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Antonakos N.,National and Kapodistrian University of Athens | Tsaganos T.,National and Kapodistrian University of Athens | Oberle V.,Jena University Hospital | Tsangaris I.,National and Kapodistrian University of Athens | And 7 more authors.
Critical Care | Year: 2017

Background: Failure of circulating monocytes for adequate cytokine production is a trait of sepsis-induced immunosuppression; however, its duration and association with final outcome are poorly understood. Methods: We conducted a substudy of a large randomised clinical trial. Peripheral blood mononuclear cells (PBMCs) were isolated within the first 24 h from the onset of systemic inflammatory response syndrome in 95 patients with microbiologically confirmed or clinically suspected gram-negative infections. Isolation was repeated on days 3, 7 and 10. PBMCs were stimulated for cytokine production. The study endpoints were the differences between survivors and non-survivors, the persistence of immunosuppression, and determination of admission clinical signs that can lead to early identification of the likelihood of immunosuppression. Results: PBMCs of survivors produced significantly greater concentrations of tumour necrosis factor-α (TNF-α), interleukin (IL)-6, IL-8, IL-10, interferon-γ and granulocyte-macrophage colony-stimulating factor after day 3. Using ROC analysis, we found that TNF-α production less than 250 pg/ml after lipopolysaccharide stimulation on day 3 could discriminate patients from healthy control subjects; this was associated with a 5.18 OR of having an unfavourable outcome (p = 0.046). This trait persisted as long as day 10. Logistic regression analysis showed that cardiovascular failure on admission was the only independent predictor of defective TNF-α production on day 3. Conclusions: Defective TNF-α production is a major trait of sepsis-induced immunosuppression. It is associated with significant risk for unfavourable outcome and persists until day 10. Cardiovascular failure on admission is predictive of defective TNF-α production during follow-up. Trial registration: ClinicalTrials.gov identifier: NCT01223690. Registered on 18 October 2010. © 2017 The Author(s).


Giamarellos-Bourboulis E.J.,National and Kapodistrian University of Athens | Pyleris E.,Sismanogleion Athens General Hospital | Barbatzas C.,Sismanogleion Athens General Hospital | Pistiki A.,National and Kapodistrian University of Athens | Pimentel M.,Cedars Sinai Medical Center
BMC Gastroenterology | Year: 2016

Background: Current knowledge suggests that small intestinal overgrowth participates in the pathogenesis of irritable bowel syndrome. It is questionable if this association is modulated by intake of proton pump inhibitors (PPIs). Methods: In a prospective study, quantitative cultures of duodenal aspirates were performed for aerobic species in 897 consecutive patients undergoing upper GI tract endoscopy. SIBO was defined as equal to or more than 103 cfu/ml. The effect of PPI intake on the relationship between SIBO and IBS was the primary endpoint. Results: Analysis among patients without any history of PPI intake (n = 713) showed that odds ratio (OR) for IBS in the event of SIBO was 5.63 (3.73-8.51, p < 0.0001); this was 4.16 (1.91-9.06) when analysis was done among patients with history of PPI intake (n = 184, p: 0.498 between patients without and with PPI intake). Multiple logistic regression analysis found that factors independently associated with SIBO were age above or equal to 60 years (OR: 2.36), body mass index more than or equal to 22 kg/m2 (OR: 0.60), presence of IBS (OR: 6.29), type 2 diabetes mellitus (OR: 1.59) and gastritis (OR: 0.47). Conclusions: The association between IBS and SIBO was completely independent from PPI intake. Although gastritis was protective against SIBO, results show that PPI intake cannot prime SIBO. © 2016 The Author(s).


PubMed | Sismanogleion Athens General Hospital, National and Kapodistrian University of Athens and Cedars Sinai Medical Center
Type: Journal Article | Journal: BMC gastroenterology | Year: 2016

Current knowledge suggests that small intestinal overgrowth participates in the pathogenesis of irritable bowel syndrome. It is questionable if this association is modulated by intake of proton pump inhibitors (PPIs).In a prospective study, quantitative cultures of duodenal aspirates were performed for aerobic species in 897 consecutive patients undergoing upper GI tract endoscopy. SIBO was defined as equal to or more than 10(3)cfu/ml. The effect of PPI intake on the relationship between SIBO and IBS was the primary endpoint.Analysis among patients without any history of PPI intake (n=713) showed that odds ratio (OR) for IBS in the event of SIBO was 5.63 (3.73-8.51, p<0.0001); this was 4.16 (1.91-9.06) when analysis was done among patients with history of PPI intake (n=184, p: 0.498 between patients without and with PPI intake). Multiple logistic regression analysis found that factors independently associated with SIBO were age above or equal to 60years (OR: 2.36), body mass index more than or equal to 22kg/m(2) (OR: 0.60), presence of IBS (OR: 6.29), type 2 diabetes mellitus (OR: 1.59) and gastritis (OR: 0.47).The association between IBS and SIBO was completely independent from PPI intake. Although gastritis was protective against SIBO, results show that PPI intake cannot prime SIBO.

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