Biomarcadores en neumonías / Biomarkers in pneumonia

Las neumonías, tanto comunitarias como nosocomiales, constituyen una importante causa de morbimortalidad a nivel global y ocasionan además importantes costos sanitarios. Como en cualquier otro proceso infeccioso, una adecuada respuesta a la infección es un fenómeno complejo que requiere un apropiado y oportuno tratamiento antibiótico, así como una apropiada respuesta inflamatoria inicial para contener la proliferación y diseminación de los microorganismos, seguida por una respuesta antiinflamatoria compensatoria que restaure la homeostasis inicial. Recientes estudios han demostrado que una excesiva respuesta inflamatoria en sepsis y NAC severa puede asociarse con efectos deletéreos y peor pronóstico. Por otro lado, una exagerada respuesta antiinflamatoria puede tener efecto negativo en la resolución de la infección. Por lo tanto, una mejor comprensión de este delicado equilibrio proinflamatorio/antiinflamatorio y sus mediadores podrán ser de gran ayuda para valorar la presencia y gravedad de la neumonía así como su probable evolución. En estudios previos varios marcadores han sido ensayados: Proteína C reactiva (PCR), Procalcitonina (PCT), diversas interleuquinas (IL1, IL6, IL8 e IL10), factor de necrosis tumoral alfa (TNFalfa), etc., como marcadores de inflamación/infección, gravedad, fallo de tratamiento y pronóstico. La presente monografía tiene por objeto hacer una revisión sintética de la literatura reciente sobre el tema, tratando de explorar y objetivar fortalezas y debilidades de tales marcadores biológicos.

Community acquired and nosocomial pneumonia are considered a global health issue and a significant cause of morbility, mortality and important economic costs. As in other infectious diseases, an appropriate therapeutic response to the infection is a complex phenomenon that requires appropriate and timely antimicrobial treatment and acorrect initial inflammatory response to stop the microbial proliferation and dissemination, followed by an anti-inflammatory response to restore the initial homeostasis. Recently published studies have showed that exaggerated inflammatory response in sepsis and severe community acquired pneumonia may be associated with poorer outcomes. On the other hand, an exagerated inflammatory response may have a deleterious effect on the infection resolution. Consequently, a better understanding of the delicate balance inflammation/anti-inflammation and their mediators could be of great help to understand the presence and severity of pneumonia and even to predict its outcome. Several marker shave been used, including C-reactive protein (CRP), procalcitonin, several interleukines [IL1, IL6, IL8, IL10], tumor necrosis factor-alpha (TNF alfa), etc, as markers of inflammation /infection, severity, therapeutic failure, severity therapeutic failure and prognostic tool. This review was performed to summarize the observations of the more recent published data on this topic, trying to explore strengths and weaknesses of these markers.

Efficacy of a new mutated recombinant tissue-type plasminogen activator in beagles with acute coronary artery thrombi / 世界急诊医学杂志（英文）

BACKGROUND:Development of new coronary thrombolytic agents is hot in the market. A new drug, mutated recombinant tissue-type plasminogen activator (rtPAm), is the product of mutation of tPA by changing binding loci with plasminogen activator inhibitor (PAI)-1 to reduce the degradation. In vitro test has demonstrated that the activity of rtPAm is much higher than rtPA in the absence of PAI. The present study is to observe the efficacy of mutated recombinant tissue-type plasminogen activator (rtPAm) in coronary thrombolytic therapy. METHODS:A total of 30 adult beagles were equally divided into 5 groups after thrombi:vehicle group, urokinase group, rtPAm low-dose group, rtPAm medium-dose group, and rtPAm high-dose group. Thrombolytic effect and myocardial infarction were observed after thrombolytic therapy. RESULTS:In the urokinase group, time to reperfusion was (15.8±3.8) minutes. TIMI 2 flow was demonstrated in 4 beagles, TIMI 3 flow in 2, and re-occlusion in 4 after 90 minutes respectively. In the low-dose rtPAm group, time to reperfusion was (15±4.5) minutes; TIMI 2 flow was demonstrated in 2 beagles, TIMI 3 flow in 4, and re-occlusion in 2 after 90 minutes. In the high-dose rtPAm group, time to reperfusion was (7.5±2.6) minutes. None of the beagles showed re-occlusion after 90 minutes. The infarction areas were (2.1+0.9)％ in the medium-dose rtPAm group and (0.7+0.4)％ in the high-dose rtPAm group, which decreased significantly than those in the low-dose rtPAm group. The aggregation rate in the medium-dose and high-dose rtPAm groups decreased significantly than that in the urokinase group. CONCLUSION:rtPAm may serve as a thrombolytic agent with platelet-targeted fibrinolysis and antiplatelet aggregation activities.