The College of American Pathologists offers these protocols to assist pathologists in providing clinically useful and relevant information when reporting results of surgical specimen examinations. The College regards the reporting elements in the “Surgical Pathology Cancer Case Summary (Checklist)” portion of the protocols as essential elements of the pathology report. However, the manner in which these elements are reported is at the discretion of each specific pathologist, taking into account clinician preferences, institutional policies, and individual practice. The College developed these protocols as an educational tool to assist pathologists in the useful reporting of relevant information. It did not issue the protocols for use in litigation, reimbursement, or other contexts. Nevertheless, the College recognizes that the protocols might be used by hospitals, attorneys, payers, and others. Indeed, effective January 1, 2004, the Commission on Cancer of the American College of Surgeons mandated the use of the checklist elements of the protocols as part of its Cancer Program Standards for Approved Cancer Programs. Therefore, it becomes even more important for pathologists to familiarize themselves with these documents. At the same time, the College cautions that use of the protocols other than for their intended educational purpose may involve additional considerations that are beyond the scope of these documents.

Introduction: During organ harvest for transplantation (TX) tissues undergo cold ischemia (C) during preservation and reperfusion during implantation. Cooling to 4 °C with specialized solutions is routinely employed to decrease tissue edema, oxidative stress and preserve membrane integrity. We have previously reported that high molecular weight polyethylene glycol (15-20,000 MW, PEG15-20) protects the intestinal epithelium against a variety of cellular stresses including radiation injury and microbial invasion by mechanisms that appear to involve lipid rafts. PEGs have also been shown to decrease lipid peroxidation and the production of reactive oxygen species in various tissues. The aim of this study was to determine if a high molecular weight PEG could more efficiently preserve the intestinal integrity of intestine grafts harvested for subsequent transplantation when compared to a standard tissue preservation solution (HTK). Methods: Twenty (20) 8 week old C57BL6 mice underwent total enterectomy in preparation for small intestinal transplantation using a well described technique of isolation and preservation of vascular inflow and outflow. Intestinal segments were preserved in either in 4C Histidine-Tryptophan-Ketoglutarate (HTK) or HTK+ 5% high molecular weight PEG co-polymer solution. Intestinal segments were analyzed histologically for tissue preservation and integrity by calculating an epithelial injury score at 9 h and 24 h following preservation. Results: Gross macroscopic exam of tissues revealed that segments from the HTK+5% PEG appeared less edematous, the vascular architecture was highly defined, and no gross necrosis was detected compared to HTK alone which displayed visible areas of necrosis and pale and ill-define vasculature (data not shown). Histology demonstrated mild lymphoplasmocytic infiltration in HTK+5% PEG compared to moderate to severe in HTK alone. Tissue architecture was intact in HTK+5% PEG and disrupted in HTK alone with visible focal ulcerations, erosions, crypt distortion, denuded epithelium and fibrosis HTK (B). Goblet cells were better preserved in HTK+5% PEG solution (data not shown).

Portal hypertensive gastropathy (PHG) and gastric antral vascular ectasia (GAVE) are unusual but important causes of gastrointestinal bleeding with characteristic endoscopic appearances and critically different therapies. However, overlapping features and poor endoscopic-histologic correlation make their distinction challenging. We sought to determine whether CD31, CD34 (vascular markers), and CD61 (platelet marker) could aid in their differentiation. Cases included 11 antral specimens with histologic diagnoses of GAVE, 11 histologically diagnosed as PHG, and biopsies of GAVE (15) or PHG (12) suspected on endoscopy but without histologic agreement. Controls consisted of endoscopically and histologically normal antrum. Image analysis of CD31 and CD34-stained sections was performed to determine mucosal microvessel density (MVD). CD61 revealed thrombi in 100% of histologically confirmed cases of GAVE and 60% of cases suspected of GAVE on endoscopy alone; control biopsies were negative. CD61 was also positive in 26% of cases originally signed out as PHG. Review of hematoxylin and eosin slides from these CD61-positive PHG cases showed other features allowing their correct reclassification as GAVE. MVD was significantly higher in GAVE than PHG. MVD in histologically confirmed PHG did not differ significantly from endoscopically suspected PHG. Review of hematoxylin and eosin slides from the latter showed active gastritis obscuring recognition of ectatic vessels. In conclusion, CD61 reliably differentiates GAVE from PHG. MVD analysis can also assist in their distinction. In PHG, the increased vascularity may be subtle in an inflammatory background; vascular markers may serve as adjunct markers for identifying the aberrant vessels.

Background and study aims: In patients with Barrett's esophagus (BE), targeted endoscopic mucosal resection (EMR) of visible lesions of high grade dysplasia (HGD) or intramucosal adenocarcinoma (IMC) is effective, but carries the risk of leaving in place synchronous lesions and Barrett's epithelium with the potential for recurrent disease. We evaluated the safety and long-term efficacy of complete Barrett's eradication EMR (CBE-EMR) for the treatment of patients with HGD or IMC, independently of the presence of macroscopically visible lesions or surgical risk.Patients and methods: 26 consecutive patients with BE and HGD or IMC underwent CBE-EMRs, which were performed with the endoscopic cap suction method and/or a 2.3-mm monofilament mucosectomy snare. Endoscopic follow up after completion of resection was carried out to assess the rate of residual or recurrent BE with or without HGD or IMC.Results: 24 patients completed the study. They underwent a total of 44 EMR sessions with a median of 3 pieces (range 1-8) removed per session. Two patients with immediate bleeding were successfully managed encloscopically. Three patients developed an early esophageal stricture that was completely resolved with a single endoscopic dilation. After a median follow-up of 28 months (range 15-51 months), persistent endoscopic and histologic eradication of BE was demonstrated in 21 patients (87.5 %). In two patients, Barrett's epithelium was detected beneath the neosquamous epithelium 3 months after completion of the resection. In the remaining patient, IMC was found in a nodule seen and removed by EMR at 12-month surveillance endoscopy.Conclusions: CBE-EMR is a safe and highly effective long-term treatment that should be offered to all patients with Barrett's esophagus with HGD and IMC.

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A 61-year-old woman was originally diagnosed with stage IVB follicular lymphoma in 1981 when she presented with lymphadenopathy, fever and night sweats. She was treated with BCNU (carmustine), cyclophosphamide, vincristine and prednisone, and achieved a complete remission. She relapsed in 1994 and over the next decade was treated several times with chemotherapy and localized radiation for recurrent disease. In August 2004, an excisional biopsy of an enlarged cervical lymph node revealed disease transformation into a large B-cell lymphoma. After two cycles of high-dose ifosfamide, etoposide and rituximab, peripheral blood progenitor cells were mobilized. She then received conditioning therapy with BNCU, etoposide, cytarabine and melphalan (BEAM). On day 0, 4.6 106/kg CD34+ autologous cells were infused. Granulocyte recovery occurred on day +10, and platelet recovery on day +15. On day +11, she developed diarrhoea, and was treated with metronidazole for a presumptive diagnosis of Clostridium difficile colitis, despite multiple negative toxin assays. She was discharged on day +15, but the diarrhoea worsened, was >1500 ml on most days, and over the next 6 weeks she lost 15 pounds. Neither skin rash, nor liver function abnormalities developed. On day +60, the patient was admitted for fever, anorexia and worsening diarrhoea. Broad-spectrum antibiotics were administered. Stool cultures, evaluation for the presence of ova and parasites, and testing for C. difficile toxin were negative. A colonoscopy revealed multiple edematous, inflamed colonic ulcerations (Figure 1). Pathology was consistent with graft-versus-host disease (GVHD) (Figure 2). No viral inclusions were seen, and an immunohistochemical stain for cytomegalovirus (CMV) was negative. Biopsy cultures for CMV and herpes simplex virus were negative, as was a serum CMV polymerase chain reaction (PCR). A thorough examination showed no other evidence of acute or chronic GVHD. Prednisone at 1 mg/kg was begun, and over the next week, the diarrhoea slightly improved from 12 to eight liquid bowel movements daily. Her appetite improved, and her weight stabilized. Ten days after the initiation of prednisone, the patient was readmitted with continued diarrhoea, fever and abdominal cramping. An infectious work-up was again unrevealing, and a repeat colonoscopy demonstrated persistent colitis. Biopsies were again consistent with GVHD. Intravenous methylprednisolone was begun at 2 mg/kg/day in two divided doses, with a marked improvement in her symptoms. The patients bowel movements were regular and well-formed, and she defervesced. She was discharged on 1 mg/kg of oral prednisone daily. Over the course of the subsequent 3 months, steroids were tapered and the patient remained well. She denied abdominal pain or fever. However, when the prednisone was reduced to 5 mg/day, she again developed severe diarrhoea with eight watery, voluminous bowel movements daily, associated with tenesmus and anorexia. Repeat colonoscopy showed numerous, non-bleeding edematous ulcers throughout the colon. Biopsies did not reveal an increase in apoptotic bodies, in contrast to the prior biopsy specimens. Cultures of stool and of colonic mucosa were again negative. There was no skin rash, and liver function tests were normal. Prednisone was increased to 30 mg daily, with a rapid and marked improvement in her symptoms within 1 week. She remains well and without evidence of disease 14 months after her auto hematopoietic cell transplantation (HCT). Prednisone was successfully tapered approximately 10 months after the second episode of auto GVHD. Acute GVHD occurs in 50–70% of patients undergoing allogeneic HCT,1 and is a major cause of post transplantation morbidity and mortality. A syndrome similar to acute GVHD has been reported after auto HCT, both spontaneously and after treatment with cyclosporine and/or interferon, and has been termed autologous GVHD (auto GVHD). Auto GVHD occurs spontaneously in 5–20% of patients undergoing auto HCT,2, 3, 4 and in 20–70% of those receiving post transplant immune modulation.5, 6, 7, 8 In comparison with acute allogeneic GVHD, auto GVHD tends to be milder. Most cases have been limited to the skin with only rare gastrointestinal (GI) involvement.1, 2, 4, 5, 6 In three recent large series of autologous transplant followed by post transplant immune modulation, GVHD developed in 42% (91/219).6, 7, 9 Only six cases of intestinal GVHD occurred, and only one was isolated to the gut.7 Auto GVHD of the liver in conjunction with intestinal GVHD has also been reported.10 A recent series from Seattle suggested that 13% of patients developed GI GVHD after auto HCT.4 Almost all cases involved upper GI GVHD. Only three of 90 patients had diarrhoea and no patients had severe diarrhoea. Our case is, to the best of our knowledge, the first case of severe stage III isolated auto GVHD of the intestine. The auto GVHD occurred spontaneously, in the absence of post transplant immune suppression. Auto GVHD should be considered in the differential diagnosis of severe unexplained diarrhoea after auto HCT.