Background/Aims: Pancreatic steatosis (PS) is a generally used term to define accumulation of fat in the pancreas. In theory PS may be able to affect the exocrine function of pancreas. In this study we aimed to determine the effect of PS on exocrine pancreas function. Materials and Methods: Forty-three patients with PS determined by 3 tesla magnetic resonance imaging (MRI) and 48 patients without PS were included in this study. Patients with PS were classified as group 1 and control patients were classified as group 2. Fecal elastase-1 levels were determined. Fecal elastase-1 levels Results: Fecal elastase-1 levels was significantly lower in group 1 compared to group 2 (319.76±45.7 vs 549.31±69.4, respectively, p=0.003). Proportion of patients with EPI was significantly higher in group 1 than group 2 (35.5% vs 12% p=0.042). There were no significant differences in terms of severity or the anatomic distribution of PS in patients with PS with EPI based on MRI (p=0.052, p=0.198, p=0.405) Conclusion: Current study demonstrates that PS can cause EPI. Cite this article as: Tahtacı M, Algın O, Karakan T, et al. Can pancreatic steatosis affect exocrine functions of pancreas? Turk J Gastroenterol 2018; 29: 588-94.

Gastric neuroendocrine neoplasms (g-NENs) or neuroendocrine tumors are generally slow-growing tumors with increasing incidence. They arise from enterochromaffin like cells and are divided into four types according to clinical characteristic features. Type 1 and 2 are gastrin dependent, whereas type 3 and 4 are sporadic. The reason for hypergastrinemia is atrophic gastritis in type 1, and gastrin releasing tumor (gastrinoma) in type 2 g-NEN. The diagnosis of g-NENs needs histopathological investigation taken by upper gastrointestinal endoscopy. g-NENs are positively stained with chomogranin A and synaptophysin. Grading is made with mitotic index and ki-67 proliferation index on histopathological analysis. It is crucial to discriminate between types of g-NENs, because the management, treatment and prognosis differ significantly between subtypes. Treatment options for g-NENs include endoscopic resection, surgical resection with or without antrectomy, medical treatment with somatostatin analogues, netazepide or chemotherapy regimens. Follow-up without excision is another option in appropriate cases. The prognosis of type 1 and 2 g-NENs are good, whereas the prognosis of type 3 and 4 g-NENs are close to the prognosis of gastric adenocancer.

Aim: To define the prevalence of polyautoimmunity (PAI) among celiac disease (CD) patients and to compare clinical and laboratory features of CD patients with or without PAI in order to determine the risk factors for PAI in CD. Material and Method: Patients diagnosed with CD in our clinic between 2007 and 2014 with at least 1 year of follow-up were retrospectively evaluated. Totally 145 patients were included in the study. Information on patient demographics and laboratory data were obtained from patient records. The study participants were divided into 2 groups. Group 1 was the CD-alone group consisting of patients without any other autoimmune diseases (AIDs), while group 2 was the PAI group consisting of patients with accompanying one or more AIDs. Results: The mean age of 145 CD patients (106 female and 39 male) included in the study was 37.2 ± 12.3 years. Of the 145 patients included, 48 (33.1%) were in the PAI group. When two groups were compared with each other in terms of the demographic features and laboratory data, the following were identified as risk factors for PAI: female gender, family history for AIDs, antigliadin IgG positivity, vitamin D deficiency, antinuclear antibody positivity ≥1/80 titer and having any musculoskeletal disease. Conclusion: To the best of our knowledge, this is one of the largest studies in the literature on CD patients for the PAI prevalence and related risk factors. Identification of the risk factors in early stages is important to explore PAI among CD patients. Larger, prospective studies are warranted about the risk factors and autoimmune characteristics of CD.

Background/Aims: The dynamic thiol/disulfide homeostasis plays pivotal roles in many physiological mechanisms in an organism. We aimed to investigate whether dynamic thiol/disulfide homeostasis changes among patients with acute pancreatitis. Materials and Methods: This prospective trial contained 45 patients with acute pancreatitis and 45 sex-and age-matched healthy volunteers as control group. Thiol/disulfide homeostasis parameters were measured by a novel and automated assay, and detected results were compared between the two groups. Results: Disulfide/total thiol percent ratio and disulfide/native thiol percent ratios were significantly higher in acute pancreatitis group; besides the native thiol, total thiol levels and native thiol/total thiol percent ratios were significantly lower (for all p Conclusion: The thiol/disulfide homeostasis is impaired in acute pancreatitis with a shift toward the oxidative status, and this deficiency might be a pathogenic factor in acute pancreatitis. The correction of this thiol/disulfide imbalance may be a new target in the management of acute pancreatitis. Cite this article as: Köseoğlu H, Alışık M, Başaran M, et al. Dynamic thiol/disulphide homeostasis in acute pancreatitis. Turk J Gastroenterol 2018; 29: 348-53.

Background: The hospital outcomes and predictors of acute peripancreatic fluid collection (APFC) have not been well-characterized. In this study, we aimed to investigate the clinical outcomes of APFC in patients with acute pancreatitis (AP) and the role of the systemic immune-inflammation index (SII), systemic inflammation response index (SIRI), and C-reactive protein (CRP) level in predicting the occurrence of APFC. Methods: In this retrospective study, the complicated group (patients with APFC) and the uncomplicated group (patients without APFC) were compared for their clinical characteristics, hospital outcomes (mortality rate, intensive care unit admission rate, and length of hospital stay), pseudocyst formation, CRP levels, SII, and SIRI on admission and at 48 hours. Results: Of 132 patients with AP, 51 (38.6%) had APFC and eight (6.1%) had pancreatic pseudocysts. Of 51 patients with APFC, 15.7% had pancreatic pseudocysts. Pseudocyst did not develop in the uncomplicated group. SII value at 48 h [median 859 (541–1740) x 10⁹/L vs. 610 (343–1259) x 10⁹/L, P = 0.01] and CRP level at 48 h [89 (40–237) mg/L vs. 38 (12–122) mg/L, P = 0.01] were higher in the complicated group than in the uncomplicated group. The length of hospital stay was longer in the complicated group, compared with the uncomplicated group [median 8 days (5–15), vs. 4 days (3–7), P < 0.001, respectively]. No significant difference was detected between the two study groups’ mortality rates and intensive care unit admission rates. Conclusions: While 38.6% of the AP patients had APFC, 6.1% of all patients and 15.7% of the patients with APFC had pancreatic pseudocysts. APFC was found to lengthen the hospital stay and to be associated with the SII value and CRP level measured at 48 h.

Malnutrition is an important and commonly seen prognostic factor in patients with cirrhosis. The diagnosis of malnutrition in cirrhosis patients may be challenging, and an easily measured and widely usable marker is lacking. Prealbumin, however, is an easily measured marker. In the current study we measured prealbumin levels in cirrhotic patients with no clinically apparent malnutrition and used it as a malnutrition marker. Another aim of this study was to evaluate the effect of nutritional support on patient with low prealbumin levels. Fifty-two patients with Child A and Child B cirrhosis were selected for the study. Prealbumin levels were studied, and Child and MELD scores were calculated. Patients with prealbumin levels ˂180 mg/L were considered to have malnutrition, and two different types of nutritional products were given to these patients. The patients given nutritional support were investigated a month later, and parameters were compared. According to the prealbumin threshold of 180 mg/L, malnutrition frequencies were 59.3% for Child A and 95% for Child B cirrhosis. After the provision of nutritional support statistically significant improvements in albumin and INR levels were detected. In addition, the MELD score decreased; however, it was not statistically significant (P: 0.088). A statistically significant decrease in the MELD score was only obtained in patients with Child B cirrhosis (P: 0.033). When the oral replacement therapies were investigated separately, a statistically significant decrease in MELD scores was detected with product 1 (P: 0.043). Prealbumin can be used as an easily measured parameter for earlier detection of malnutrition in patients with cirrhosis and without clinically apparent malnutrition. Oral nutritional support, especially with products containing relatively high carbohydrate levels and low protein, may have a favorable effect on MELD scores.