Sathya Jaganmohan

Antiviral Therapy Reduces Risk of Hepatocellular Carcinoma in Patients With Hepatitis C Virus–Related Cirrhosis

BACKGROUND & AIMS The effects of antiviral therapy on prevention of hepatocellular carcinoma (HCC) in patients with hepatitis C virus (HCV)-related cirrhosis are unclear. We performed a systematic review and meta-analysis to assess HCC risk reduction in patients with HCV-related cirrhosis who have received antiviral therapy. METHODS Twenty studies (4700 patients) were analyzed that compared untreated patients with those given interferon (IFN) alone or ribavirin. Risk ratios (RRs) determined effect size using a random effects model. RESULTS Pooled data showed reduced HCC risk in the treatment group (RR, 0.43; 95% confidence interval [CI], 0.33-0.56), although the data were heterogenous (chi(2) = 59.10). Meta-regression analysis showed that studies with follow-up durations of more than 5 years contributed to heterogeneity. Analysis of 14 studies (n = 3310) reporting sustained virologic response (SVR) rates with antiviral treatment showed reduced HCC risk in patients with an SVR, compared with nonresponders (RR, 0.35; 95% CI, 0.26-0.46); the maximum benefits were observed in patients treated with ribavirin-based regimens (RR, 0.25; 95% CI, 0.14-0.46). Meta-analysis of 4 studies assessing the role of maintenance IFN in nonresponders did not show HCC risk reduction (RR, 0.58; 95% CI, 0.33-1.03). No publication bias was detected by the Egger test analysis (P > 0.1). CONCLUSIONS The risk of HCC is reduced among patients with HCV who achieve an SVR with antiviral therapy. Maintenance therapy with IFN does not reduce HCC risk among patients who do not respond to initial therapy. View this articles video abstract atwww.cghjournal.org.

Clinical Challenges and Images in GI

C uestion: A 40-year-old Hispanic woman with unremarkble past medical history presented to the emergency deartment (ED) with generalized fatigue and dyspnea on xertion. Her symptoms started about 3 months ago. There as no history of weight loss or anorexia. She denied menrrhagia, melena, hematochezia, and hematemesis. On hysical examination, she was normotensive, tachypneic, nd tachycardic with a heart rate of 116. Examination of the onjunctiva revealed marked pallor. The rest of the physical xamination was unremarkable, except for a positive guaiac est. Laboratory data revealed a hemoglobin 6.2 g/dl (noral range, 11.5–15.5) and a mean corpuscular volume of 67 (normal range, 80–96). Patient underwent esophagogasroduodenoscopy (EGD) and colonoscopy to evaluate the ource of blood loss. EGD revealed numerous, red-colored, yperemic, smooth, polypoid lesions in the body and the ntrum of the stomach (Figure A). Multiple polyps were esected using snare cautery and sent for pathology. All the esected polyps exhibited the same histopathological feaures as shown in Figure B (hematoxylin and eosin; original agnification, 20x).

T1468: Neuroendocrine Tumors of Gastrointestinal Tract and the Pancreas: Diagnostic Modalities, Accuracy, and Outcomes

Purpose: Th e aim of the study was to evaluate the utility of various diagnostic modalities including computed tomography (CT) scan, endoscopy, and endoscopic ultrasound (EUS) in gastrointestinal (GI) neuroendocrine tumors (NET). Methods: Retrospective chart review of patients who underwent endoscopic evaluation from January 2003 to June 2009 at a cancer center was done. Th e accuracy of EUS-guided fi ne needle aspiration (FNA) was evaluated. Th e Tand Nstaging of NET by EUS was compared to histological staging. Results: Results: A total of 85 patients (35 men) with a mean age 60.3 years were found to have GI NET. Th ere were 50 patients with pancreatic endocrine neoplasm (PEN) including 5 with multiendocrine neoplasia 1 (MEN1), 15 with duodenal carcinoids, 2 ampullary carcinoids, 12 gastric carcinoids, 3 rectal carcinoids, 1 ileal carcinoid, 2 NET of unknown primary. Among PEN, 5 were in the uncinate process, 14 in the head, 3 in the neck, 8 in the body, and 15 in the tail, and 5 MEN1. Th e median size was 2.3 cm (range; 0.52-7 cm) for PEN, 1cm (range; 0.6-7 cm) for gastric carcinoids, 1cm (range; 0.5-3 cm) for duodenal carcinoids, and 1.8 cm (range; 0.5-3.1 cm) for rectal carcinoids. EUS was performed in 78 patients. Th e CT fi ndings were unremarkable in 25, positive for a mass in 26, and metastasis in 30. For patients with no abnormalities seen on CT scan (25 patients), upper endoscopy (EGD) and sigmoidoscopy showed a discrete nodule or lesion in all patients. 46 had EUS for PEN; EUS FNA was performed in 33 and all were positive (accuracy 100%). EUS staging was compared to histologic staging for carcinoids and the accuracy for T-staging was 61% (if T1a and T1b were separated, accuracy was 52%) with understaging of 13% and overstaging of 26%. All carcinoids smaller than 1cm in the stomach (2), duodenum (3), and rectum (1) did not progress aft er endoscopic resection and/or biopsy during a median follow-up period of 92 days (range 24-758). No complications were seen in endoscopic procedures. Conclusion: Endoscopic evaluation is the most sensitive modality in detecting and diagnosing carcinoids smaller than 1cm. EUS FNA is highly accurate in the diagnosis of PEN. EUS is moderately accurate in T-staging of carcinoids. Carcinoids, smaller than 1cm in the stomach, duodenum, and rectum, may not have an aggressive behavior in a short term follow-up period. [245] Analysis of senstivities for EUS-guided trucut biopsy for pancreatic masses

T1386 Risk of Pancreatic Cancer Development in Cancer Survivors in the United States – A Population-Based Epidemiological Study Using the SEER Cancer Database

Introduction Smokers are at risk for pancreatic cancer and other pancreatic diseases. Cigarette smoking also aggravates the risk of pancreatic cancer in patients with hereditary and chronic pancreatitis and results in a higher incidence of acute pancreatitis and relapses in chronic pancreatitis. Both pancreatic cancer and chronic pancreatitis are characterized by a progressive fibrosis. Recently, two studies on rats reported that tobacco smoking is associated with chronic pancreatic inflammation with fibrosis, and scarring of pancreatic acinar structures. In this study we aim to confirm a relation between cigarette smoking and pancreatic fibrosis (PF) in humans. Methods In this retrospective study, pancreatic tissue acquired during autopsy was collected and revised. Pancreatic fibrosis (PF) was gradually scored by analyzing intra-lobular, extra-lobular and total PF: grade 0 (normal or mild; 0-25% PF), grade 1 (moderate; 25-50%PF), grade 2 (severe; >50%). Information on smoking habits was extracted from (electronic) medical files. Results Of 900 autopsies, performed from January 2005 till December 2007, the minority of available histology material (n=111) was of significant quality to be included for analysis. Grade 2-3 total PF and intra-lobular PF was significantly more present in “smokers” versus “never smokers” (total: 42.9% vs 26.5%, p=0,027 and intra-lobular: 39.3% vs 15.6%, p=0.013), whereas no differences could be found between “never smokers” and “abstinent smokers” and “abstinent smokers” and “smokers”. When taking into account interlobular PF, no differences between all groups were observed. Conclusion To date no human study studied the effect of tobacco smoking on pancreatic tissue. We demonstrate for the first time that current cigarette smoking is associated with total pancreatic fibrosis and more specific intra-lobular pancreatic fibrosis, compared to non-smokers.