2011 August 19

CSI: a severity index for Clostridium difficile infection at the time of admission.

Aug 192011

CSI: a severity index for Clostridium difficile infection at the time of admission.

J Hosp Infect. 2011 Aug 15;

Authors: Lungulescu OA, Cao W, Gatskevich E, Tlhabano L, Stratidis JG

Abstract
Clostridium difficile is a common cause of nosocomial diarrhoea in the USA. To develop a score model that would help to identify severe versus mild or moderate C. difficile infection (CDI) upon admission we performed a retrospective cohort study. Between January 2004 and December 2007, 255 patients met inclusion criteria for this study. Severe CDI was defined as cases that required colectomy, intensive care unit management, ended in death, or hospitalisation of >10 days. Data recorded included past medical history, physical examination on admission, laboratory data and imaging/colonoscopy data. To create the CDI severity index (CSI) score, we included four risk factors for severe CDI that were identified by univariate analysis: history of malignancy, white blood cell count at admission >20,000/dL, blood albumin <3.0mg/dL, and creatinine at admission >1.5-fold the baseline value. One point was assigned to each of the risk factors. As indicated by a c-statistic of 0.78, the CSI score predicted severe CDI much better than chance (c-statistics of 0.50). The risk of developing severe CDI increased by a factor of 2.9 (95% CI: 1.82-4.59) for each 1-point increase in the CSI score. A CSI score with a cut-off value of 2 had a sensitivity and specificity of 82% and 65%, respectively. The CSI score may quantify the risk of severe CDI at the time of admission, and help in early identification of patients who may benefit from more aggressive treatment.

PMID: 21849220 [PubMed - as supplied by publisher]

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Assessing adrenal insufficiency of corticosteroid secretion using free versus total cortisol levels in critical illness.

Intensive Care Med Start a Discussion »

Aug 192011

Assessing adrenal insufficiency of corticosteroid secretion using free versus total cortisol levels in critical illness.

Intensive Care Med. 2011 Aug 18;

Authors: Molenaar N, Johan Groeneveld AB, Dijstelbloem HM, de Jong MF, Girbes AR, Heijboer AC, Beishuizen A

Abstract
PURPOSE: To study the value of free versus total cortisol levels in assessing relative adrenal insufficiency during critical illness-related corticosteroid insufficiency. METHODS: A prospective study in a mixed intensive care unit from 2004 to 2007. We consecutively included 49 septic and 63 non-septic patients with treatment-insensitive hypotension in whom an adrenocorticotropic hormone (ACTH) test (250 ?g) was performed. Serum total and free cortisol (equilibrium dialysis), corticosteroid-binding globulin (CBG) and albumin were assessed. RESULTS: Although a low CBG resulted in a high free cortisol level relative to total cortisol, free and total cortisol and their increases were well correlated (r = 0.77-0.79, P < 0.001). In sepsis, hypoalbuminemia did not affect total and free cortisol, and increases in total cortisol upon ACTH predicted increases in free cortisol regardless of low binding proteins. In non-sepsis, total cortisol was lower with than without hypoalbuminemia; free cortisol did not differ, since hypoalbuminemia concurred with a low CBG. Increases in total cortisol depended less on binding proteins than on raw levels. The areas under the receiver operating characteristic curve for predicting increases in free from total cortisol were 0.93-0.97 in sepsis and 0.79-0.85 in non-sepsis (P = 0.044 or lower for sepsis vs. non-sepsis). CONCLUSIONS: Although the biologically active free cortisol fraction depends on binding proteins, total cortisol correlates to free cortisol in treatment-insensitive hypotension during critical illness. In sepsis, albumin is not an important binding molecule. Subnormal increments in total cortisol upon ACTH suffice in assessing relative adrenal insufficiency, particularly in sepsis.

PMID: 21850531 [PubMed - as supplied by publisher]

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Efficacy of Fidaxomicin Versus Vancomycin as Therapy for Clostridium difficile Infection in Individuals Taking Concomitant Antibiotics for Other Concurrent Infections.

Clin Infect Dis Start a Discussion »

Aug 192011

Efficacy of Fidaxomicin Versus Vancomycin as Therapy for Clostridium difficile Infection in Individuals Taking Concomitant Antibiotics for Other Concurrent Infections.

Clin Infect Dis. 2011 Sep;53(5):440-7

Authors: Mullane KM, Miller MA, Weiss K, Lentnek A, Golan Y, Sears PS, Shue YK, Louie TJ, Gorbach SL

Abstract
Background.?Treatment guidelines recommend stopping all implicated antibiotics at the onset of Clostridium difficile infection (CDI), but many individuals have persistent or new infections necessitating the use of concomitant antibiotics (CAs). We used data from 2 phase 3 trials to study effects of CAs on response to fidaxomicin or vancomycin. Methods.?Subjects with CDI were treated for 10 days with fidaxomicin 200 mg every 12 hours or vancomycin 125 mg every 6 hours, assessed for resolution of symptoms, and followed up for an additional 4 weeks for evidence of recurrence. Rates of cure, recurrence, and global cure (cure without recurrence) were determined for subgroups of subjects defined by CA use and treatment group. Results.?CAs were prescribed for 27.5% of subjects during study participation. The use of CAs concurrent with CDI treatment was associated with a lower cure rate (84.4% vs 92.6%; P < .001) and an extended time to resolution of diarrhea (97 vs 54 hours; P < .001). CA use during the follow-up was associated with more recurrences (24.8% vs 17.7%; not significant), and CA administration at any time was associated with a lower global cure rate (65.8% vs 74.7%; P = .005). When subjects received CAs concurrent with CDI treatment, the cure rate was 90.0% for fidaxomicin and 79.4% for vancomycin (P = .04). In subjects receiving CAs during treatment and/or follow-up, treatment with fidaxomicin compared with vancomycin was associated with 12.3% fewer recurrences (16.9% vs 29.2%; P = .048). Conclusions.?Treatment with CAs compromised initial response to CDI therapy and durability of response. Fidaxomicin was significantly more effective than vancomycin in achieving clinical cure in the presence of CA therapy and in preventing recurrence regardless of CA use.

PMID: 21844027 [PubMed - in process]

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Predictive value of interferon-? release assays for incident active tuberculosis: a systematic review and meta-analysis.

Lancet Infect Dis Start a Discussion »

Aug 192011

Predictive value of interferon-? release assays for incident active tuberculosis: a systematic review and meta-analysis.

Lancet Infect Dis. 2011 Aug 14;

Authors: Rangaka MX, Wilkinson KA, Glynn JR, Ling D, Menzies D, Mwansa-Kambafwile J, Fielding K, Wilkinson RJ, Pai M

Abstract
BACKGROUND: We aimed to assess whether interferon-? release assays (IGRAs) can predict the development of active tuberculosis and whether the predictive ability of these tests is better than that of the tuberculin skin test (TST). METHODS: Longitudinal studies of the predictive value for active tuberculosis of in-house or commercial IGRAs were identified through searches of PubMed, Embase, Biosis, and Web of Science and complementary manual searches up to June 30, 2011. Eligible studies included adults or children, with or without HIV, who were free of active tuberculosis at study baseline. We summarised incidence rates in forest plots and pooled data with random-effects models when appropriate. We calculated incidence rate ratios (IRR) for rates of disease progression in IGRA-positive versus IGRA-negative individuals. FINDINGS: 15 studies had a combined sample size of 26?680 participants. Incidence of tuberculosis during a median follow-up of 4 years (IQR 2-6), even in IGRA-positive individuals, was 4-48 cases per 1000 person-years. Seven studies with no possibility of incorporation bias and reporting baseline stratification on the basis of IGRA results showed a moderate association between positive results and subsequent tuberculosis (pooled unadjusted IRR 2·10, 95% CI 1·42-3·08). Compared with test-negative results, IGRA-positive and TST-positive results were much the same with regard to the risk of tuberculosis (pooled IRR in the five studies that used both was 2·11 [95% CI 1·29-3·46] for IGRA vs 1·60 [0·94-2·72] for TST at the 10 mm cutoff). However, the proportion of IGRA-positive individuals in seven of 11 studies that assessed both IGRAs and TST was generally lower than TST-positive individuals. INTERPRETATION: Neither IGRAs nor the TST have high accuracy for the prediction of active tuberculosis, although use of IGRAs in some populations might reduce the number of people considered for preventive treatment. Until more predictive biomarkers are identified, existing tests for latent tuberculosis infection should be chosen on the basis of relative specificity in different populations, logistics, cost, and patients' preferences rather than on predictive ability alone. FUNDING: Special Programme for Research and Training in Tropical Diseases (WHO), Wellcome Trust, Canadian Institutes of Health Research, UK Medical Research Council, and the European and Developing Countries Clinical Trials Partnership.

PMID: 21846592 [PubMed - as supplied by publisher]

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Differing risk factors for vancomycin-resistant and vancomycin-sensitive enterococcal bacteraemia.

Clin Microbiol Infect Start a Discussion »

Aug 192011

Differing risk factors for vancomycin-resistant and vancomycin-sensitive enterococcal bacteraemia.

Clin Microbiol Infect. 2011 May 31;

Authors: Peel T, Cheng AC, Spelman T, Huysmans M, Spelman D

Abstract
Clin Microbiol Infect ABSTRACT: Enterococcus is an important cause of bacteraemia. Previous epidemiological studies examining risk factors for enterococcal bacteraemia have used traditional case-control study designs, which can be potentially biased. This case-case-control study examining risk factors for enterococcal bacteraemia was conducted over 10 years (January 2000 to December 2009) in a tertiary, university-affiliated hospital. There were 440 episodes of enterococcal bacteraemia, 80 of which were caused by vancomycin-resistant Enterococcus (VRE). Two multivariable models were generated, comparing VRE and vancomycin-susceptible Enterococcus (VSE) with the same control group. VRE bacteraemia was associated with central venous catheter use (OR 11.6, 95% CI 2.6-51.5), neutropenia (OR 16.9, 95% CI 2.4-120.2), and allogenic bone marrow transplantation (OR 18.0, 95% CI 2.4-133.4). In contrast, VSE bacteraemia risk factors included: age (OR 1.0, 95% CI 1.0-1.1), exposure to metronidazole (OR 8.7, 95% CI 1.7-43.5), and gastrointestinal disease (OR 6.4, 95% CI 1.2-34.5). Meropenem use decreased the risk of VSE bacteraemia (OR 0.3, 95% CI 0.1-0.9). Hypoalbuminaemia was the only factor identified in both models (VRE, OR 6.0, 95% CI 1.7-21.1; VSE, OR 3.3, 95% CI 1.4-7.7). The absence of substantial overlap of risk factors for VRE and VSE argues in favour of differences in pathogenesis. These data suggest that environmental sources are more important in VRE bacteraemia. Endogenous sources, particularly the gastrointestinal tract, play a pivotal role in VSE bacteraemia. This study highlights the importance of infection control protocols to reduce the risk of VRE bacteraemia.

PMID: 21848977 [PubMed - as supplied by publisher]

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Increased risk of venous thrombosis in persons with clinically diagnosed superficial vein thrombosis: results from the MEGA study.

Blood Start a Discussion »

Aug 192011

Increased risk of venous thrombosis in persons with clinically diagnosed superficial vein thrombosis: results from the MEGA study.

Blood. 2011 Aug 17;

Authors: van Langevelde K, Lijfering WM, Rosendaal FR, Cannegieter SC

Abstract
Superficial vein thrombosis (SVT) is regarded a self-limiting disorder, although recent studies showed that ultrasonographically diagnosed SVT is a precursor for venous thrombosis. We aimed to determine whether the same holds true for clinically diagnosed SVT, and to what extent it is associated with thrombophilia in a population-based case-control study (MEGA). We found that a history of clinical SVT was associated with a 6.3-fold (95%CI 5.0-8.0) increased risk of deep-vein thrombosis and a 3.9-fold (95%CI 3.0-5.1) increased risk of pulmonary embolism. Blood group non-O and factor V Leiden showed a small increase in SVT risk in controls, with odds ratios of 1.3 (95%CI 0.9-2.0) and 1.5 (95%CI 0.7-3.3), respectively. In conclusion, clinically diagnosed SVT was a risk factor for venous thrombosis. Given that thrombophilia was only weakly associated with SVT, it is likely that other factors (varicosis, obesity, stasis) also play a role in its etiology.

PMID: 21849479 [PubMed - as supplied by publisher]

Link to Article at PubMed

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