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In this case report, we present a case of autoimmune pancreatitis (AIP) diagnosis in a patient after a 7-year history of suspicious pancreatic cancer. Kim's and Japanese criteria were used to diagnose AIP. Our case avoided undesirable invasive procedures and recovered thanks to the proper diagnosis and timely treatment with prednisone. Early and accurate diagnosis of AIP, in this case, had a significant impact on the treatment and prognosis process. (C) 2021 The Author(s) Published by S. Karger AG, Basel

Aim The aim of this study was to evaluate nutritional status and sarcopenia in patients with inflammatory bowel disease (IBD) in clinical remission. Methods A total of 344 patients with IBD in clinical remission were included in this cross-sectional study. Patients with clinical activity (Harvey-Bradshaw index >5 for Crohn's disease and partial Mayo scores ≥5 for ulcerative colitis) were excluded. Sociodemographic, clinical, and anthropometric data were recorded. BMI was categorized according to WHO criteria. Nutritional status was assessed using the Mini Nutritional Assessment (MNA) questionnaire. Body composition included fat-free mass (FFM) analyzed with Tanita-330 ST. Muscle strength was measured with a Takei digital hand grip dynamometer using a standard protocol. Physical performance was measured as 4-m gait speed. Sarcopenia was defined based on the European Working Group on Sarcopenia in Older People 2 criteria. Results Overall, 5.5% of patients were underweight, 9.9% were malnourished, and 39.5% were at risk of malnutrition. Sarcopenia and probable sarcopenia were diagnosed in 41.3% of patients. Total number of flares requiring hospitalization (100%) was the most important predictor of sarcopenia, followed by total number of flares (80.1%), FFMI (46.5%), age (44.6%), BMI (31.8%), MNA score (27.7%), serum creatinine (23.6%), anti-tumor necrosis factor alpha use (23.3%), and gender (17.8%). Conclusion In conclusion, our findings revealed a considerable proportion of IBD patients in clinical remission to be malnourished or at risk of malnutrition along with a high rate of sarcopenia. This emphasizes the need for concomitant screening for nutritional status and body composition analysis in patients with IBD for provision of appropriate nutritional support, even during the remission period, and prevention of sarcopenia-related surgical and poor clinical outcomes.

Post Endoscopic Retrograde Cholangiopancreatography (ERCP) pancreatitis is one of the most serious complications of ERCP. Our study aims to investigate the risk, predisposing factors and prognosis of pancreatitis after ERCP in elderly patients. Patients referred to the ERCP unit between April 2008 and 2012 and admitted to the hospital at least 1 day after the ERCP procedure were included to the study. Information including patient’s demographics, diagnosis, imaging findings, biochemical analysis, details of the ERCP procedure and complications were recorded. The severity of post ERCP pancreatitis (PEP) was determined by revised Atlanta Criteria as well as APACHE II and Ranson scores. A total of 2902 ERCP patients were evaluated and 988 were included to the study. Patients were divided into two groups as ≥ 65 years old (494 patients, 259 F, 235 M) and

Amaç: Pankreas kanserlerinin epidemiyolojisi ve genel sağkalım (GSK) özelliklerinin araştırılmasıdır.Gereç ve Yöntem: Ege Üniversitesi Kanserle Savaş Uygulama ve Araştırma Merkezine (EÜKAM) 1992-2017 yıllarında kayıtlı Ege Üniversitesi Tıp Fakültesi (EÜTF) kanser verileri retrospektif olarak taranmıştır. CANREG özel bilgisayar programına kayıtlı veriler, WHO ve Surveillance, Epidemiology, and End Results (SEER) sistemlerinde gruplanarak analizler yapılmıştır. İstatistiksel analizlerde Ki-kare, General Linear Model (GLM), Kaplan-Meier sağ kalım analizleri kullanılmıştır.Bulgular: Toplam 117.139 kanser olgusunun 2.507’si pankreas kanseridir. Olgularımızın 1.493’ü (%59,5) erkek, 1.014’ü (%40,5) kadın olup pankreas kanseri iki cinsiyette benzer oranlarda izlenmektedir. Pankreas başı, en sık yerleşim yeridir. Genellikle ileri evrede tanı konulan kuyruk yerleşimli tümörler, erkeklerde daha sıktır (%11,5 vs. %6,2; p=0,047). Erkeklerde en sık 60 69 yaş arasında, kadınlarda ise 70 yaş üzerinde izlenmektedir. Ekzokrin tümörler, endokrin tümörlerden anlamlı oranda fazla karşılaşılmaktadır (%95 vs. %5; p=0,002). 1992 yılından 2014 yılı sonuna kadar kaydedilen pankreas kanseri olgularında doğrusal bir artış mevcuttur ve yıllara göre olan bu artış anlamlıdır (GLM: F=10,91, p, Aim: To determine epidemiological and overall survival (OS) characteristics of pancreatic cancer patients.Materials and Methods: Data of Ege University Cancer Control and Research Center between 1992-2017 were screened retrospectively. Data recorded in CANREG program were grouped and analyzed in WHO and Surveillance, Epidemiology, and End Results (SEER) systems. Chi-square test, General Linear Model (GLM) and Kaplan-Meier survival analysis were used for statistical analysis.Results: Number of pancreatic cancer cases was 2,507 among 117,139 cancer cases. 1,493 (59.5%) of our cases were male and 1,014 (40.5%) were female. Pancreatic head was the most common location. Tail located tumors were more common in males (11.5% vs. 6.2%; p =0.047). It was most common in males between the ages of 60 and 69, in females over the age of 70. Exocrine tumors were significantly higher than endocrine tumors (95% vs. 5%; p=0.002). There was a linear increase in pancreatic cancer cases recorded from 1992 to the end of 2014, and this increase over the years was significant (GLM: F=10.91, p

Background/Aims: Ledipasvir (LDV) and sofosbuvir (SOF) as single-tablet regimen (STR) has been approved for treatment of chronic HCV infection (CHC) for treatment-naive or experienced cirrhotic or non-cirrhotic patients. Our aim was to analyse the effectiveness and safety of 12-24 weeks treatment of LDV/SOF (90mg/400 mg)+/- ribavirin in a real-life setting in Turkey. Materials and Methods: Between May-Dec 2016, 104 treatment-naive or experienced adult patients with CHC and with or without cirrhosis (including decompensated cirrhosis) were included in this observational study. Patients were administered LDV/SOF STR +/- ribavirin once daily for 12-24 weeks. SVR12 rates and effects of the baseline characteristics on SVR12 rates were assessed. Results: Out of 104 enrolled patients (61.5% female, mean age 62.0 years); 60.6% were cirrhotic, 76.0% previously used peg-IFN, 94.2% had GT1. At the end of the treatment, 77.8% (77/99, no data for 21 patients) had undetectable HCV-RNA and 98.9% (94/95) had SVR12. in the baseline characteristics subgroups, the SVR12 rates varied between 94.4% and 100%, and none of the baseline characteristics had a significant effect on the SVR12 rates. During the study, 6 (5.8%) patients died and none of the deaths was suspected to be related to the LDV/SOF. No treatment-emergent adverse event was reported. Conclusion: in conclusion, LDV/SOF +/- ribavirin yielded very high SVR12 rates, without any safety or tolerability concern in Turkey. the effectiveness of the LDV/SOF treatment was not affected by the patient demographics or medical characteristics such as fibrosis level, cirrhosis status, previous treatment status, HCV-RNA level or HCV genotype., Gilead Sciences, TurkeyGilead Sciences, This study was supported by Gilead Sciences, Turkey for editorial support in the preparation of this manuscript.

[Abstract Not Available]

WOS: 000429745000008, Triple-A syndrome is a rare, multi-systemic disease and is characterized by adrenal insufficiency, achalasia, or alacrima. The symptoms may also involve neurologic manifestations, including pyramidal findings and peripheral motor neuropathy. Other findings include autonomic dysfunction and cerebellar ataxia. In the present study, we present the case of two siblings with triple-A syndrome with neurologic manifestations. The neurologic abnormalities can lead to misdiagnosis owing to resemblance to the manifestations of other neurologic disorders. Therefore, the cases with triple-A syndrome should be carefully evaluated and examined for clinical and neurophysiologic signs.

Background/aims This study aimed to compare the causes of nonvariceal upper gastrointestinal bleeding (NVUGB), demographics, risk factors, and outcomes of patients during two periods between 1993 and 2016 in a tertiary health-care center in Turkey. Materials and methods We compared the causes of NVUGB and clinical outcomes in 421 patients hospitalized between January 1993 and December 1995 with those of 231 patients with NVUGB hospitalized between January 2015 and September 2016. We also compared epidemiological characteristics, risk factors, and the rates of endoscopic hemostatic procedures. Results We observed significant increases in patients' mean age, in the percentage of patients with comorbid conditions, and in the percentage of patients who received direct-acting oral anticoagulants before bleeding. We also observed a statistically nonsignificant increase in the diagnoses of gastric ulcer, along with a significant concordant decrease in diagnoses of duodenal ulcer as a cause of bleeding. The use of emergency surgical hemostasis decreased among cases of peptic ulcer bleeding. The overall rate of mortality from bleeding did not significantly change between the two periods. Conclusion Over the 23 years studied, the causes of NVUGB changed, probably because the population was increasingly elderly population and because of the use of anticoagulants and better therapeutic approaches to chronic duodenal ulcers. The use of emergency surgical hemostasis reduced, but mortality rate did not significantly change between the two specific periods.

INTRODUCTION:Crosstalk between hepatocytes and immune cells is the key point that ultimately leads to inflammation and fibrosis. This is well-known entity underlying the decompansation of liver failure. Recently, it has been shown that the ratio of lymphocyte to monocytes that can be measured easily in peripheral blood reflects many inflammatory processes. In this study, we aimed to find the novel inflammatory parameters predicting subclinical hepatic encephalopathy in patients with liver failure who were routinely followed up in outpatient clinics.METHODS:Seventy-six cirrhotic patients who were followed up in Ege University Medical Faculty Hospital Gastroenterology-Hepatology out-patient clinic were included in the study. Thirteen similar healthy volunteers in terms of age and gender were also recruited. We applied psychometric hepatic encephalopathy score (PHES) and Critical flicker frequency test (CFF) for both patient groups (with and without covert hepatic encephalopathy (CHE)). We analyzed neutrophil-to-lymphocyte ratio (NLR), lymphocyte-to-monocyte ratio (LMR), mean platelet volume as well as INR, CRP, albumin, total bilirubines and platelet counts from routine clinic testing samples, retrospectively.RESULTS:According to West-Haven criteria, CHE was detected in 41 patients and not detected in 35 patients. When CFF test was applied, patients with CHE completed by reacting late compared to non-CHE patients (pCONCLUSION:LMR and NLR, which are cheap and easily available hemogram parameters, can provide early warning to clinicians for cirrhotic patients in outpatient follow-up.

GIRIS ve AMAC: Uzun donem Methotrexat kullanimi artmis karaciger hasari ve fibrozis riski ile iliskilidir. Leflunomid hastalik modifiye edici bir ilactir. Leflunomid nukleer faktor kappa B aktivasyonunun guclu bir inhibitorudur. Ayni zamanda anti-oksidan aktivitesi de vardir. Bu deneysel calismada Methotrexat'in neden oldugu karaciger toksisitesinde Leflunomid tedavisinin etkinligi arastirilmistir. YONTEM ve GERECLER: 39 rat 4 gruba ayrilmistir. Methotrexat'a bagli karaciger toksisitesi tek doz 20mg/kg Methotrexat'in periton icine injeksiyonu ile olusturulmustur. Ardindan Leflunomid 5 gun boyunca 10 mg/kg dozda verilmistir. Ardindan serum ornekleri ve homojenize karaciger ornekleri toplanmistir. Serum alanin aminotransferaz, alkalin fosfataz, superoxide dismutaz, myeloperoxidaz aktivitesi, glutatyon duzeyleri calisilmis ve histopatolojik degerlendirme yapilmistir. BULGULAR: Leflunomid tedavisi tedavi almayan gruba gore karaciger semikantitatif skalaya bagli histopatolojik degerlendirmede anlamli duzelme saglamistir (Patolojik skor 1.1+0.7 ve 5.1+2, p

Crigler-Najjar syndrome presents as severe unconjugated hyper-bilirubinemia and is characteristically caused by a mutation in the UGT1A1 gene, encoding the enzyme responsible for bilirubin glucuronidation. Here we present a patient with Crigler-Najjar syndrome with a completely normal UGT1A1 coding region. Instead, a homozygous 3 nucleotide insertion in the UGT1A1 promoter was identified that interrupts the HNF1 alpha binding site. This mutation results in almost complete abolishment of UGT1A1 promoter activity and prevents the induction of UGT1A1 expression by the liver nuclear receptors CAR and PXR, explaining the lack of a phenobarbital response in this patient. Although animal studies have revealed the importance of HNF1 alpha for normal liver function, this case provides the first clinical proof that mutations in its binding site indeed result in severe liver pathology stressing the importance of promoter sequence analysis. (C) 2015 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved.

We aimed to measure the diurnal changes of critical flicker frequency in healthy subjects and cirrhotic patients and to investigate their relationship with sleep disturbance.Cirrhotic patients and healthy volunteers were included. All groups completed the Pittsburgh Sleep Quality Index and a simple sleep questionnaire. Sleep disturbance was defined as a Pittsburgh Sleep Quality Index score of5. Critical flicker frequency was measured twice a day to detect diurnal abnormalities.Overall, 59 cirrhotic patients (54.2% males, Mean Age 59 ± 11 years) and 18 controls (39.9% males, Mean Age 58 ± 9 years) were included. Sleep disturbances were more common in cirrhotics (66.1%) than controls (38.9%, p0.05). In cirrhotics, the critical flicker frequency was not related to decompensation. The nocturnal values were higher than the morning values in cirrhotics (64.4%), but not in controls (p0.0001). Additionally, sleep disturbances were more common in cirrhotics who had higher nocturnal values (p0.05).Changes in the diurnal critical flicker frequency were observed in cirrhotics but not in controls. Sleep disturbances in cirrhotics appear to be associated with deviations of the diurnal rhythm of critical flicker frequency rather than with clinical parameters such as the clinical stages of cirrhosis and the Model For End-Stage Liver Disease and Child-Pugh scores.

Celiac disease is a gluten-induced enteropathy controlled by gluten restriction. Celiac disease is occasionally associated with T-cell lymphoma. We report a case with celiac disease who presented with duodenal ulcer-like symptoms and endoscopic findings. The persistent symptoms despite a strict diet led to the suspicion of an associated malignancy. Intensive evaluation revealed a case with celiac disease associated with B-cell lymphoma. Although B-cell lymphoma is rare, it should be kept in mind especially in female patients with persistent symptoms and refractory celiac disease.

Background: Eradication rates of Helicobacter pylori have declined to unacceptable levels in recent years. New and effective treatment options are warranted both as a first and second line treatment. Aim: To test an effectiveness of modified sequential therapy with levofloxacin for H. pylori eradication in Turkey. Material and Methods: Helicobacter pylori infected dyspeptic patients were included to the study. Subjects were treated with modified sequential therapy consisting of rabeprazole 20 mg b.i.d. and amoxicillin 1 g b.i.d., for 7 days followed by rabeprazole 20 mg b.i.d, levofloxacin 500 mg q.d. and metronidazole 500 mg b.i.d for the remaining 7 days. Results: Sixty-three treatment naive patients and 37 previous treatment failures were enrolled to the study (59 F, 41 M, age: 21–80 years). There was five drop out. Helicobacter pylori eradication was achieved in 80 patients, intention-to-treat (ITT): 80% (95% CI: 71–87%) and per-protocol (PP): 84.2% (95% CI: 75–91%), totally. In treatment naive patients ITT and PP eradication rates were 82.5% (95% CI: 71–91%), and 86.7% (95% CI: 75–94%), respectively. As a second line treatment eradication was successful in ITT 75.7%.(95% CI: 59–88%), and PP 80% (95% CI: 63–92%).Mild side effects were reported by 8 patients (8.4%). Conclusions: Sequential therapy using “rabeprazole and amoxicillin 7 days followed by rabeprazole, metronidazole and levofloxacin for 7 days” is a new regimen with acceptable eradication rates in naive patients in Turkey. Further modifications in the dose or duration of this new sequential therapy might increase its effectiveness as both first and second line treatment.

Background: Non-alcoholic fatty liver disease (NAFLD) is common in obese and diabetics. Serine protease inhibitor Kazal-1 (SPINK-1) protein is highly expressed in the liver and adipose tissue of diabetic and obese suggesting its role in NAFLD. SPINK-1 also behaves as an acute phase reactant protein. Some genetic factors including the genetic variations in SPINK-1 protein have been linked to chronic pancreatitis and diabetes. We therefore hypothesized that SPINK-1 mutations might be a risk factor for the development of NAFLD. Methods: Liver biopsy proven fifty NAFLD cases (20 steatohepatitis, 30 diffuse fatty liver disease and 44 healthy controls were included to the study. Liver function tests were measured. Body mass index was calculated. Insulin resistance was determined by using a homeostasis model assessment (HOMA-IR). Ultrasound evaluation was performed for each subject. Common genetic mutations in the third exon of SPINK-1 gene were analyzed by direct sequencing method. Results: We found two cases with a SNP at N34S location in NAFLD group (allele frequency %4). One subject with diffuse fatty liver disease and other with liver cirrhosis due to NAFLD had N34S mutation. No SNPs were detected in healthy controls. In conclusions, in limited number of patients SPINK-1 mutations were not considered as a risk factor alone for NAFLD development.

Background/Aims: The diagnosis of an underlying myeloproliferative neoplasm (MPN) is often problematic in patients with Budd Chiari syndrome (BCS) or portal vein thrombosis (PVT). This study aimed to assess the diagnostic value of the JAK2 gene V617F gain-of-function mutation for MPN in splanchnic vein thrombosis patients. Materials and Methods: One hundred eleven patients (80 with PVT, 27 with BCS, and 4 with BCS and PVT) were investigated. The control group included 56 volunteers without any known diseases. LightCycler SNP genotyping was performed to detect the JAK2 V617F mutation in DNA extracted from peripheral blood. Results: The JAK2 V617F mutation was identified in six of 28 patients (21.4%) with idiopathic PVT or BCS and in eight of 45 patients (17.8%) with PVT or BCS secondary to a known prothrombotic factor, but in only one of 38 patients (2.6%) with PVT and cirrhosis (p=0.049). Conclusion: The JAK2 V617F mutation is a noninvasive molecular marker for occult MPNs and can be used for the diagnosis of latent MPNs presenting with thrombotic events. Analysis of JAK2 mutation in the patients with idiopathic PVT or BCS showed that 20% had latent MPNs. In addition to this JAK2 mutation, prothrombotic events were observed in a significant number of patients with splanchnic vein thrombosis. JAK2 gene analysis should be included in the research panel for BCS and PVT patients without cirrhosis.

WOS: 000395365500001, PubMed ID: 28261279, Gastroenteropancreatic neuroendocrine tumors (GEPNETs) are a relatively rare, heterogeneous group of diseases in which important advances have been observed in the diagnosis and treatment as well as in our understanding of the biology and genetics of the disease in recent years. Given the insufficient scientific data available on evidence-based management of GEPNETs and the differences in circumstances in individual countries, a multidisciplinary study group was established to provide guidelines for the management of GEPNETS. This study group consisted of a medical oncologist, endocrinologist, surgeon, pathologist, gastroenterologist, and a nuclear medicine specialist, who aimed to prepare a practical guide in the light of existing scientific data and international guidelines, to be used in common clinical practice., RocheRoche Holding; PfizerPfizer; Celgene, Suayib Yalcin has had advisory board role in Novartis, Roche, Pfizer, Amgen and speaker Bureau role for Gen ilac, Novartis, Roche, Pfizer and travel grant from Roche and Pfizer, and research grant from Celgene.

Alcoholic chronic pancreatitis is a severe, disabling, chronic inflammatory condition of the pancreas that is seen in fewer than 5% of alcoholics. The severity and unpredictability of this condition has lead to several theories on the mechanism causing chronic pancreatitis based on careful clinical observation. Hypothetical mechanisms were applied to various animal models. Finally, following multiple lines of evidence, there is a convergence of thought and development of some new models that are quite instructive. Taken together, chronic alcohol consumption by rats results in multiple effects on the pancreas that increase the risk of acute pancreatitis, including ongoing acinar cell injury that lowers the threshold for hyperstimulation-induced acute pancreatitis, neurohormonal injury, and adaptation that results in acinar cell hyperstimulation, increased susceptibility to viral mediated acute pancreatitis, and possibly other factors. After acute pancreatitis initiates the inflammatory process, the chronic inflammation and fibrosis of alcoholic chronic pancreatitis are driven by diet, the acinar cell stress response to continued alcohol that may be potentiated by toxic alcohol metabolites, hypoxia, hyperstimulation, and partial duct obstruction; plus the effects of proinflammatory immunocytes and cytokines; and by stellate cell-mediated fibrosis driven by anti-inflammatory cytokines, alcohol, and alcohol metabolites. The factors determining which alcoholic will develop alcoholic chronic pancreatitis likely involve genetic factors, dietary factors, and susceptibility to pancreatic injury through several mechanisms ranging from trauma to gallstones to viruses.

OBJECTIVES Acute pancreatitis is a multifactorial disease caused by activation of several inflammatory mediators. Leukotrienes, beside other mediators, may be involved in acute pancreatitis. The aim of this study was to investigate the effects of 'zafirlukast', a leukotriene receptor antagonist, in acute pancreatitis and its relation with prostaglandin synthesis. METHODS Eighty rats were randomly divided into eight groups. Acute pancreatitis was induced by subcutaneous injection of cerulein (20 microg/kg), four times at 1-h intervals. Zafirlukast (20 mg/kg) was applied intraperitoneally as a pretreatment. Prostaglandin synthesis was inhibited by low-dose indomethacin (5 mg/kg subcutaneously). Pancreatic histopathology, serum amylase activity and pancreatic myeloperoxidase activity were determined to assess the severity of pancreatitis. RESULTS Zafirlukast pretreatment alone did not induce any inflammation and fatty necrosis in pancreatic tissue. However, it increased the histopathological score from 3.70 +/- 0.57 to 6.62 +/- 0.53 in rats with acute pancreatitis (P < 0.001). Fatty necrosis was especially prominent in the zafirlukast-treated acute pancreatitis group compared with the untreated group (2.62 +/- 0.26 versus 0.40 +/- 0.22, respectively; P < 0.001). Inhibition of prostaglandin synthesis by indomethacin partially suppressed the harmful effects of zafirlukast in acute pancreatitis. It decreased the pathological score (4.62 +/- 0.73) and fatty necrosis (1.50 +/- 0.32) in that group. CONCLUSION Interestingly, leukotriene receptor antagonism by zafirlukast increased the pancreatic histopathological score and fatty necrosis in rats with acute pancreatitis. Blocking of cysteinyl leukotriene receptors might cause an induction of mediator synthesis via other pathways. Effects of leukotriene receptor antagonism on the pancreas must be evaluated extensively in further studies.

BACKGROUND: Many interrelationships exist between the thyroid gland and the gastrointestinal tract. Several past and recent studies have shown that the thyroid gland profoundly influences the structure and function of the exocrine pancreas in the rat. In the present study we investigated the effect of methimazole (METZ), an antithyroid drug, on cerulein induced acute pancreatitis (AP) in rats. METHODS: Rats were divided into 3 groups (10-12 weeks age, 200-250 g weight, n: 10). Group B was made hypothyroid with methimazole 5 mg/kg daily for 10 days and the others were untreated euthyroid groups. After 10 days, acute pancreatitis was induced with four doses of 20 microg/kg body weight of cerulein administered s.c at hourly intervals in group A and B while the control group C was given 4 doses of I ml saline. Pancreas wet weight (mg), plasma amylase activity (IU/l) and pancreatic histology were used as endpoints to quantify the severity of the AP. RESULTS: Plasma tri-iodothyronine (T3) (ng/dl) and thyroxine (T4) (microg/dl) levels were significantly reduced after METZ treatment for 10 days (p < 0.01). METZ pretreatment reduced significantly the cerulein induced increase in pancreatic weight (1,205 +/- 12 mg in METZ treated AP group versus 1,617 +/- 14 mg in AP group, p < 0.05) and the rise in amylase activity (7,078 +/- 816 IU/l in METZ treated AP group versus 8,611 +/- 830 IU/l in AP group p < 0.05). CONCLUSION: METZ reduces the severity of cerulein induced AP in rats. This effect might be through its antithyroid property.

Background & Aims The association between pancreatic intraductal papillary mucinous neoplasms (IPMNs) and extrapancreatic neoplasms (EPNs) is controversial. We performed a multicenter observational study to assess the incidence of EPNs after an IPMN diagnosis. Methods 1340 patients with IPMNs were evaluated from 2000 through 2013 at 4 academic institutions in Europe for development of EPN. To estimate the actual incidence of EPN, we excluded patients with an EPN previous or synchronous to the IPMN, and patients who had been followed for less than 12 months, resulting in a study population of 816 patients. The incidence of EPN was compared with sex-specific, age-adjusted European cancer statistics; the standardized incidence ratio (SIR), and the 5- and 10-year cumulative incidence rates were calculated. Results A total of 290/1340 patients had a history of EPN (prevalence of 21.6%). In this subgroup of patients, the IPMN was discovered incidentally in 241. Among the 816 patients included in the incidence analysis, 50 developed an EPN after a median time of 46 months from study enrollment. The incidence of any EPN was not greater in patients with than without IPMN with a SIR of 1.48 (95% confidence interval, 0.94–2.22) in males and of 1.39 (95% CI 0.90–2.05) in females. The 5- and 10-year cumulative incidence rates for development of EPN in patients with IPMN were 7.9% and 16.6% in men, and 3.4% and 23.1% in women. Conclusions Patients with IPMN do not have a significantly higher incidence of EPNs than the general European population. It might not be necessary to screen patients with IPMN for EPN.

Objectives: Nuclear factor-κB (NF-κB) is a potent mediator in several steps of acute pancreatitis. Leflunomide is a novel immunomodulating drug that is also a potent inhibitor of NF-κB activation. The aim of this study was to investigate the effects of leflunomide pretreatment in severe necrotizing pancreatitis in rats. Methods: Fifty rats were randomly divided into 5 groups. Severe necrotizing pancreatitis was induced by retrograde injection of 3% sodium taurocholate into the common biliopancreatic duct. Leflunomide (10 mg/kg) was given intragastrically for 2 doses before the experiment. Serum amylase activity, pancreatic histopathologic condition, malondialdehyde level, myeloperoxidase enzyme activity, nitric oxide level, and pulmonary changes were assessed. Results: Leflunomide pretreatment significantly ameliorated pancreatic hemorrhage, edema, and neutrophil infiltration and decreased histopathological score compared with the untreated severe necrotizing pancreatitis group (pathological score [mean ± SEM]: 6.70 ± 1.19 vs 12.36 ± 1.08 in the leflunomide treated and untreated groups, respectively, P < 0.01). Pulmonary changes was decreased in the leflunomide treated group (3.90 ± 0.45 vs 4.75 ± 0.25, respectively). Change in pulmonary alveolar distention was significant. Although serum amylase levels also decreased, the difference was not significant (5922 ± 3290 vs 15547 ± 5090 U/mL). Conclusions: Leflunomide is a beneficial agent in the severe form of acute pancreatitis in rats and should be considered as a potential agent for treatment of acute pancreatitis. Copyright © 2010 by Lippincott Williams & Wilkins.

Pancreatic renin-angiotensin system has been implied to play a role in the regulation of pancreatic functions and could be a new therapeutic target in acute pancreatitis. The aim of this study was to evaluate the therapeutic potential of angiotensin-converting-enzyme inhibition by captopril and angiotensin II type 1 receptor inhibition by L-158809 and losartan experimentally in acute pancreatitis.Rats were randomly divided into 15 groups. Acute edematous pancreatitis was induced by injection of cerulein 20microg/kg SC four times at hourly intervals. Severe necrotizing pancreatitis was induced by retrograde injection of 3% taurocholate into the biliary-pancreatic duct.Captopril, L-158809 and losartan were given intraperitoneally. Main outcome features: pancreatic pathology, pancreatic myeloperoxidase activity and serum amylase activity were assessed.Captopril decreased serum amylase (10,809+/-1867 vs. 4085+/-1028U/L, p0.01), myeloperoxidase activity (3.5+/-0.5 vs. 1.5+/-0.1, p0.05) and histopathological score (5.0+/-0.4 vs. 1.1+/-0.5, p0.01) in acute edematous pancreatitis. In taurocholate induced severe necrotizing pancreatitis captopril ameliorated histopathological score (10.1+/-1.2 vs. 3.4+/-0.5, p0.01), pancreatic parenchymal necrosis (4.5+/-0.6 vs. 0.0+/-0.0, p0.001), fatty necrosis (2.8+/-0.9 vs. 0.1+/-0.1, p0.01) and edema (2.1+/-0.3 vs. 1.4+/-0.3, p0.05). However, L-158809 did not have similar beneficial effects on acute pancreatitis in rats while losartan decreased pancreatic parenchymal necrosis and neutrophil infiltration.This study not only demonstrated the differential effects of captopril, losartan and L-158809 in acute pancreatitis but also showed that there is still much to investigate about pancreatic renin-angiotensin system. Inhibition of angiotensin-converting enzyme should be evaluated carefully as a potential new therapeutic target in acute pancreatitis.

OBJECTIVES Budd-Chiari syndrome (BCS) is characterized by hepatic venous outflow obstruction and may be caused by various prothrombotic disorders. We aimed to study the role of hyperhomocysteinaemia, factor V Leiden mutation and G20210A prothrombin gene mutation in the pathogenesis of the syndrome. METHODS Thirty-two patients (16 male, 16 female, aged 19-45 years) with angiographically verified BCS and 33 age-matched and sex-matched voluntary healthy controls (15 male, 18 female, aged 19-45 years) were included into the study. Factor V Leiden and prothrombin gene mutations were determined in extracted DNA from peripheric mononuclear cells, using a light cycler amplification system. Plasma homocysteine levels were measured by fluorescence polarization immunoassay. RESULTS The homozygote factor V Leiden mutation was diagnosed in four BCS patients and the heterozygote mutation was diagnosed in five. The frequency of the mutant allele was 20.3% in BCS patients and 7.6% in the controls (P < 0.05). There was no significant difference in prothrombin gene mutation frequency between the two groups. Serum homocysteine levels were significantly higher in the BCS group than in the controls (16.4 +/- 8.8 vs 11.0 +/- 2.7 micromol/l; P < 0.01). BCS patients with the mutant factor V Leiden allele have significantly higher levels of serum homocysteine (22.1 +/- 13.3 vs 14.4 +/- 5.9 mumol/l; P < 0.05). CONCLUSIONS Hyperhomocysteinaemia, especially when associated with the factor V Leiden mutation, is an important risk factor for the development of BCS.

Background: Infected necrosis in acute pancreatitis is the main factor in determining the prognosis of the disease. Early and accurate diagnosis of infected pancreatic necrosis might decrease mortality. The aim of the present study is to identify a reliable marker for the onset infection in three different experimentally induced pancreatitis models. Methods: Ninety female Wistar albino rats were randomly divided into nine groups. In three different experimental models, including cerulein induced acute oedematous pancreatitis (AEP), sterile pancreatic necrosis due to taurocholate-induced acute pancreatitis (SPN) and infected pancreatic necrosis taurocholate-induced acute pancreatitis (IPN). Serum levels of procalcitonin (PCT), C-reactive protein (CRP), tumour necrosis factor a (TNF-α), interleukin 6 (IL-6) and interleukin 8 (IL-8), amylase were measured. The degree of pancreatic damage also evaluated pathologically. Results: Procalcitonin levels were increased significantly in AEP, SPN and IPN compared to control groups (P < 0.05). PCT and IL-6 level were the highest in the IPN group (P < 0.05). Serum amylase, CRP, TNF-α, IL-2, and IL-8 levels were similar between IPN and SPN groups (P > 0.05), but higher than in other groups. The results of histological evaluation also correlated with the advent of the disease. Conclusion: Procalcitonin and IL-6 acts as reliable acute phase reactant in an experimental model of AEP, SPN and IPN in the rat. PCT and IL-6 combination might be surrogate marker of infected pancreatic necrosis and should be preferred to other markers assay especially in severe pancreatitis.

AIM: In this study we aimed to clarify the role of mast cells in the development and progression of inflammation in cerulein-induced acute pancreatitis (AP) in rats. We have also examined the effects of ketotifen; a mast-cell stabilizing agent in the treatment of acute pancreatitis and its relation with nitric oxide (NO) synthesis. METHODS: In the first part of the study we planned to examine the effects mast cell stabilization in acute pancreatitis, while the second part was focused on examining the relation between NO synthesis and the potential effects of ketotifen in AP. Wistar albino rats were randomly divided into 6 groups (n: 10). In the first part of the study, AP was induced by four subcutaneous (sc) injections of 20 microg/kg body weight of cerulein at hourly intervals in Groups A and B while Group C was treated with saline as the control group. Group B was pretreated with ketotifen 1 mg/kg (ip). In the second part, the study design was similar except for the inhibition of nitric oxide synthesis by N-nitro L-arginine methyl ester (L-NAME) 30 mg/kg (ip) in Groups D, E and F. Group D was treated with L-NAME and cerulein and Group E was treated with ketotifen, L-NAME and cerulein. Group F was treated with L-NAME and saline as the control group. Serum amylase activity and pancreatic myeloperoxidase activity (MPO) were measured. Pancreatic histology and mast-cell count in pancreatic tissue were evaluated. RESULTS: Mast cell count was found to be increased in the pancreatic tissue in cerulein-induced AP. (2.93+/-0.26 vs 1.98+/-0.26; p

Background: Eradication rates for Helicobacter pylori (H. pylori) have declined to unacceptable levels worldwide in recent years. Since we have high H. pylori prevalence but low eradication rates due to clarithromycin resistance, new and effective treatment options are warranted both as a first and second line treatment in Turkey. Sequential therapy including PPI and amoxicillin for 5 days followed by PPI, clarithromycin and tinidazole for an additional five days is emerging as an alternative to triple therapy for the initial treatment of patients infected with H. pylori. However, this regimen has not been so successful in countries with high clarithromycin resistance (over 50%). Our aim was to test an effectiveness of modified sequential therapy with levofloxacin in H. pylori eradication as a first and second line treatment. Materials and Methods: H. pylori infected dyspeptic patients including both treatment naive cases and previous treatment failures were included to the study. H. pylori infection was diagnosed histopathologically and by rapid urease test in endoscopic biopsies taken from gastric antrum and corpus or via 13C urea breath test. Subjects were treated with modified sequential therapy consisting of rabebrazole 20 mg b.i.d and amoxicillin 1 gr b.i.d., for 7 days followed by rabebrazole 20 mg b.i.d, levofloxacin 500 mg q.d and metronidazole 500 mg b.i.d for the remaining 7 days. Outcome was assessed 6 weeks after ending the therapy by 13C urea breath test. Results: Sixty-three treatment naive patients and 37 previous treatment failures were enrolled to the study (59 F, 41 M, age: 21-80 years). Fifteen patients were diagnosed with gastric or duodenal ulcers. There was five drop out during the study. H. pylori eradication was achieved in 80 subjects totally (PP 84.2%, ITT 80 %). In treatment naive patients H. pylori eradication was achieved in 52 revealing PP 86.7% and ITT 82.5% eradication success. As a second line treatment, modified sequential regimen achieved eradication in 28 patients revealing PP 80 % and ITT 75.7% success rates. Mild side effects were reported by 8 patients (8.4%). Treatment was not discontinued in any patients due to side effects. Conclusions: Sequential therapy using rabebrazole and amoxicillin seven days followed by rabebrazole, metronidazole and levofloxacin for the remaining seven days is an effective regimen in H. pylori eradication both as a first and second line treatment. This regimen with especially acceptable level of eradication rate as a second line treatment and high compliance might be the preferred regimen in countries with high H. pylori prevalence and high clarithromycin resistance.

WOS: 000264933100001, PubMed ID: 19222849, Background: Both C reactive protein (CRP) and procalcitonin (PCT) are well known acute phase reactant proteins. CRP was reported to increase in metabolic syndrome and type-2 diabetes. Similarly altered level of serum PCT was found in chronic liver diseases and cirrhosis. The liver is considered the main source of CRP and a source of PCT, however, the serum PCT and CRP levels in non-alcoholic fatty liver disease (NAFLD) were not compared previously. Therefore we aimed to study the diagnostic and discriminative role of serum PCT and CRP in NAFLD. Methods: Fifty NAFLD cases and 50 healthy controls were included to the study. Liver function tests were measured, body mass index was calculated, and insulin resistance was determined by using a homeostasis model assessment (HOMA-IR). Ultrasound evaluation was performed for each subject. Serum CRP was measured with nephalometric method. Serum PCT was measured with Kryptor based system. Results: Serum PCT levels were similar in steatohepatitis (n 20) and simple steatosis (n 27) patients, and were not different than the control group (0.06 +/- 0.01, 0.04 +/- 0.01 versus 0.06 +/- 0.01 ng/ml respectively). Serum CRP levels were significantly higher in simple steatosis, and steatohepatitis groups compared to healthy controls (7.5 +/- 1.6 and 5.2 +/- 2.5 versus 2.9 +/- 0.5 mg/dl respectively p < 0.01). CRP could not differentiate steatohepatitis from simple steatosis. Beside, three patients with focal fatty liver disease had normal serum CRP levels. Conclusion: Serum PCT was within normal ranges in patients with simple steatosis or steatohepatitis and has no diagnostic value. Serum CRP level was increased in NAFLD compared to controls. CRP can be used as an additional marker for diagnosis of NAFLD but it has no value in discrimination of steatohepatitis from simple steatosis.