Raltitrexed induces systemic inflammatory reactions and toxidermia in patients with colorectal carcinoma

31st Congress of the European-Society-for-Medical-Oncology -- SEP 29-OCT 03, 2006 -- Istanbul, TURKEYWOS: 000248078900410European Soc Med Onco

Reactive oxygen species and chemokines: Are they elevated in the esophageal mucosa of children with gastroesophageal reflux disease?

AIM: To determine the role of inflammatory cytokines and reactive oxygen species (ROS) in childhood reflux esophagitis

Evaluation of Risk Factors for Antibiotic Resistance in Patients with Nosocomial Infections Caused by Pseudomonas aeruginosa

Background. Pseudomonas aeruginosa (P. aeruginosa) is resistant to various antibiotics and can cause serious nosocomial infections with high morbidity and mortality. In this clinical study, we investigated the risk factors in patients who were diagnosed with P. aeruginosa-related nosocomial infection. Methods. A retrospective case control study including patients with P. aeruginosa-related nosocomial infection. Patients who were resistant to any of the six antibiotics (imipenem, meropenem, piperacillin-tazobactam, ciprofloxacin, amikacin, and ceftazidime) constituted the study group. Results. One hundred and twenty isolates were isolated. Various risk factors were detected for each antibiotic in the univariate analysis. In the multivariate analysis, previous cefazolin use was found as an independent risk factor for the development of imipenem resistance (OR = 3.33; CI 95% [1.11-10.0]; = 0.03), whereas previous cerebrovascular attack (OR = 3.57; CI 95% [1.31-9.76]; = 0.01) and previous meropenem use (OR = 4.13; CI 95% [1.21-14.07]; = 0.02) were independent factors for the development of meropenem resistance. For the development of resistance to ciprofloxacin, hospitalization in the neurology intensive care unit (OR = 4.24; CI 95% [1.5-11.98]; = 0.006) and mechanical ventilator application (OR = 11.7;]; = 0.004) were independent risk factors. Conclusion. The meticulous application of contact measures can decrease the rate of nosocomial infections

A review of intussusception cases involving failed pneumatic reduction and re-intussusception

BACKGROUND: The aim of the present study was to evaluate cases in which intussusception was unsuccessfully treated with pneumatic reduction (PR), and intussusception recurred following PR

Risk Factors For Linezolid-Associated Thrombocytopenia And Negative Effect Of Carbapenem Combination

Introduction: Linezolid is a synthetic antimicrobial agent with a broad spectrum of activity against virtually all Gram-positive bacteria. Although linezolid is generally well tolerated, the prolonged use of linezolid can lead to myelosuppression, including neutropenia, thrombocytopenia, and anemia. The aim of this study was investigating the risk factors for thrombocytopenia in patients who received linezolid therapy. Methodology: This retrospective study was performed on patients who received linezolid therapy between July 2007 and December 2017. Thrombocytopenia was defined as either a platelets count of < 100x10(9)/L or a 25% reduction from the baseline platelet count. Results: A total of 371 patients, (198 (53%) male and 173(47%) female were included into the study. Mean duration of therapy was 12.81 +/- 5.19 days. Linezolid-induced thrombocytopenia was detected in a total of 111 patients. Using the univariate analysis advanced sex, serum urea concentration, baseline platelet level and low eGFR value were found to be risk factors for linezolid associated thrombocytopenia (p < 0.05). According to a multivariate analysis, patients undergoing carbapenem treatment combination therapy (p = 0.003) and with a baseline platelet level of < 200x10(9)/L (p = 0.00) were found to have a high risk of developing thrombocytopenia. Conclusions: Several factors may influence of linezolid associated thrombocytopenia. Platelet count should be monitored during therapy and thrombocytopenia should be kept in mind in patients with baseline platelet level of < 200x10(9)/L, low eGFR, linezolid-carbapenem combination therapy.WoSScopu

Neuroprotective effects of melatonin upon the offspring cerebellar cortex in the rat model of BCNU-induced cortical dysplasia

WOS: 000248658500014PubMed ID: 17572393Cortical dysplasia is a malformation characterized by defects in proliferation, migration and maturation. This study was designed to evaluate the alterations in offspring rat cerebellum induced by maternal exposure to carmustine-[1,3-bis (2-chloroethyl)-1-nitrosoure] (BCNU) and to investigate the effects of exogenous melatonin upon cerebellar BCNU-induced cortical dysplasia, using histological and biochemical analyses. Pregnant Wistar rats were assigned to five groups: intact-control, saline-control, melatonin-treated, BCNU-exposed and BCNU-exposed plus melatonin. Rats were exposed to BCNU on embryonic day 15 and melatonin was given until delivery. Immuno/histochemistry and electron microscopy were carried out on the offspring cerebellum, and levels of malondialdehyde and superoxide dismutase were determined. Histopathologic ally, typical findings were observed in the cerebella from the control groups, but the findings consistent with early embryonic development were noted in BCNU-exposed cortical dysplasia group. There was a marked increase in the number of TUNEL positive cells and nestin positive cells in BCNU-exposed group, but a decreased immunoreactivity to glial fibrillary acidic protein, synaptophysin and transforming growth factor beta 1 was observed, indicating a delayed maturation, and melatonin significantly reversed these changes. Malondialdehyde level in BCNU-exposed group was higher than those in control groups and melatonin decreased malondialdehyde levels in BCNU group (P<0.01), while there were no significant differences in the superoxide dismutase levels between these groups. These data suggest that exposure of animals to BCNU during pregnancy leads to delayed maturation of offspring cerebellum and melatonin protects the cerebellum against the effects of BCNU. (C) 2007 Elsevier B.V. All rights reserved

Changes in antimicrobial resistance and outcomes of health care-associated infections

To describe the change in the epidemiology of health care-associated infections (HAI), resistance and predictors of fatality we conducted a nationwide study in 24 hospitals between 2015 and 2018. The 30-day fatality rate was 22% in 2015 and increased to 25% in 2018. In BSI, a significant increasing trend was observed for Candida and Enterococcus. The highest rate of 30-day fatality was detected among the patients with pneumonia (32%). In pneumonia, Pseudomonas infections increased in 2018. Colistin resistance increased and significantly associated with 30-day fatality in Pseudomonas infections. Among S. aureus methicillin, resistance increased from 31 to 41%

Effect of Hepatosteatosis on the Virological Response in Entecavir and Tenofovir Therapies

Objective: Both chronic hepatitis B (CHB) and hepatosteatosis may lead to necroinflammation in liver. Therefore, the presence of hepatosteatosis might negatively affect the efficacy of antiviral therapy. We aimed to determine the effect of hepatosteatosis on virological response in patients with CHB receiving entecavir (ETV) and tenofovir (TDF) treatment

Broadly effective metabolic and immune recovery with C5 inhibition in CHAPLE disease

Complement hyperactivation, angiopathic thrombosis and protein-losing enteropathy (CHAPLE disease) is a lethal disease caused by genetic loss of the complement regulatory protein CD55, leading to overactivation of complement and innate immunity together with immunodeficiency due to immunoglobulin wasting in the intestine. We report in vivo human data accumulated using the complement C5 inhibitor eculizumab for the medical treatment of patients with CHAPLE disease. We observed cessation of gastrointestinal pathology together with restoration of normal immunity and metabolism. We found that patients rapidly renormalized immunoglobulin concentrations and other serum proteins as revealed by aptamer profiling, re-established a healthy gut microbiome, discontinued immunoglobulin replacement and other treatments and exhibited catch-up growth. Thus, we show that blockade of C5 by eculizumab effectively re-establishes regulation of the innate immune complement system to substantially reduce the pathophysiological manifestations of CD55 deficiency in humans