Biomarkers in medicine
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The increased incidence of sepsis, a systemic response to infection that occurs in some patients, has stimulated interest in identifying infected patients who are at risk and intervening early. When this condition progresses to severe sepsis (characterized by organ dysfunction), mortality is high. Hospitals that have implemented recommendations of the Surviving Sepsis Campaign have seen a reduction in mortality rate for hospital-acquired severe sepsis. ⋯ Sepsis is a complicated syndrome with many physiological derangements and many emerging laboratory markers of sepsis have been proposed as adjuncts to clinical evaluation. The list includes cytokines, acute phase proteins, neutrophil activation markers, markers of abnormal coagulation and, recently, markers of suppression of both the innate and adaptive immune response. The perfect biomarker would accurately identify patients at risk of developing severe sepsis and then guide targeted therapy.
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Biomarkers in medicine · Feb 2011
ReviewFunctional testing methods for the antiplatelet effect of P2Y12 receptor antagonists.
Dual antiplatelet therapy with aspirin and a P2Y(12) receptor antagonist is the cornerstone of management in patients with acute coronary syndrome and those with coronary artery disease who have undergone coronary stent implantation. Clopidogrel is the most commonly used P2Y(12) antagonist. ⋯ The consistent observation that a lack of clopidogrel effect based on these tests is associated with poor clinical outcome has led to the promise of an individualized, patient-centered approach to antiplatelet therapy. Over the past few years, a wealth of data have helped bring this promise closer to reality, and upcoming clinical trials of platelet function testing could at last bring personalized medicine into routine clinical practice.
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The diagnosis of acute myocardial infarction currently rests on the measurement of troponin, a biomarker of myocardial necrosis. Unfortunately, the current generation troponin assays detect troponin only 6-9 h after symptom onset. This can lead to a delay in diagnosis and also excessive resource utilization when triaging patients who, ultimately, have noncardiac causes of acute chest pain. ⋯ These include markers of myocardial injury, such as myoglobin, heart-type fatty acid binding protein, glycogen phosphorylase BB; hemostatic markers, such as D-dimer; and finally, inflammatory markers, such as matrix metalloproteinase 9. Recently, highly sensitive troponin assays have reported an early sensitivity for myocardial infarction of greater than 95%, although at a cost of reduced specificity. The optimal strategy with which to use these novel biomarkers and highly sensitive troponins has yet to be determined, and interpretation of their results in light of thorough clinical assessment remains essential.