METABOLIC SYNDROME PROMOTES PRE-NEOPLASTIC CHANGES OF THE COLONIC MUCOSA

METABOLIC SYNDROME PROMOTES PRE-NEOPLASTIC CHANGES OF THE COLONIC MUCOSA

S28 Abstracts / Digestive and Liver Disease 41S (2009), S1–S167 OC.07.3 METABOLIC SYNDROME PROMOTES PRE-NEOPLASTIC CHANGES OF THE COLONIC MUCOSA E. ...

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S28

Abstracts / Digestive and Liver Disease 41S (2009), S1–S167

OC.07.3 METABOLIC SYNDROME PROMOTES PRE-NEOPLASTIC CHANGES OF THE COLONIC MUCOSA E. De Masi 1 , F. Franceschi ∗ ,2 , M.G. Mancino 1 , G. Cammarota 2 , A. Cazzato 2 , D. Roccarina 2 , G. Gigante 2 , B. Giupponi 2 , G. De Marco 2 , A. Gasbarrini 2 , G. Gasbarrini 2 1 Ospedale

San Carlo, Roma; 2 Ospedale Gemelli, Roma

Background and aim: Metabolic syndrome (MS) is a pathological condition defined by the presence of obesity, blood hypertensionn, type 2 diabetes mellitus, hyperinsulinemia and dyslipidemia. MS is a well known risk factor for cardiovascular diseases but recent studies have also hypothesized a potential role for certain kind of tumors, including colorectal adenoma and adenocarcinoma. Since there are no definite data on this topic, we desigend a study aimed at assessing the role of MS in the occurrence of either colorectal adenoma or adenocarcinoma. Material and methods: 3 different groups of subjects were enrolled: Group 1: 200 patients (90 males, mean age 68±7 years) with colorectal adenoma (122 patients, 55 males, mean age 67±8 years; single adenoma in 56 patients, multiple adenomas in 66 patients), or adenocarcinoma (78 patients, 35 males, mean age 69±6 years; co-existing adenoma in 24 patients); Group 2: 180 patients (96 males, mean age 67±6 years) with MS but without any family history of colorectal neoplasia; Group 3: 185 controls (91 males, mean age 69±8 years), without MS or any history of colorectal neoplasia. Patients from Group 1 were fully evaluated for MS, while patients from Group 2 and 3 underwent pancolonoscopy with biopsies, where indicated. Results: Group 1: 110 patients (48 males, mean age 68±5 years) showed MS compared to 90 subjects (40 males, mean age 68±9 years) without any sign of MS (p=0.15). Among subjects with MS, 40 patients (18 males, mean age 70±7 years) were affected by colorectal adenocarcinoma, while 70 (32 males, mean age 66±3 years) presented single or multiple colorectal adenomas (p<0.0001). No significant association was found between number of pre-neoplastic or neoplastic polyps, in the same patient,and presence of MS. Group 2 and 3: 51 of 180 Group 2 patients (28 males, mean age 67±8 years) reported at least one pre-neoplastic lesion compared to 18 of 185 Group 3 patients (8 males, mean age 69±6 years) (p<0.001). Moreover, 4 Group 2 patients (2 males, mean age 70±7 years) showed colorectal adenocarcinoma compared to only 1 Group 3 patient (1 male, 72 years) (p<0.09). Conclusions: MS increases the risk of developing pre-neoplastic colorectal lesions. Further studies are now needed in order to fully elucidate the mechanisms by which MS affects the carcinogenic process of the colonic mucosa. # D. Colorectal diseases 2. Pre-cancerous lesions

OC.07.4 ROLE OF microRNA IN THE PATHOGENESIS OF COLORECTAL CANCER: POSSIBLE INVOLVEMENT OF miRNA-143 AND miRNA-21 G. Biscaglia ∗ , A. Panza, A.M. Gentile, F. Di Mola, P. di Sebastiano, A. Piepoli, A. Andriulli Ospedale Casa Sollievo Della Sofferenza IRCCS, San Giovanni Rotondo Background and aim: Colorectal cancer (CRC) is one of the major causes of cancer death worldwide. Recent studies showed a link between colorectal cancer development and microRNA (miRNA) function. MiRNAs are small, non coding RNA molecules which negatively modulates the expression of many cellular proteins by targeting coding mRNA. Some miRNA genes are located in cancer-associated genomic regions or in fragile sites, suggesting that miRNAs may play a more important role in the pathogenesis of human cancers. Aim of this study is to evaluate the role of two miRNA, miRNA-143 e

miRNA-21, in colorectal cancers. Material and methods: The expression levels of miRNA-143 and miRNA-21 using quantitative PCR (qPCR) were investigated in 11 CRC samples analysing colon carcinomas matched to normal tissues of the same patients. For all patients, RNA was extracted using standard TRIZOL methods. cDNA was synthesized from total RNA using genespecific primers according to the TaqMan MicroRNA Assay protocol. Quantitative PCR was performed using an Applied Biosystems 7700 Sequence Detection System. Features of cancers were evalueted. Results: High levels of miRNA-21 were observed in patients with age > 50 and high degree of local invasion (Dukes C) with metastasis or lynph node involvement, whereas lower expression of miR143 in patients with age < 50 years regardless of degree disease. Conclusions: These results suggest an involvement of miRNA-143 in young patients and of miRNA-21 in metastatic CRC. # J. GI Oncology 2. Genetic

OC.07.5 GASTRIC CARCINOID TYPE I: PREVALENCE, INCIDENCE AND RISK FACTORS A. Sbrozzi-Vanni ∗ ,1 , L. Vannella 1 , R. Baldini 2 , E. Lahner 1 , C. Bordi 3 , E. Di Giulio 1 , G. Delle Fave 1 , B. Annibale 1 1 Dept.

Digestive and Liver Disease University Sapienza, Roma; 2 Dept. Epidemiology University Sapienza, Roma; 3 Dept. Pathology University Parma, Parma Background and aim: Gastric carcinoids (GC) are rare well-differentiated neuroendocrine tumors arising from the enterochromaffin-like (ECL) cells of the gastric oxyntic mucosa. Type I is associated with Atrophic Body Gastritis (ABG), with or without pernicious anaemia. Achlorhydria in ABG leads to G cell hyperplasia and chronic hypergastrinemia, ECL cell hyperplasia and if necessary development of ECL carcinoids. Few data exist on the prevalence, incidence and risk factors for type I GC. Aim: to assess the prevalence and incidence of GC type I in a consecutive series of ABG patients and identify risk factors for the GC. Material and methods: 367 consecutive ABG patients [240 F, median age 56 (20-95), 151 with pernicious anaemia] were enrolled in this study between 1990 and 2006 as the result of a screening programme for early detection of ABG. 55.8% of ABG patients underwent to Hp eradication treatment. 215 (144 F) ABG patients were followed and the median follow-up was 59 months (12-198). Variables concerning personal, family history, GI symptoms, biochemical and histological data were collected at the time of diagnosis of ABG and were used for univariate (Mann-Whitney and Fisher tests) and logistic regression analyses. Results: 8/367 (2.2%) ABG patients had GC type I at the time of diagnosis of ABG, while in 6/215 (2.8%) GC was diagnosed during the follow-up. The logistic regression confirmed as risk factors for the development of type I GC the presence of dyspepsia (OR 7, 95%CI 2-26) and presence of gastric polyps (OR 32, 95%CI 8-134). Carcinoids (n=14)

ABG (n=353)

P

Males 5/14 (35,7%) 122/353 (34,6%) 1 Median age (yrs) 60 (23-72) 56 (20-95) 0,8745 Severe corporal atrophy 11/14 (78,5%) 194/353 (55%) 0,10196 Smoke 7/13 (53,8%) 121/323 (37,5%) 0,254374 Dyspepsia 7/13 (53,8%) 69/351 (19,6%) 0,019694 Fasting Serum Gastrin (pg/ml) 832,5 (220-2800) 500 (49-2700) 0,0105 Chromogranin A (ng/ml) 171 (60-405) 100 (30-547) <0,0001 Gastric polyps 11/14 (78,5%) 35/353 (9,9%) <0,000001

Conclusions: Type I GC had a prevalence rate of 21.8/1000 ABG patients and an incidence rate of 5/1000 ABG patients/year, showing that this endocrine neoplasia occurs not infrequently in ABG patients. Gastroscopical follow-up of ABG patients is advised in the manage-