ARAGANGLIOMA SYNDROME(PGL) is a clinical term that has been introduced to describe a group of diseases in which patients may have neoplasias of several paraganglia. 1,2 For at least 4 decades, it has been known that such conditions may be heritable. 3 In addition, thoracic, retroperitoneal, and adrenal lo-cations (eg, extra-adrenal or adrenal pheochromocytomas) are also wellrecognized components of PGL. 4,5 Thus, Author Affiliations and a complete list of the members of the European-American Paraganglioma Study Group appear at the end of this article.

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Objectives: The objectives were to evaluate the diagnostic accuracy for sepsis in an emergency department (ED) population of the cluster of differentiation-64 (CD64) glycoprotein expression on the surface of neutrophils (nCD64), serum levels of soluble triggering receptor expressed on myeloid cells-1 (s-TREM-1), and high-mobility group box-1 protein (HMGB-1).Methods: Patients with any of the following as admission diagnosis were enrolled: 1) suspected infection, 2) fever, 3) delirium, or 4) acute hypotension of unexplained origin within 24 hours of ED presentation. Levels of nCD64, HMGB-1, and s-TREM-1 were measured within the first 24 hours of the first ED evaluation. Baseline clinical data, Sepsis-related Organ Failure Assessment (SOFA) score, Acute Physiology and Chronic Health Evaluation (APACHE II) score, daily clinical and microbiologic information, and 28-day mortality rate were collected. Because there is not a definitive criterion standard for sepsis, the authors used expert consensus based on clinical, microbiologic, laboratory, and radiologic data collected for each patient during the first 7 days of hospitalization. This expert consensus defined the primary outcome of sepsis, and the primary data analysis was based in the comparison of sepsis versus nonsepsis patients. The cut points to define sensitivity and specificity values, as well as positive and negative likelihood ratios (LRs) for the markers related to sepsis diagnosis, were determined using receiver operative characteristics (ROC) curves. The patients in this study were a prespecified nested subsample population of a larger study.Results: Of 631 patients included in the study, 66% (95% confidence interval [CI] = 62% to 67%, n = 416) had sepsis according with the expert consensus diagnosis. Among these sepsis patients, SOFA score defined 67% (95% CI = 62% to 71%, n = 277) in severe sepsis and 1% (95% CI = 0.3% to 3%, n = 6) in septic shock. The sensitivities for sepsis diagnosis were CD64, 65.8% (95% CI = 61.1% to 70.3%); HMGB-1, 57.5% (95% CI = 52.7% to 62.3%); and s-TREM-1, 60% (95% CI = 55.2% to 64.7%). The specificities were CD64, 64.6% (95% CI = 57.8% to 70.8%), HMGB-1, 57.8% (95% CI = 51.1% to 64.3%), and s-TREM-1, 59.2% (95% CI = 52.5% to 65.6%). The positive LR (LR+) for CD64 was 1.85 (95% CI = 1.52 to 2.26) and the negative LR (LR-) was 0.52 (95% CI = 0.44 to 0.62]; for HMGB-1 the LR+ was 1.36 (95% CI = 1.14 to 1.63) and LR-was 0.73 (95% CI = 0.62 to 0.86); and for s-TREM-1 the LR+ was 1.47 (95%

SummaryIt has been experimentally shown that endotoxin induces a significant increase in the blood levels of a plasminogen activator inhibitor (PAI). We evaluated the effect of different doses of heparin (5 to 20IU kg−1 h−1), antithrombin III (10 to 40 U kg−1 h−1 and 240 U/kg as bolus) and of a combination of the two on: 1) the elevation of PAI activity, 2) fibrin deposition in kidneys and 3) mortality in rabbits infused with E. coli lipopoly-saccharide. Our results show that heparin plus AT III is able to significantly reduce the generation of endotoxin-induced PAI activity in rabbits' circulation. Low dose of heparin and a bolus injection of AT III both cause a decrease in the generation of PAI at 2 but not at 6 hours of endotoxin infusion. Moreover, fibrin deposits in kidneys of animals receiving heparin plus AT III or a bolus injection of AT III were significantly reduced as compared to control rabbits. The association between low levels of PAI and decreased fibrin deposits is strengthened by the significant correlation (p < 0.05) found between these two parameters. Finally, the plasma levels of PAI activity at 2 and 6 hours of endotoxin infusion in surviving animals were lower than those observed in animals that died within 2 hours after the end of treatment. We conclude that heparin plus AT III partially prevents the endotoxin-induced generation of PAI activity which seems to correlate with the reduced presence of fibrin deposits in kidneys and with a reduced mortality.

Background: Recent data have suggested that 18 million of new sepsis cases occur each year worldwide, with a mortality rate of almost 30%. There is not consensus on the clinical definition of sepsis and, because of lack of training or simply unawareness, clinicians often miss or delay this diagnosis. This is especially worrying; since there is strong evidence supporting that early treatment is associated with greater clinical success. There are some difficulties for sepsis diagnosis such as the lack of an appropriate gold standard to identify this clinical condition. This situation has hampered the assessment of the accuracy of clinical signs and biomarkers to diagnose sepsis.

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