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Common patterns and disease-related signatures in tuberculosis and sarcoidosis.

In light of the marked global health impact of tuberculosis (TB), strong focus has been on identifying biosignatures. Gene expression profiles in blood cells identified so far are indicative of a persistent activation of the immune system and chronic inflammatory pathology in active TB. Definition of a biosignature with unique specificity for TB demands that identified profiles can differentiate diseases with similar pathology, like sarcoidosis (SARC).

Here, we present a detailed comparison between pulmonary TB and SARC, including whole-blood gene expression profiling, microRNA expression, and multiplex serum analytes. Our analysis reveals that previously disclosed gene expression signatures in TB show highly similar patterns in SARC, with a common up-regulation of proinflammatory pathways and IFN signaling and close similarity to TB-related signatures. microRNA expression also presented a highly similar pattern in both diseases, whereas cytokines in the serum of TB patients revealed a slightly elevated proinflammatory pattern compared with SARC and controls.

Our results indicate several differences in expression between the two diseases, with increased metabolic activity and significantly higher antimicrobial defense responses in TB. However, matrix metallopeptidase 14 was identified as the most distinctive marker of SARC.

Described communalities as well as unique signatures in blood profiles of two distinct inflammatory pulmonary diseases not only have considerable implications for the design of TB biosignatures and future diagnosis, but they also provide insights into biological processes underlying chronic inflammatory disease entities of different etiology.

Current status of new anticoagulants in the management of venous thromboembolism.

Venous Thromboembolism, manifested as deep venous thrombosis and pulmonary embolism, is a common problem associated with significant morbidity, mortality, and resource expenditure.

Unfractionated heparin, low-molecular-weight heparin, and vitamin K antagonists are the most common treatment and prophylaxis, and have demonstrated their efficacy in a vast number of previous studies. Despite their broad use, these agents have important limitations that have led to the development of new drugs in a bid to overcome the disadvantages of the old ones without decreasing their therapeutic effect. These novel medications, some approved and others in different stages of development, include direct thrombin inhibitors like dabigatran etexilate, and direct activated factor X inhibitors like rivaroxaban.

The current paper will review the characteristics, clinical trial results, and current and potential therapeutic uses of these new agents with a focus on the categories of direct thrombin inhibitors and activated factor X inhibitors.

Prognostic clinical prediction rules to identify low-risk pulmonary embolism: a systematic review and meta-analysis.

Background: Prognostic assessment is important for the management of patients with pulmonary embolism (PE). A number of CPRs have been proposed for stratifying PE mortality risk. Aim of this systematic review is to assess the performance of prognostic clinical prediction rules (CPRs) in identifying low-risk PE.

Methods: MEDLINE and EMBASE databases were systematically searched until August 2011. Derivation and validation studies that assessed the performance of prognostic CPRs in predicting adverse events-risk in PE patients were included. Weighted mean proportion and 95% confidence intervals (CIs) of adverse events were then calculated and pooled using a fixed and a random-effects model. Statistical heterogeneity was evaluated through the use of I(2) statistics.

Results: Of 1125 references in the original search, 33 relevant articles were included. Nine CPRs were assessed in 37 cohorts, for a total of 35,518 patients. Pulmonary Embolism Severity Index and prognostic Geneva CPR were investigated in 22 and 6 cohorts, respectively. Eleven (29.7%) cohorts were of high quality. Median follow-up was 30 days. In low-risk PE patients, pooled short-term mortality (within 14 days or less) was 0.7% (95% CI 0.3-1.1%, random-effects model; I² = 49.6%), 30-day mortality was 1.7% (95% CI 1.1-2.3%, random-effects model; I² = 82.4%), and 90-day mortality was 2.2% (95% CI 1.2-3.4%, random-effects model; I² = 59.8%).

Conclusions: Prognostic CPRs efficiently identify PE patients at low risk of mortality. Before implementing prognostic CPRs in the routine care of PE patients, well-designed management studies are warranted. © 2012 International Society on Thrombosis and Haemostasis.

Pleural effusion in pulmonary embolism.

Pulmonary embolism is a common and potentially lethal disease that recurs frequently and is associated with long-term impairment and suffering. Patients with pulmonary embolism are at risk of death, recurrence of embolism, or chronic morbidity. Appropriate therapy can reduce the incidence of all. Pulmonary embolism is the most commonly overlooked disorder in patients with pleural effusion. Recent findings of pleural effusions due to pulmonary embolism are discussed in this review.

RECENT FINDINGS: The presence of pleuritic chest pain in a patient with a pleural effusion is highly suggestive of pulmonary embolism. Nearly all pleural effusions due to pulmonary embolism are exudates, frequently hemorrhagic, and with a marked mesothelial hyperplasia. Patients with a pleural effusion are likely to have an embolus in the central, lobar, segmental, or subsegmental pulmonary arteries and these are the regions in which spiral computed tomography pulmonary angiography (CTPA) can detect an embolus. No specific treatment is required for pleural effusion. The presence of bloody pleural fluid is not a contraindication for the administration of anticoagulant therapy.

SUMMARY: Pulmonary embolism is probably responsible for a significant percentage of undiagnosed exudative pleural effusions. Spiral CTPA is the best way to evaluate the possibility of pulmonary embolism in a patient with a pleural effusion. The treatment protocol of the patient with pleural effusion secondary to pulmonary embolism is the same as that for any patient with pulmonary embolism.

Timing of troponin I measurement in pulmonary embolism.

Troponin I (TnI) is an important prognostic marker and risk-stratification tool in patients with pulmonary embolism (PE). However, the best timing for this biomarker measurement is still unclear.

OBJECTIVE: To analyse the kinetics of TnI in patients hospitalised for PE in order to better ascertain the evolution of the biomarker in this disease. In particular, we attempted to determine which measurement is the most appropriate to assess the PE risk according to this biomarker's status.

DESIGN, SETTING, PATIENTS AND MAIN OUTCOME MEASURES: This was a prospective, single center, cohort study. TnI (Beckman Access method) was measured on admission, then every 8 h for 72 h in 200 stable patients hospitalised for PE in our cardiology department. Patients were classified into two groups: TnI-(negative) or TnI +.

RESULTS: Mean TnI peak occurred at H8: 0.67±0.55 ng/ml. TnI values then decreased quickly, but remained positive (>0.06 ng/ml) beyond the 72-h surveillance period. The TnI biological profile varied widely after admission. Of the patients TnI- on the first assessment, 15% were positive at the second measurement. Among patients hospitalised less than 24 h after the onset of symptoms, 30% were misclassified on admission. In all cases, the second assessment, eight hours after admission, gave the biomarker's true status.

CONCLUSION: Our study clarifies the kinetics of TnI in PE and highlights the situations in which an early TnI can be false negative. Many misclassifications could be avoided by taking into account the value of this biomarker obtained at H8.

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