Value of cardiac biomarkers in patients with acute pulmonary embolism

Prognostic stratification of patients with PE is important in management and potentially improve clinical outcome. Cardiac biomarkers are used as an adjunct to clinical and echocardiographic risk stratification in a variety of circumstances, [Creatine-kinase-MB [CK-MB]] and cardiac troponin I [cTnl] are most widely used because of their high sensitivities, and very high specificity of troponin for heart muscle injury. Evidence is mounting that myoglobin's sensitivity for myocardial necrosis combined with its unique release and clearance properties may render it particularly attractive as a risk marker either alone or in combination with other markers. The aim of the current study is to assess the levels of cardiac specific biomarkers in relation to different clinical, ECG and echocardiogrphic findings in patients with acute PE, as well as evaluating the prognostic value of these biomarkers for inhospital mortality and adverse clinical events. This study comprised 40 patients with proved PE [22 males and 18 females], their mean age was 50.05 +/- 13.09 years [range 22-70 years]. The following investigations were performed for all patients; 12-leads ECG, Full echo Doppler study, spiral CT of the chest, and laboratory testing: arterial blood gas, serum myoglobin, serum troponin, total CK and CK-MB, kidney and liver function tests. Significant elevation of CK-MB [> 10 micro/L] was noted only in 7.5% of patients, while cardiac cTnl was elevated [>/= 0.07 ng/ml] in 45% of patients and elevated serum myoglobin was found very early after symptoms [<4 h] in 55% of patients. Elevated serum cTnl and myoglobin were significantly associated with ECG signs of right ventricular strain and echocardiographic evidence of right ventricular dysfunction. The results of the present study demonstrate the prognostic value of cardiac specific biomarkers, cardiac troponin I and myoglobin in acute pulmonary embolism. Thus, the current data combined with the results of previous studies strongly support the integration of troponin and myoglobin testing into the risk stratification and management of patients with established acute PE

The role of protein kinases in antigen-activation of peripheral blood mononuclear cells of Schistosoma mansoni infected individuals

T cell recognition of antigens displayed on the surface of antigen presenting cell results in rapid activation of protein tyrosine kinases and kinases C. This process leads to second messengers, such as inositol phosphates and diacylglycerol, and phosphorylation of multiple proteins. The role of different protein kinases in the activation of peripheral blood mononuclear cells (PBMC) from Schistosoma mansoni infected individuals was evaluated using genistein and H-7, specific inhibitors of protein tyrosine kinase and kinase C, respectively. Our results showed that proliferation in response to soluble egg antigen or adult worm antigen preparation of S. mansoni was reduced when PBMC were cultured in presence of protein kinase inhibitors. Using these inhibitors on in vitro granuloma reaction, we also observed a marked reduction of granuloma index. Taken together, our results suggest that S. mansoni antigen activation of PBMC involves protein kinases activity.

Activity of a platelet protein kinase that phosphorylates fibrinogen and histone in Argentine hemorragic fever

La actividad de una proteinoquinasa plaquetaria que fosforila la cadena alfa del fibrinógeno y la histona como substrato exógeno, se evaluo en 28 pacientes con fiebre hemorrágica argentina, agrupados de acuerdo a la forma clínica en: 13 leves, 6 comunes y 9 graves. Las muestras de sangre se obtuvieron antes del tratmiento con plasma inmune, 4 dias después y en la convalescencia. La fosforilación de la histona exógena y del fibrinógeno se estudió con 25 Ci/mmol ( gamma-32p)-ATP. Simultaneamente se efectuó el recuesto de plaquetas y se midió la actividad del interferon alfa (IFN). La fosforilación de la histona se halló por debajo de los valores normales en todos los pacientes durante la fase aguda de la enfermedad. Esta reducción fue coincidente con los titulos más altos de IFN. La fosforilación del fibrinógeno estuvo igualmente disminuida. La fosforilación de la histona y del fibrinógeno estaban aun disminuidos 4 dias después del tratamiento, cuando el IFN era practicamente no dosable. El bajo nivel de fosforilación no puede atribuirse solamente a una disminución del número de plaquetas y podría ser otra evidencia de la existencia de una alteración plaquetaria en los pacientes con fiebre hemorragica argentina