99 43rd European Pancreatic Club (EPC) Meeting June 22–25, 2011, Magdeburg, Germany Guest Editor: Halangk, W. (Magdeburg) (available online only) 276 Erratum 277 IAP Society News 278 EPC Society News No. 3

Somatic mutations of MMR gene are not often present in HNPCC and in sporadic RER+ colorectal cancers. Complete studies were made according to Bethesda and Amsterdam Criteria, and 35 patients belonged to the group with sporadic colorectal cancer, and 9 patients belonged to HNPCC group. The results of our studies showed that there is no significant difference between RER phenotype of HNPCC and sporadic cancer (p>0,05) in regard to microsatellite status. It can be a good indicator that there are so called 'susspected' on HNPCC among sporadic cancers which were not detected yet. The reason for this was an incomplete familial history of illness of patients and as such it was selected as sporadic cancer. Microsatellite analysis together with medical and familial history of illness can be a successful instrument for efficient HNPCC identification. However, successful solving of this problem lies in making an accurate diagnosis in comparative findings, which can be provided by genetic and clinical tests.

Colorectal cancer with its frequency, high mortality rate as well as many etiological unknowns is a challenge to contemporary science. Finally, genetic information could be used in near future for prevention of colorectal cancer, its early diagnosis and selection for the most suitable hospital treatment. In this study, we analysed genetic alterations of tumor suppressor genes and the possibility of quick and efficient screening method for identification of colorectal cancer. The study consisted of 54 samples of tumor and surrounding healthy tissue of patients with colorectal cancer, which is clasificated according to Bethesda and Amsterdams criterias. The investigation showed that genetic alterations of tumor suppressor gene NM 23 were present in 19/35 (54,29%) samples, and tumor suppressor gene p53 in 18/35 (51,43%), APC in 18/35 (51,43%), DCC2 tumor suppressor gene in 12/35 (34,29%), tumor suppressor gene RB1 in 8 /35 (22, 86%) and DCC 1 in 10/35 ( 28,57%) tumor tissue.

their poor general condition and because it would be difficult to discriminate between necrotic and normal tissue during the sur-gery. Besides, the risk of uncontrolled hem-orrhage during or immediately after the surgery would be very high. Open necrosectomy results in signifi-cant deterioration of organ dysfunction scores after the procedure [2]. M IPN is less aggressive compared to open surgery but it is a much more aggressive method com-pared to percutaneous catheter drainage (PCD) using 8- or 10-Fr catheters under ultrasound or CT control (general anes-thesia, progressive dilatation of the drain tract to 30 Fr allowing insertion of a trocar, using grasping forceps for removal of ne-crotic tissue) [1, 3]. P CD seems technically feasible in the vast majority of patients with necrotizing pancreatitis [4, 5] . B-esides, with this method a few catheters can be simultaneously introduced into liquid areas of necroses (into different pancreatic and peripancreatic regions) without gen-eral anesthesia and with fewer traumas, performing vigorous irrigation with simi-lar or better effects than by MIPN. On the basis of our long-term experi-ence [4, 6] , we believe that necrosecto-my (including MIPN) as a primary treat-ment may represent overtreatment of IPN. Therefore, we consider that sole conserva-tive treatment with proper intravenous hy-dration and administration of proper an-tibiotics should be performed at the begin-ning of the disease. PCD with vigorous D e a rE d itor, We read with great interest the article by Ahmad et al. [1] published in issue 1 of Pancreatology 2 011, volume 11. The article describes a case series outlining the expe-rience and results of retroperitoneal mini-mally invasive pancreatic necrosectomy (MIPN) and demonstrates that MIPN can be performed with acceptable morbidity and mortality and with good end results. The authors note that multiple MIPNs may be needed to eradicate the necrosis satisfactorily [1] . However, we wish to highlight certain issues regarding the statement that multiple MIPNs represent the optimal treatment for infected pancre-atic necroses (IPN). In the beginning of acute necrotizing pancreatitis, pancreatic and peripancreatic necroses are solid and the discrimination between necrotic tissue and normal tissue is very difficult. However, during the course of IPN, after the transition from solid ne-crotic tissue to more liquid contents takes place, there is a chance of a higher success rate in evacuating the necrotic tissue from the cavities, regardless of the method that is used. The presence of infection and vigor-ous irrigation can accelerate the process of transition from solid necrotic tissue to more liquid content. In those conditions, patients with necrotizing pancreatitis are not good candidates for surgery because of

Background Bosnia and Herzegovina (B&H) is one of the Eastern European countries that lacks data on the epidemiology of ulcerative colitis (UC). Aims We aimed to assess the epidemiological and clinical characteristics of UC in Tuzla Canton of B&H during a 12-year period (1995–2006). Patients and methods We retrospectively evaluated hospital records of both UC inpatients and outpatients residing in Tuzla Canton of B&H (total of 496 280 inhabitants) between 1995 and 2006. Patients that firmly satisfied the diagnostic criteria for UC were included in the study. Incidence rates were calculated with age standardization using European population standards. Trends in incidence were evaluated as moving 3-year averages. Results During the observed period, 214 patients met the diagnostic criteria for UC. The average age-standardized incidence was found to be 3.43/105 inhabitants [95% confidence interval (CI) = 2.97–3.89], ranging from 0.22 to 7.44 per 105. The mean annual crude incidence in the last 5 years of study (2002–2006) was 5.55/105 (95% CI = 4.63–6.48). The prevalence of UC during the observed period was found to be 43.1/105 (95% CI = 37.3–48.8). The incidence of UC increased dramatically from the average of 1.01/105 in the period between 1995 and 1997 to 6.04/105 between 2004 and 2006, as did the number of colonoscopies performed, from 29 in 1995 to 850 in 2006. The average yearly incidence of confirmed UC cases detected on colonoscopy was 5.56 per 100 colonoscopies per year (95% CI = 4.81–6.30) and only 3.92 per 100 colonoscopies (95% CI = 3.26–4.57) in the last 5 years of the observed period. Conclusion Tuzla Canton of B&H is a region with an increasing incidence of UC, which is most likely a direct consequence of a wider use of colonoscopy. We believe that in the next few years, the incidence of UC in this region will probably reach the annual incidence rate of 6 per 105 inhabitants.

HNPCC (Hereditary non-polyposis colorectal cancers) development is caused by mutation of genes included in system of mismatch repair genes. The mutation exists at 60% of patients in hMSH2 gene, 30% in hMLH1 and 10% both in hPMS1and hPMS2 genes. RER+ exists in about 90% in hereditary non-polyposis colorectal cancer and about 15-28% in sporadic cancers. The purpose of the study was to determine highly sensitive microsatellite markers which can be fast and efficient way of microsatellite screening for detection of HNPCC patients. Moreover, we have analysed the loss of heterozygosity of tumour suppressor genes which could have the diagnostic value in detection of HPNCC patients.

Considering its frequency, high mortality rate as well as many etiological mysteries colorectal cancer is a challenge to contemporary science. In our study we analyzed RER + and RER--phenotypes and their relations with clinical-pathological characteristics of sporadic colorectal cancers. We also analyzed genetic alterations of tumor suppressor genes as well as their relation with microsatellite instability. The study was based on 54 tumor samples and 54 samples of the surrounding healthy tissue of patients with colorectal cancer. According to Amsterdam Criteria and Bethesda Criteria 35/54 or 64,81% belonged in the group of sporadic colorectal cancer. Mononucleotide marker Bat 25 showed instability in 48,57%; Bat 26 in 45,71% and Bat 40 in 29/35 82,86% of tumor samples. Considering dinucleotide markers, TP 53 showed instability in 54,29% and DS123 in 37,14% of tumor samples. Genetic alterations in tumor suppressor genes were found in tumor tissue: NM 23 in 54,29% samples, p53 in 51,43%, APC in 51,43%, DCC2 in 34,29%, RB1 in 22, 86% and DCC 1 in 28,57%. Our studies confirmed that genetic instability had an important role in the development of tumor type. Our results showed that mononucleotide marker Bat 40 might be used for an easy and fast screening procedure in Bosnian population, because it exhibited high percent of microsatellite instability and was in relation with RER+ phenotype. This investigation showed that different genetic alterations may occur during cancer development in each individual patient's tumor. These changes result in MMR inactivation, which causes RER+ phenotype. Our results suggest a connection between alteration in some tumor suppressor genes and MSI phenotype of sporadic colorectal cancer in Bosnian population.

Objective To determine (i) the prevalence of HBV infection in families of confirmed chronic carriers, (ii) possible routes of transmission and risk factors for the intrafamilial transmission, (iii) vaccination rate among family members of chronic carriers and (iv) family members with highest risk for infection. Methods A total of 172 family members of 67 hepatitis B surface antigen chronic carriers were tested for hepatitis B markers; 716 first-time blood donors from the same area were used as controls. Results Prevalence of hepatitis B surface antigen was higher (P<0.001) among family members of index cases (12.2%; 21/172) than among controls (3.6%; 26/716) with relative risk of 3.3 (95% confidence Intervals=1.9–5.8; P<0.05). Rate of exposure among family members was 37.8% (65/172); only 8.7% (15/172) had been vaccinated for hepatitis B virus. Difference (P<0.001) in exposure existed among family members; exposure increased with age (ρs=0.34; P<0.001). Prevalences of hepatitis B surface antigen positivity and hepatitis B virus exposure were higher among parents of index cases (P<0.005) and among offspring of female index cases (P<0.001). There were more (P<0.001) hepatitis B surface antigen-positive family members among those with mother–children relationship with index case (13/31; 41.9%) than among those with father–children (19/85; 22.4%) and horizontal (siblings and spouses) relationship (2/56; 3.6%). Significantly more (P<0.001) hepatitis B surface antigen-positive and hepatitis B virus-exposed offspring were found in families where only mother was hepatitis B surface antigen positive. Among family members of HBeAg-positive cases more hepatitis B surface antigen-positive cases and hepatitis B virus-exposed cases have been found (P<0.001). Combination of HBeAg positivity and female sex of index case significantly increased risk for chronic carriage among family members (relative risk=24.06; 95% confidence interval=8.88–65.21; P<0.05). Conclusion In the area studied, both horizontal and vertical transmission exists, but maternal route is predominant. Female sex, HBeAg positivity of index carrier and presence of hepatitis B surface antigen-positive mother inside family increased risk for hepatitis B surface antigen positivity and exposure among family members. Vaccination rate of family members of index cases is alarmingly low.