Objective: To determine the role of serum procalcitonin levels in predicting ascites infection in hospitalized cirrhotic and non-cirrhotic patients.Methods: A total of 101 patients (mean age: 63.4±1.3, 66.3% were males) hospitalized due to cirrhosis (n=88) or malignancy related (n=13) ascites were included in this study. Spontaneous bacterial peritonitis (SBP, 19.8%), culture-negative SBP (38.6%), bacterascites (4.9%), sterile ascites (23.8%) and malign ascites (12.9%) groups were compared in terms of procalcitonin levels in predicting ascites infection. Receiver operating characteristic (ROC) curves were used to evaluate the diagnostic performance of procalcitonin levels and predicting outcome of procalcitonin levels was compared with C-reactive protein (CRP).Results: Culture positivity was determined in 26.7% of overall population. Serum procalcitonin levels were determined to be significantly higher in patients with positive bacterial culture in ascitic fluid compared to patients without culture positivity (median (min-max): 4.1 (0.2-36.4) vs. 0.4 (0.04-15.8), p<0.001). Using ROC analysis, a serum procalcitonin level of <0.61 ng/mL in SBP (area under curve (AUC): 0.981, CI 95%: 0.000-1.000, p<0.001), <0.225 ng/mL in culture-negative SBP (AUC: 0.743, CI 95%: 0.619-0.867, p<0.001), <0.42 ng/mL in SBP and culture-negative SBP patients (AUC: 0.824, CI 95%: 0.732-0.916, p<0.001), and <1.12 ng/mL in bacterascites (AUC: 0.837, CI 95%: 0.000-1.000, p=0.019) were determined to accurately rule out the diagnosis of bacterial peritonitis. Predictive power of serum procalcitonin levels in SBP + culture-negative SBP group (AUCs: 0.824 vs 0.622, p=0.004, Fig 4), culture-positive SBP (AUCs: 0.981 vs 0.777, p=0.006, Fig 5) and (although less powerfull) in culture-negative SBP (AUCs: 0.743 vs 0.543, p=0.02, Fig 6) were found significantly higher than CRP.Conclusion: According to our findings determination of serum procalcitonin levels seems to provide satisfactory diagnostic accuracy in differentiating bacterial infections in hospitalized patients with liver cirrhosis related ascites.

BackgroundBlastocystosis is a frequent bowel disease. We planned to to evaluate the prevalence of Blastocystis spp. in patients who applied to the same internal medicine-gastroenterology clinic with or without gastrointestinal complaints to reveal the association of this parasite with diagnosed IBS and IBD.MethodsA total of 2334 patients with gastrointestinal symptoms composed the study group, which included 335 patients with diagnosed inflammatory bowel disease and 877 with irritable bowel syndrome. Patients without any gastrointestinal symptoms or disease (n = 192) composed the control group. Parasite presence was investigated by applying native-Lugol and formol ethyl acetate concentration to stool specimens, and trichrome staining method in suspicious cases.ResultsBlastocystis spp. was detected in 134 patients (5.74%) in the study group and 6 (3.12%) in the control group (p = 0.128). In the study group, Blastocystis spp. was detected at frequencies of 8.7% in ulcerative colitis (24/276), 6.78% in Crohn’s disease (4/59), 5.82% in irritable bowel syndrome (51/877), and 4.9% in the remaining patients with gastrointestinal symptoms (55/1122). Blastocystis spp. was detected at a statistically significant ratio in the inflammatory bowel disease (odds ratio [OR] = 2.824; 95% confidence interval [CI]: 1.149-6.944; p = 0.019) and ulcerative colitis (OR = 2.952; 95% CI: 1.183-7.367; p = 0.016) patients within this group compared to controls. There were no statistically significant differences between the control group and Crohn’s disease or irritable bowel syndrome patients in terms Blastocystis spp. frequency (p = 0.251, p = 0.133).ConclusionsBlastocystosis was more frequent in patients with inflammatory bowel disease, especially those with ulcerative colitis. Although symptomatic irritable bowel syndrome and Crohn’s disease patients had higher rates of Blastocystis spp. infection, the differences were not significant when compared to controls.

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Background/Aim. To identify the etiological role of Helicobacter pylori (Hp) and nonsteroidal anti-inflammatory drugs (NSAIDs) in endoscopically diagnosed duodenal ulcers (DUs). Methods. Patients undergoing esophagogastroduodenoscopy in two major hospitals in Antalya and Adiyaman were included in this study and assigned as duodenal ulcer (n = 152; median age: 41.0 (16–71) years; 58.6% males) or control group (n = 70; median age: 41.0 (18–68) years; 57.1% males). Patient demographics, risk factors, and NSAID/acetylsalicylic acid (ASA) use were recorded. Results. HP was more commonly located in the corpus (75.0 versus 50.0%; odds ratio [OR] = 3.00; 95% confidence interval [CI]: 1.66–5.44; P < 0.001), incisura (75.7 versus 60.0%; OR = 2.07; 95% CI: 1.13–3.79; P = 0.017), and antrum (80.3 versus 60.0%; OR = 2.71; 95% CI: 1.45–5.05; P = 0.001) among DU patients than controls. Hp positivity was 84.9% while Hp was negative in 15.1% of patients including those accompanied with NSAID and/or ASA use (9.2%), and those were negative for all three etiological factors (5.9%). Conclusion. Our findings indicate the substantial role of Hp in the pathogenesis of DU disease as identified in 84.9% of DU patients compatible with the background prevalence of 61.4% among age-matched control subjects. Hp was the single causative factor in 44.1% of our patients, while NSAID/ASA exposure was in 9.2%.