small bowel infarctionspecimens that is identical to experimental NSAID small bowel injury, isdescribed. The findings support the hypothesis that NSAIDs damage the smallbowel by primary mechanisms that involve ischaemia to the bowel wall.P47Audit of colorectal cancer histopathology staging at Maidstoneand Tunbridge wells NHS Trust.AA Zainab 1 , J Schofield 2 .1 Darent and Valley NHS Trust, Dartford,Kent,UK, 2 Preston Hall Hospital,Maidstone, Kent ,UKMethod:The national minimum data sets for all colorectal cancer cases over 12 monthperiod (Jan.2007 to Dec.2007) were examined. The stage, lymph node countand presence of extramural vascular invasions were analysed. The reportingpractice is sub-specialised, two consultants report colorectal cancer excision atMaidstone Hospital (Pathologist A and B), while at Pembury Hospital, only oneconsultant with another consultant to cover for any leaves.Results:PATHOLOGISTA B C DTotal number 45 27 84 18of casesColon 35 18 68 12Rectum 10 9 16 6T stagepT4 (overall) 18 (40%) 9 (33.3%) 21 (25%) 5 (27.7%)pT4 (rectum) 2 (20%) 1 (11.1%) 2 (12.5%) 1 (11%)pT4 (colon) 16 (45.7%) 8 (44.4%) 21 (30.8%) 4 (33%)Lymph node 7-39 9-42 9-41 10-29rangeMean17.3 20.6 15.5 16.3lymph nodecountEMVI 16 (35.5%) 9 (33.3%) 39 (46%) 8 (44.4%)Discussion:New national guidance has been published with audit standards suggested forEMVI (at least 25%) and T4 rate (at least 20% for colonic and 10% for rectaltumours). The existing guidance of a mean of 12 lymph nodes remains. All fourpathologists are achieving all three of these audit standards.P46Management of colorectal liver metastases: a single institutionexperienceA Treacy 1 ,DPower 1 , A Behabahani 1 , G McEntee 1 , P Kelly 1 ,J McCaffrey 1 .1 Mater Misericordiae University Hospital, Dublin, IrelandIntroduction: Metastatic colorectal cancer (CRC) to liver has been associatedwith poor outcome. As CRC is a common disease with approximately 25% ofpatients presenting with liver metastases, and an additional 25% developingliver metastases, management of these patients has been the focus of muchresearch.Methods: We identified all new patients with CRC who presentedwith/developed liver metastases from July 1 st 2005-June 30 th 2007. Resectablepatients had upfront liver resections, and unresectable patients were assessedfor ‘neoadjuvant’ chemotherapy and targeted therapy. Response tochemotherapy was evaluated using response evaluation criteria in solid tumours(RECIST) and then liver resection was revisited. All findings at surgery werediscussed and concordance with radiology assessed.Results:185 patients were diagnosed with CRC. 29 (73%) of these patients wereunresectable due to poor performance score, excess number or location ofmetastases, and presence of extra-hepatic disease. 18 patients with unresectabledisease received ‘neo-adjuvant’ treatment with FOLFOX6 and Bevacizumab.13 of these patients went for resection with 11 having a partial response (PR)and 2 patients having a complete response (CR) on imaging. 11 patients had‘curative’ resections. Discordance between surgery and radiology was seen in 3cases. Chemotherapy was well tolerated in the majority of cases and there wasno significant postoperative morbidity.Conclusion: Liver is the most common site of colorectal metastases. Ourexperience in the management of liver metastases from CRC shows that 38% ofunresectable liver disease is rendered resectable with modern chemotherapy.P48MYH-Associated Hyperplastic Polyposis Syndrome – A CaseReportABP Peckham-Cooper 1 , KA Laughlan 1 ,OBoyle 1 ,NS Ambrose 1 ,NScott 21 John Goligher Colorectal Unit, Leeds General Infirmary, 2 Leeds GeneralInfirmaryHyperplastic Polyposis Syndrome (HPS) is rare, usually characterized bymultiple, large hyperplastic polyps. MutY-human-homolog (MYH) associatedHPS (MAP) is a recently characterized autosomal recessive variant usuallycausing adenomatous polyposis with fewer polyps than seen in classical FAPcaused by APC mutation. Rarely, MYH-mutations have been described inassociation with hyperplastic and adenomatous polyps fulfilling current criteriafor hyperplastic polyposis.A 64-year-old female presented with simple fresh per rectal bleeding over atwo-month period. Colonoscopy revealed 100 colonic hyperplastic polyps and30-50 colonic adenomas, histology was highly suspicious of HPS. Followingdiscussion at MDT she underwent a panproctocolectomy and formation ofileostomy. Approximately 250 polyps were identified in the proctocolectomyspecimen. The majority of the polyps were identified as hyperplastic polyps,although larger than typical sporadic hyperplastic polyps and demonstratedunusual architectural features including inversion. Tubular and tubulovillousadenomas were predominantly found in the proximal colon while hyperplasticpolyps and serrated adenomas were mainly present in the distal colon. Mutationanalysis of APC and the MYH genes identified 2 MYH variants and a diagnosisof MAP was made. Screening colonoscopy of her two children revealed noevidence of polyposis.In conclusion, MAP is a rare variant of HPS. Responsible for 1.4% of alladenamatous polyposis, it is the first human cancer predisposition disorder to belinked to defects in the BER-pathway with mutations occurring in the MUTYHgene. This syndrome has defined pathological and genetic properties, raisingimportant questions for screening with 1:100 of the population being affectedby the mutation.Summer Meeting (194 th ) 1–4 July 2008 Scientific Programme43