17 research outputs found

    Cryptococcus gattii infection in an immunocompetent host in Greece

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    We report a case of a 31-year-old otherwise healthy female with pulmonary cryptococcoma along with cryptococcal meningitis due to Cryptococcus gattii molecular type VGI, in Greece. Combined antifungal treatment and surgical excision of pulmonary cryptococcoma yielded a good response

    Decreases in the Serum VLDL-TG/Non-VLDL-TG Ratio from Early Stages of Chronic Hepatitis C: Alterations in TG-Rich Lipoprotein Levels

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    BACKGROUND: The liver secretes very-low-density lipoproteins (VLDLs) and plays a key role in lipid metabolism. Plasma total triglyceride (TG) level variations have been studied in patients with hepatitis C virus (HCV)-related chronic hepatitis (CH-C). However, the results of these studies are variable. A homogenous assay protocol was recently proposed to directly measure the TG content in VLDL (VLDL-TG) and VLDL remnants. METHODOLOGY/PRINCIPAL FINDINGS: Using the assay protocol, we determined serum VLDL-TG levels in 69 fasting patients with biopsy-proven HCV-related chronic liver disease and 50 healthy subjects. Patients were classified into stages F0-F4 using the 5-point Desmet scale. Serum total TG levels in patients with non-cirrhotic (F1-F3) CH-C did not demonstrate significant differences compared with healthy subjects, but serum VLDL-TG levels did demonstrate significant differences. Mean serum VLDL-TG levels tended to decrease with disease progression from F1 to F4 (cirrhosis). Compared with healthy subjects, serum non-VLDL-TG levels significantly increased in patients with stages F2 and F3 CH-C; however, we observed no significant difference in patients with liver cirrhosis. Furthermore, the serum VLDL-TG/non-VLDL-TG ratio, when taken, demonstrated a significant decrease in patients with CH-C from the mildest stage F1 onward. CONCLUSIONS/SIGNIFICANCE: The decrease in serum VLDL-TG levels was attenuated by increase in non-VLDL-TG levels in patients with non-cirrhotic CH-C, resulting in comparable total TG levels. Results of previous studies though variable, were confirmed to have a logical basis. The decrease in the serum VLDL-TG/non-VLDL-TG ratio as early as stage F1 demonstrated TG metabolic alterations in early stages of CH-C for the first time. The involvement of TG metabolism in CH-C pathogenesis has been established in experimental animals, while conventional TG measurements are generally considered as poor indicators of CH-C progression in clinical practice. The serum VLDL-TG/non-VLDL-TG ratio, which focuses on TG metabolic alterations, may be an early indicator of CH-C

    ©2010 Academic Journals Full Length Research paper Comparison of community and hospital-acquired bacteremia in a Greek university hospital: One year

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    blood culture results from the microbiology department of our hospital. One thousand three hundred and sixty six cases were detected in 1336 patients. The rate of true bacteremia which was 13.1 and 10.7 % of cultures were contaminated. Of the 1366 episodes of bloodstream infection, 55.3 % were community-acquired and 44.7 % were health-care associated. Gram-positive bacteria prevailed (58.5%), followed by gram negative bacilli (38.5%). Polymicrobial bacteremia was detected in 2.2 % of cases. Coagulase-negative staphylococci (CoNS) were the leading cause (550/1366 = 40.3%), whilst enterococci, Staphylococcus aureus and Streptococci represented 8, 6.4 and 3.8 % respectively. Pseudomonas aeruginosa was the commonest gram-negative isolate (155/1366 = 11.3%), followed by Escherichia coli (8.2%) and Acinetobacter sp. (7.3%). Fungi were isolated in the 3 % of the isolates and Candida albicans accounted for the 70.7 % of them. Fatal outcome due to bloodstream infections was 15.3 % and 5.7 % in hospital (HA) and community-acquired (CA) episodes, respectively (P < 0.0005).The highest mortality occurred in patients with bacteremia due to Acinetobacter (41%) in HA episodes, and in patients with bacteremia due to S. aureus (34.0%) in CA incidents. Key words: Bacteraemia, pathogens, antimicrobial resistance
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