Biomedical subjects

Jesús M Cesar

Publications and source records attributed to Jesús M Cesar.

4 recordsLinked to original sources

PubMed2005

Lactate production by thrombin-activated platelets of patients with primary thrombocythemia.

INTRODUCTION: Platelet activation needs a high energy demand which is supplied by the degradation of glucose into lactate. Platelet response to agonists in patients with primary thrombocythemia is defective. We studied the production of lactate by the platelets of patients with this disease and defective platelet aggregation. MATERIAL AND METHODS: Ten patients suffering from primary thrombocythemia and ten controls were included in this study. The lactate generation was measured in resting and thrombin activated platelets in absence or presence of glucose. RESULTS: Resting platelets incubated for 30 min in phosphate-buffered saline (PBS) generated the same amount of lactate in patients (44.6+/-21.6 micromol/10(11) cells) and controls (41.0+/-17.3 micromol/10(11) cells). Addition of glucose led to similar increases in lactate formation by platelets in patients (82.2+/-26.4 micromol/10(11) cells) and controls (88.1+/-34.5 micromol/10(11) cells). The addition of thrombin in absence of glucose did not modify the lactate formation respective to PBS. Finally, the incubation of platelets with both glucose and thrombin caused further increases in the generation of lactate in both groups, patients (236.9+/-83.9 micromol/10(11) cells) and controls (228.6+/-63.5 micromol/10(11) cells) without differences between them. The production of lactate in both groups was also similar when platelets were incubated for 10 min or 20 min with both thrombin and glucose. However at 5 min, platelets of patients generated more lactate (97.8+/-23.7 micromol/10(11) cells) than controls (66.5+/-38.7 micromol/10(11) cells, p<0.05). CONCLUSIONS: These results suggest that thrombin is able to induce an initial hyperactivity of those pathways involved in the platelet energy production of patients with primary thrombocythemia.

Adolescent↗

PubMed2005

Platelet dysfunction in primary thrombocythemia using the platelet function analyzer, PFA-100.

We measured platelet function by standard aggregometric tests and by the PFA-100 (Dade Behring, Newark, DE) in samples from 55 patients with primary thrombocythemia (PT) and 26 healthy volunteers. Platelet function was evaluated in platelet-rich plasma by aggregation tests. PFA-100 studies (closure time) were performed in citrated whole blood using collagen-adenosine diphosphate (ADP) and collagen-epinephrine cartridges. Plasma levels of von Willebrand factor (vWF) also were measured. The mean +/- SD closure time for patients vs volunteers for the collagen-epinephrine cartridge was prolonged (210.8 +/- 62.2 vs 118.1 +/- 19.6 seconds; P < .001); results were abnormal for 38 patients (69%). Results with the collagen-ADP cartridge also were abnormal in patients (134.3 +/- 58.4 seconds) vs volunteers (87.3 +/- 15.6 seconds; P < .001); closure time was prolonged in 23 patients (42%). A decreased response to epinephrine (38.4% +/- 34.2% vs 82.5% +/- 10.3%; P < .001), the main defect detected by platelet aggregation tests, affected 32 patients (58%). Platelet response to collagen also was abnormal (52.0% +/- 34.6% vs 86.0% +/- 10.1%; P < .01) but affected only 21 patients (38%). vWF levels for patients were normal. The results seem to confirm that platelet function in patients with PT is abnormal and show that platelet function can be assessed by an easy, reproducible, and sensitive method, the PFA-100. Closure time usually was prolonged; this feature could be applied in the diagnosis of PT.

Adult↗

PubMed2004

Aging and oral anticoagulant therapy using acenocoumarol.

We evaluated the influence of aging, gender and indications of anticoagulant therapy on acenocoumarol requirements in 1845 patients from 30 to 99 years old receiving acenocoumarol therapy who were monitored in our hospital outpatient anticoagulation clinic from March 1993 through September 1999. The patients were stratified in seven age groups, comprising older than 80 years and the five decades between 30 years and 80 years. We found a progressive decrease in the acenocoumarol requirements from 30 years to 80 years (rho=-0.98), which was estimated as 2.7 mg/week per decade (11.5% per decade). This decrease was not the consequence of a different range of anticoagulation or differences in body weight. We did not find correlation between the decrease of acenocoumarol requirements and different biochemical parameters including, creatinine, calcium and alanine aminotransferase. We detected a progressive decrease in levels of serum total proteins but changes in this parameter did not correlate with the amount of acenocoumarol requirements. The dose of acenocoumarol (mg/week per patient) of those patients suffering from venous thromboembolism were higher than the remainder of the patients (18.4 +/- 9.3 versus 14.5 +/- 7.8, P <0.0001). This finding was also detected, after stratifying the patients by decades, from 60 years to 80 years. In conclusion, requirements of acenocoumarol decrease with aging; this decrease represents an important amount from 30 years to 80 years and it should be kept in mind to choose the initial dose of acenocoumarol. Patients with venous thromboembolism required a higher dose of acenocoumarol.

Acenocoumarol↗

PubMed2002

Thrombopoietin inside the pulmonary vessels in patients with and without pulmonary hypertension.

There is substantial evidence that platelet production and release take place in the lungs. Thrombopoietin (Tpo) stimulation can cause platelet release in the pulmonary vasculature. On the other hand, myelofibrosis can occur in Tpo-overexpressing transgenic mice models, and there is unexplained pulmonary hypertension in chronic myeloproliferative disorders including primary myelofibrosis. In this study, we aimed to assess local Tpo concentrations inside the pulmonary artery and associated vessels in humans. We measured Tpo concentrations in plasma samples taken concurrently from the right ventricle, the pulmonary artery, and the left ventricle during cardiac catheterization in patients with and without pulmonary hypertension. The study group comprised 10 patients with normal pulmonary arterial pressure (Group A, male/female 4/6, mean age 48 +/- 19) and 14 patients with pulmonary hypertension (Group B, male/female 9/5, mean age 57 +/- 16). The Tpo levels inside the right ventricle, the pulmonary artery and the left ventricle were 33.3 +/- 15.6, 47.2 +/- 33.9, and 34.4 +/- 18.6 pg/ml, respectively, in Group A; and 85.0 +/- 39.8, 128.4 +/- 50.4, and 81.5 +/- 35.5 pg/ml, respectively, in Group B. Levels of the Tpo were significantly higher in all three localizations in Group B compared to Group A. Moreover, the Tpo concentration inside the pulmonary artery is significantly higher than the Tpo concentrations in the right and left ventricles in Group B patients. There were positive correlations between the Tpo levels and pulmonary artery systolic pressure over the whole patient group. In conclusion, there could be an association between pulmonary hypertension and Tpo level. Moreover, lung vasculature holding the major regulatory thrombopoietic hormone, Tpo, may be an important place for megakaryocytopoiesis.

Adult↗