Biomedical subjects
I Benet
Publications and source records attributed to I Benet.
Allogeneic peripheral blood progenitor cell transplantation: analysis of short-term engraftment and acute GVHD incidence in 33 cases. allo-PBPCT Spanish Group.
The results of 33 allogeneic peripheral blood progenitor cells transplants (allo-PBPCT) in adult patients with hematologic malignancies were analyzed in a retrospective and multicenter study. In 21 of 33 cases (63%) the disease was refractory or in advanced stage and eight of the 33 cases (24%) were second transplants after relapse. Donors were treated with a median of 10 (4-16) micrograms/kg/day of rhG-CSF subcutaneously for 5-7 days. Three required a central venous line for harvesting. Peripheral blood leukapheresis product contained a median of 5.9 (1.8-13) 10(6)/kg CD34+ cells and a median of 309.5 (153-690) 10(6)/kg CD3+ cells. After a myeloablative regimen, all patients received PBPC from HLA-identical donors as the sole source of progenitor cells. Cyclosporin A (CsA) alone (n = 2), CsA and steroids (n = 9), and CsA and methotrexate (MTX) (n = 22) were used for GVHD prophylaxis. Growth factors post-transplant were given to 11 patients (33%). The median follow-up of the patients was 3 months. Actuarial median day for hemopoietic recovery was: neutrophils to >0.5 (>1) x 10(9)/l, day 14 (15); platelets to >20 (>50) x 10(9)/l, day 14 (21). The quantity of CD34+ cells infused did not significantly affect the engraftment kinetics, from a starting cutoff of 2.5 x 10(6)/kg. The speed of neutrophil recovery seemed to be influenced strongly by using rhG-CSF post-transplant and marginally by the type of GVHD prophylaxis. Actuarial probability for grade II-IV acute GVHD of the whole group was 37% (95% Cl, 20-54%).
[Effect of treatment with 13-cis-retinoic acid and ara-C on the hematopoietic stem cells of patients with myelodysplastic syndromes].
PURPOSE: To assess the "in vivo" effect of 13-cis-retinoic acid and low dose Ara-C in MDS as well as to establish "in vitro" advantage of retinoid dose-related growth pattern on bone marrow cultures as defined by culture timing and CFU-GM proliferative response. PATIENTS AND METHODS: We evaluated 28 patients diagnosed of MDS according to FAB classification, of whom 4 cases had RA, 8 cases SRA, 14 cases RAEB and 2 cases RAEB-T. Patients who had RA and SRA were treated with oral 13-cis-retinoic acid at doses of 20-40 mg daily for 4 months and those cases with RAEB and RAEB-T had subcutaneous Ara-C at doses of 3 mg/m2 twice a day for 21 days. The "in vivo" and "in vitro" effect of retinoic acid on the haemopoietic differentiation was evaluated by the growth CFU-GM in semisolid cell culture methods. RESULTS: Increasing in vitro concentrations of 13-cis retinoic acid did not enhance the growth of myelodysplastic progenitors. Nevertheless, our study did not find any beneficial therapeutic effect of retinoic compounds in MDS patients. In this study, low-dose Ara-C (3 mg/m2) showed similar effects when compared with higher doses reported by others. Furthermore, in terms of CFU-GM proliferation the concentration of colonies before and after treatment were fairly similar in all but two patients. CONCLUSIONS: The results drawn from our study demonstrated that there is no beneficial advantage of 13-cis-retinoic acid as a differentiation inducing agent on myelodysplastic patients. In contrast, lower doses of Ara-C showed similar effects on haemopoiesis of MDS patients than standard doses of 10-20 mg/m2 but with less side effects.
Chromosome 5 abnormalities in acute lymphoblastic leukemia.
We report two cases of acute lymphoblastic leukemia with involvement of chromosome 5. One of them showed a del(5)(q13q33) in a 5-year-old boy who had previously received antineoplastic chemotherapy for an L1-ALL that had been diagnosed nine months before. The other one showed a t(5;7)(q12-13;q36) together with a t(8;14)(q24;q32) and a der(1) in a 66-year-old man with an L3-ALL. Both chromosome 5 aberrations are interpreted as evolutionary events. In the first case, it was secondary to chemotherapy treatment; in the second, an evolutionary chromosome rearrangement, considering the translocation between chromosomes 8 and 14 as the primary cytogenetic event.
[Toxicity and hematopoietic regeneration produced by adjuvant chemotherapy in patients with neoplasia of the breast].
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[Technics of platelet separation from their plasma medium. Evaluation of the sepharose gel filtration].
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[Evaluation of heparin therapy: sensitivity of the various methods].
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[Systemic mastocytosis associated to thrombopathy. Ultrastructural findings].
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[Functional study of the platelets of the newborn].
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[Study of an inhibitor of platelet aggregation [prostacycline] derived from rat arterial wall (author's transl)].
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[Platelet osmotic shock. I. Assessment and ultrastructural changes (author's transl)].
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[Osmotic shock of platelets. II. Influence of different chemicals. Osmotic shock on filtered platelets (author's transl)].
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[A functional assay of fibrinoformation in the newborn (author's transl)].
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[A structural study of foetal fibrinogen (author's transl)].
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[Hemocoagulation disorders in a patient with prostatic cancer and hepatic cirrhosis].
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[Platelet anti-aggregating activity of furosemide (author's transl)].
The effect of furosemide on platelet aggregation, factor 3 availability, and response to hypotonic stress has been studied. Furosemide greatly inhibits platelet aggregation, with ADP, epinephrine, collagen, ristocetin, thrombin and serotonin. The use of heparin as anticoagulant does not alter this effect. Furosemide action is not conducted through calcium chelation. Platelet factor 3 availability is not modified by furosemide. There is a direct correlation between furosemide concentration and inhibition in the second phase of platelet response to hypotonic stress. The possibility of a disorder furosemide induced on the platelet metabolism, is suggested.