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author:("pekin, tesim")
1.  Evaluation of Vancomycin Resistance 3 Multiplexed PCR Assay for Detection of Vancomycin-Resistant Enterococci from Rectal Swabs 
Annals of Laboratory Medicine  2013;33(5):326-330.
Background
Active screening for vancomycin-resistant enterococci (VRE) using rectal specimens is recommended to limit the spread of antimicrobial resistance within certain high-risk populations. We evaluated the diagnostic performance of Vancomycin Resistance 3 Multiplexed Tandem PCR assay (AusDiagnostics, Australia), a rapid multiplex real-time PCR assay that detects vanA and/or vanB.
Methods
Two-hundred-and-eleven rectal swabs from Hematology and Oncology unit were submitted for VRE surveillance via direct detection of vanA and/or vanB by culture and by using Vancomycin Resistance 3 Multiplexed Tandem PCR assay. Enterococci were identified to the species level by using standard biochemical tests and BD Phoenix Automated Microbiology System (BD Diagnostic Systems, USA). Vancomycin susceptibility of enterococci was determined using Etest (BioMerieux, France).
Results
Compared to the culture method, Vancomycin Resistance 3 Multiplexed Tandem PCR assay had a sensitivity of 84.0%, specificity of 98.8%, positive predictive value (PPV) of 91.3%, and negative predictive value (NPV) of 97.6%. The assay failed to detect 18 (8.5%) specimens because of the presence of PCR inhibitors; of the remaining 193 specimens, 25 (12.9%) were positive, 23 for vanA, and 2 for vanB. Although both sensitivity and specificity for vanA VRE was 100% compared to the culture method, all vanB-positive specimens tested negative by VRE culture.
Conclusions
Vancomycin Resistance 3 Multiplexed Tandem PCR assay is a rapid and laborsaving option for VRE surveillance for direct use on rectal swabs. However, the high rate of PCR failure owing to the inhibitors in the specimens and the low specificity for vanB should be considered when interpreting the results.
doi:10.3343/alm.2013.33.5.326
PMCID: PMC3756236  PMID: 24003422
Vancomycin resistance; Enterococcus faecium; PCR
2.  The Role of Serum Procalcitonin Levels in Predicting Ascitic Fluid Infection in Hospitalized Cirrhotic and Non-cirrhotic Patients 
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.
doi:10.7150/ijms.6014
PMCID: PMC3752724  PMID: 23983598
Procalcitonin; ascitic fluid infection; hospitalized patients; cirrhosis; malignancy; cut-off value.
3.  The Role of Helicobacter pylori and NSAIDs in the Pathogenesis of Uncomplicated Duodenal Ulcer 
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%.
doi:10.1155/2012/189373
PMCID: PMC3463179  PMID: 23049545
4.  Blastocystosis in patients with gastrointestinal symptoms: a case–control study 
BMC Gastroenterology  2012;12:122.
Background
Blastocystosis 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.
Methods
A 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.
Results
Blastocystis 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).
Conclusions
Blastocystosis 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.
doi:10.1186/1471-230X-12-122
PMCID: PMC3444885  PMID: 22963003
Ulcerative colitis; Crohn’s disease; Irritable bowel syndrome; Blastocystis spp

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