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3. Micafungin as antifungal prophylaxis in non-transplanted haemotological patients

Author

Villaescusa, T, Vázquez, L, Bergua, J M, García, J, Romero, A, Olave, M T, García Belmonte, D, Queipo de Llano, M P, and Grupo de Infecciones en pacientes hematológicos. Sociedad Andaluza de Hematología y Hemoterapia.

Subjects
0301 basic medicine, Male, Antifungal Agents, Lymphoma, Original, Aspergillosis, 0302 clinical medicine, Toxicity profile, toxicicidad, Aged, 80 and over, Candidiasis, Anemia, Aplastic, General Medicine, Middle Aged, Precursor Cell Lymphoblastic Leukemia-Lymphoma, Leukemia, Myeloid, Acute, hongos, 030220 oncology & carcinogenesis, fungal, Candida spp, Female, prophylaxis, medicine.drug, Microbiology (medical), Antifungal, Adult, medicine.medical_specialty, Aspergilllus, medicine.drug_class, 030106 microbiology, echinocandins, 03 medical and health sciences, Young Adult, medicine, Humans, In patient, Aged, Retrospective Studies, Pharmacology, Immunosuppressive treatment, Gynecology, business.industry, Eortc criteria, profilaxis, Micafungin, toxicity, equinocandinas, medicine.disease, Hematologic Diseases, business
Abstract

espanolIntroduccion. Las infecciones fungicas son una importante causa de morbilidad y mortalidad en los pacientes hematologicos. Estas infecciones son principalmente debidas a Candida spp.y Aspergillus spp. La mortalidad debida a estas infecciones es alta, pero ha descendido a lo largo de las ultimas series gracias a los mejores agentes antifungicos. Las equinocandinas son, in vitro, muy activas contra Candida y Aspergillus spp. El objetivo de este estudio es analizar la eficacia y seguridad de micafungina en la profilaxis antifungica de pacientes hematologicos en tratamiento quimioterapico. Material y metodos. Un estudio multicentrico, observacional, retrospectivo se llevo a cabo en 7 servicios de Hematologia en Espana. Se incluyeron los pacientes ingresados con quimioterapia o tratamiento inmunosupresor que hubieran recibido micafunfina como profilaxis entre el 1 de enero de 2009 y el 31 de diciembre de 2014. Resultados. Hubo 5 casos de infeccion fungica probable o probada (4,8%) segun los criterios de la EORTC de 2008: 2 probadas, 3 probables. Las infecciones fungicas fueron 3 aspergilosis y 2 candidiasis. No hubo ningun abandono de la profilaxis con micafungina debido a toxicidad. Conclusion. Micafungina es un agente antifungico que, usado en profilaxis, ha demostrado buena eficacia y excelente perfil de toxicidad, siendo una opcion interesante en pacientes que requieren profilaxis antifungica durante su hospitalizacion. EnglishIntroduction. Fungal infections are a major cause of morbidity and mortality in the haematological patients. These infections are mainly due to Candida spp. and Aspergillus spp. Mortality by these infections is high, but rates have descended in the latest series due to better antifungal agents. Echinocandins are, in vitro, very active against Candida and Aspergillus spp. The objective of the study is to analyse the efficacy and safety of micafungin in the antifungal prophylaxis of haematological patients on chemotherapy. Material and methods. A multicentre, observational retrospective study was performed in 7 Haematology Departments in Spain. Patients admitted to these departments with chemotherapy or immunosuppressive treatment, and who had received antifungal prophylaxis with micafungin between 1 January 2009 and 31 December 2014 were included. Results. There were 5 cases of probable or proven fungal infection (4.8%) according to the 2008 EORTC criteria: 2 proven, 3 probable. The types of fungal infection were 3 aspergillosis and 2 candidiasis. There were no drop-outs from the prophylaxis with micafungin due to toxicity. Conclusion. Micafungin is an antifungal agent which, used in prophylaxis, has demonstrated good efficacy and an excellent toxicity profile, making it an apparently interesting option in patients requiring antifungal prophylaxis during their hospitalisation episode.

Published
2019

5. Germline polymorphisms may improve prognostic stratification in intermediate risk acute myeloblastic leukaemia

Author

Urbano-Ispizua, A., Brunet, S., Monzó, M., Perea, G., Navarro, A., Esteve, J., Berlanga, J., Ribera, J. M., Bueno, J., Llorente, A., Besalduch, J., Guàrdia, R., Tormo, M., Pedro, C., Sánchez, J. M., Torres, P., Queipo de Llano, M. P., Font, L. L., Moraleda, J. M., Martí, J. M., Vivancos, P., Peñarrubia, M. J., Nomdedéu, J. F., Montserrat, E., and Sierra, J.

Published
2005

7. Cardiopoietic cell therapy for advanced ischemic heart failure : results at 39 weeks of the prospective, randomized, double blind, sham-controlled CHART-1 clinical trial

Author

Bartunek, Jozef, Terzic, Andre, Davison, Beth A, Filippatos, Gerasimos S, Radovanovic, Slavica, Beleslin, Branko, Merkely, Bela, Musialek, Piotr, Wojakowski, Wojciech, Andreka, Peter, Horvath, Ivan G, Katz, Amos, Dolatabadi, Dariouch, El Nakadi, Badih, Arandjelovic, Aleksandra, Edes, Istvan, Seferovic, Petar M, Obradovic, Slobodan, Vanderheyden, Marc, Jagic, Nikola, Petrov, Ivo, Atar, Shaul, Halabi, Majdi, Gelev, Valeri L, Shochat, Michael K, Kasprzak, Jaroslaw D, Sanz Ruiz, Ricardo, Heyndrickx, Guy R, Nyolczas, Noémi, Legrand, Victor, Guédès, Antoine, Heyse, Alex, Moccetti, Tiziano, Fernandez Aviles, Francisco, Jimenez Quevedo, Pilar, Bayes Genis, Antoni, Hernandez Garcia, Jose Maria, Ribichini, Flavio, Gruchala, Marcin, Waldman, Scott A, Teerlink, John R, Gersh, Bernard J, Povsic, Thomas J, Henry, Timothy D, Metra, Marco, Hajjar, Roger J, Tendera, Michal, Behfar, Atta, Alexandre, Bertrand, Seron, Aymeric, Stough, Wendy Gattis, Sherman, Warren, Cotter, Gad, Wijns, W. i. l. l. i. a. m. Collaborators Clinical investigators, Dens, sites Belgium: Ziekenhuis Oost Limburg: J., Dupont, M., Mullens, W., Janssens, M., Dolatabadi, Hoˆpital Civil de Charleroi: D., De Bruyne, Y., Lalmand, J., Dubois, P., El Nakadi, B., Aminian, A., De Vuyst, E., Gurnet, P., Gujic, M., Blankoff, I., Guedes, CHU Mont Godinne UCL: A., Gabriel, L., Seldrum, S., Doyen, C., Andre´, M., Heyse, AZ Glorieux: A., Van Durme, F., Verschuere, J., Legrand, Domaine Universitaire du Sart Tilman: V., Gach, O., D’Orio, V., Davin, L., Lancellotti, P., Baudoux, E., Ancion, A., Dulgheru, R., Vanderheyden, OLV Ziekenhuis Aalst – Cardiologie: M., Bartunek, J., Wijns, W., Verstreken, S., Penicka, . M., Gelev, P. Meeus Bulgaria: Tokuda Hospital Sofia: V., Zheleva Kichukova, I., Parapunova, R., Melamed, R., Sardovski, S., Radev, O., Yordanov, A., Radinov, A., Nenov, D., Amine, I., Petrov, City Hospital Clinic Cardiology Center: I., Kichukov, K., Nikitasov, L., Stankov, Z., Stoyanov, H., Tasheva Dimitrova, I., Angelova, M., Dimitrov, E., Minchev, M., Garvanski, I., Botev, C., Polomski, P., Alexandrovska University Hospital, Vassilev, Sofia: D., Karamfiloff, K., Tarnovska Kadreva, R., Vladimirova, L., Dimitrov, G., Hadzhiev, E., Tzvetkova, G., Andreka, . M. Atanasova Hungary: Gottsegen Gyo¨ rgy Orszagos Kardiologiai Inte´zet: P., Fontos, G., Fabian, J., Csepregi, A., Uzonyi, G., Gelei, A., Edes, Debreceni Egyetem Orvos e´s Ege´szse´gtudomanyi Centrum Altalanos Orvostudomanyi Kar Kardiologia Inte´zet: I., Balogh, L., Vajda, G., Darago, A., Gergely, S., Fulop, T., Jenei, C., Horvath, Pe´csi Tudomanyegyetem Klinikai Ko¨zpont Szıvgyogyaszati Klinika: I., Magyari, B., Nagy, A., Cziraki, A., Faludi, R., Kittka, B., Alizadeh, H., Merkely, Semmelweis Egyetem Varosmajori Szıv e´s Ergyogyaszati Klinika: B., Geller, L., Farkas, P., Szombath, G., Foldes, G., Skopal, J., Kovacs, A., Kosztin, A., Gara, E., Sydo, N., Nyolczas, MH Ege´szse´gu¨gyi Ko¨zpont Kardiologiai Osztaly: N., Kerecsen, G., Korda, A., Kiss, . M., Borsanyi, T., Polgar, B., Muk, B., Sharif, Z. Bari Ireland: HRB Clinical Research Facility: F., Atar, Y. M. Smyth Israel:Western Galilee Hospital: S., Shturman, A., Akria, L., Kilimnik, M., Brezins, M., Halabi, Ziv Medical Center: M., Dally, N., Goldberg, A., Aehab, K., Rosenfeld, I., Levinas, T., Saleem, D., Katz, Barzilai Medical Center: A., Plaev, T., Drogenikov, T., Nemetz, A., Barshay, Y., Jafari, J., Orlov, I., Nazareth Hospital EMMS: M. Omory, N. Kogan Nielsen, Shochat, Hillel Yaffe Medical Center: M., Shotan, A., Frimerman, A., Meisel, S., Asif, A., Sofer, O., Blondheim, D. S., Vazan, A., Metra, L. Arobov Italy: A. O. Spedali Civili di Brescia: M., Bonadei, I., Inama, L., Chiari, E., Lombardi, C., Magatelli, M., Russo, D., Lazzarini, V., Carubelli, V., Vassanelli, AOUI Verona – Borgo Trento Hospital: C., Ribichini, Flavio Luciano, Bergamini, C., Krampera, Mauro, Cicoria, M. A., Zanolla, L., Dalla Mura, D., Gambaro, A., Rossi, A., Pesarini Poland: Jagiellonian University Department of Cardiac, G., Musialek, Vascular Diseases at John Paul II Hospital in Krakow: P., Mazurek, A., Drabik, L., Ka˛dzielski, A., Walter, Z., Dzieciuch Rojek, M., Rubis, P., Plazak, . W., Tekieli, L., Podolec, J., Orczyk, W., Sutor, U., Zmudka, K., Olszowska, M., Podolec, P., Gruchala, Uniwersyteckie Centrum Kliniczne: M., Ciecwierz, D., Mielczarek, M., Burakowski, S., Chmielecki, M., Zielinska, M., Frankiewicz, A., Wdowczyk, J., Stopczynska, I., Bellwon, J., Mosakowska, K., Nadolna, R., Wroblewska, J., Rozmyslowska, M., Rynkiewicz, M., Marciniak, I., Raczak, G., Tarnawska, M., Taszner, M., Kasprzak, Bieganski Hospital: J., Plewka, M., Fiutowska, D., Rechcinski, T., Lipiec, P., Sobczak, M., Weijner Mik, P., Wraga, M., Krecki, R., Markiewicz, M., Haval Qawoq, D., Wojakowski, Gornosla˛skie Centrum Medyczne Sla˛skie j. Akademii Medycznej: W., Ciosek, J., Dworowy, S., Gaszewska Zurek, E., Ochala, A., Cybulski, W., Jadczyk, T., Wanha, W., Parma, Z., Kozlowski, M., Dzierzak, M., Markiewicz Serbia: Clinical Hospital Center Zvezdara, M., Arandjelovic, Cardiology Clinic: A., Sekularac, N., Boljevic, D., Bogdanovic, A., Zivkovic, S., Cvetinovic, N., Loncar, G., Clinical Centre of Serbia, Beleslin, Cardiology Clinic: B., Nedeljkovic, M., Trifunovic, D., Giga, V., Banovic, M., Nedeljkovic, I., Stepanovic, J., Vukcevic, V., Djordjevic Dikic, A., Dobric, M., Obrenovic Kircanski, B., Seferovic, Cardiology Clinic: P., Orlic, D., Tesic, M., Petrovic, O., Milinkovic, I., Simeunovic, D., Jagic, Clinical Center of Kragujevac: N., Tasic, M., Nikolic, D., Miloradovic, V., Djurdjevic, P., Sreckovic, M., Zornic, N., Clinical Hospital Center Bezanijska Kosa, Radovanovic, Cardiology Department: S., Saric, J., Hinic, S., Djokovic, A., Ðordevic, S., Bisenic, V., Markovic, O., Stamenkovic, S., Malenkovic, V., Tresnjak, J., Misic, G., Cotra, D., Tomovic, L., Vuckovic, V., Clinic of Emergency Internal Medicine, Obradovic, Military Medical Academy: S., Jovic, Z., Vukotic, S., Markovic, D., Djenic, N., Ristic Andjelkov, A., Bayes Genis, D. Ljubinka Spain: Hospital Universitario Germans Trias I. Pujol: A., Rodriguez Leor, O., Labata, C., Vallejo, N., Ferrer, E., Batlle, M., Fernandez Aviles, Hospital General Universitario Gregorio Mara~non: F., Sanz Ruiz, R., Casado, A., Loughlin, G., Zatarain, E., Anguita, J., Ferna ndez Santos, M. E., Pascual, C., Bermejo, J., Hernandez Garcia, Hospital Clinico Universitario Virgen de la Victoria: J. M., Jimenez Navarro, M., Dominguez, A., Carrasco, F., Mu~noz, A., Garcia Pinilla, J. M., Ruiz, J., Queipo de Llano, M. P., Hernandez, A., Fernandez, A., Jimenez Quevedo, Hospital Clinico San Carlos: P., Guerra, R., Biagioni, C., Gonzalez, R. A., Gomez deDiego, J. J., Mansson Broberg, L. Perez de Isla Sweden: Karolinska University Hospital: A., Sylve´n, C., Leblanc, K., Winter, R., Blomberg, P., Gunyeli, E., Ruck, A., Silva, C., Fo¨rstedt Switzerland: CardioCentro Ticino, J., Moccetti, Switzerland: T., Rossi, M., Pasotti, E., Petrova, I., Crljenica, C., Monti, C., Murzilli, R., Su¨rder, D., Moccetti, M., Turchetto, L., Locicero, V., Chiumiento, L., Maspoli, S., Mombelli, M., Anesini, A., Biggiogero, M., Ponti, G., Camporini, C., Polledri, S., Hill, G. Dolci United Kingdom: Kings College Hospital: J., Plymen, C., Amin Youssef, G., Mcdonagh, T., Drasar, E., Mijovic, A., Jouhra, F., Mcloman, D., Dworakowski, R., Webb, I., Byrne, J., and Potter, V.

Subjects
0301 basic medicine, Male, Cardiopoiesis, Cardiovascular disease, Disease severity, Marker, Precision medicine, Regenerative medicine, Stem cell, Target population, Adult, Aged, Double-Blind Method, Female, Heart Failure, Humans, Mesenchymal Stem Cell Transplantation, Middle Aged, Myocardial Ischemia, Prospective Studies, Treatment Outcome, Young Adult, Cardiology and Cardiovascular Medicine, Cell- and Tissue-Based Therapy, mesenchymal stem-cells, 030204 cardiovascular system & hematology, Cardiorespiratory Medicine and Haematology, outcomes, Fast-Track Clinical Research, Sudden cardiac death, 0302 clinical medicine, Ischemia, cardiovascular disease, Clinical endpoint, target population, CHART Program, Ejection fraction, bone-marrow, Heart Failure/Cardiomyopathy, 3. Good health, Cohort, Cardiology, Fast Track, disease severity, delivery, medicine.medical_specialty, precision medicine, Clinical Sciences, regenerative medicine, 03 medical and health sciences, cardiopoiesis, Internal medicine, medicine, Adverse effect, marker, disease, business.industry, medicine.disease, mortality, Confidence interval, Clinical trial, stem cell, Editor's Choice, 030104 developmental biology, predictors, Cardiovascular System & Hematology, Heart failure, business
Abstract

Altres ajuts: This work was supported by Celyad, SA (Mont-Saint-Guibert, Belgium). Celyad has received research grants from the Walloon Region (Belgium, DG06 funding). Cardiopoietic cells, produced through cardiogenic conditioning of patients' mesenchymal stem cells, have shown preliminary efficacy. The Congestive Heart Failure Cardiopoietic Regenerative Therapy (CHART-1) trial aimed to validate cardiopoiesis-based biotherapy in a larger heart failure cohort. This multinational, randomized, double-blind, sham-controlled study was conducted in 39 hospitals. Patients with symptomatic ischaemic heart failure on guideline-directed therapy (n = 484) were screened; n = 348 underwent bone marrow harvest and mesenchymal stem cell expansion. Those achieving > 24 million mesenchymal stem cells (n = 315) were randomized to cardiopoietic cells delivered endomyocardially with a retention-enhanced catheter (n = 157) or sham procedure (n = 158). Procedures were performed as randomized in 271 patients (n = 120 cardiopoietic cells, n = 151 sham). The primary efficacy endpoint was a Finkelstein–Schoenfeld hierarchical composite (all-cause mortality, worsening heart failure, Minnesota Living with Heart Failure Questionnaire score, 6-min walk distance, left ventricular end-systolic volume, and ejection fraction) at 39 weeks. The primary outcome was neutral (Mann–Whitney estimator 0.54, 95% confidence interval [CI] 0.47–0.61 [value > 0.5 favours cell treatment], P = 0.27). Exploratory analyses suggested a benefit of cell treatment on the primary composite in patients with baseline left ventricular end-diastolic volume 200–370 mL (60% of patients) (Mann–Whitney estimator 0.61, 95% CI 0.52–0.70, P = 0.015). No difference was observed in serious adverse events. One (0.9%) cardiopoietic cell patient and 9 (5.4%) sham patients experienced aborted or sudden cardiac death. The primary endpoint was neutral, with safety demonstrated across the cohort. Further evaluation of cardiopoietic cell therapy in patients with elevated end-diastolic volume is warranted.

Published
2017

8. The expression level of BAALC-associated microRNA miR-3151 is an independent prognostic factor in younger patients with cytogenetic intermediate-risk acute myeloid leukemia

Author

Díaz-Beyá, M, primary, Brunet, S, additional, Nomdedéu, J, additional, Cordeiro, A, additional, Tormo, M, additional, Escoda, L, additional, Ribera, J M, additional, Arnan, M, additional, Heras, I, additional, Gallardo, D, additional, Bargay, J, additional, Queipo de Llano, M P, additional, Salamero, O, additional, Martí, J M, additional, Sampol, A, additional, Pedro, C, additional, Hoyos, M, additional, Pratcorona, M, additional, Castellano, J J, additional, Nomdedeu, M, additional, Risueño, R M, additional, Sierra, J, additional, Monzó, M, additional, Navarro, A, additional, and Esteve, J, additional

Published
2015
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9. Favorable outcome of patients with acute myeloid leukemia harboring a low-allelic burden FLT3-ITD mutation and concomitant NPM1mutation: relevance to post-remission therapy

Author

Pratcorona, Marta, Brunet, Salut, Nomdedéu, Josep, Ribera, Josep Maria, Tormo, Mar, Duarte, Rafael, Escoda, Lourdes, Guàrdia, Ramon, Queipo de Llano, M. Paz, Salamero, Olga, Bargay, Joan, Pedro, Carmen, Martí, Josep Maria, Torrebadell, Montserrat, Díaz-Beyá, Marina, Camós, Mireia, Colomer, Dolors, Hoyos, Montserrat, Sierra, Jorge, and Esteve, Jordi

Abstract

Risk associated to FLT3internal tandem duplication (FLT3-ITD) in patients with acute myeloid leukemia (AML) may depend on mutational burden and its interaction with other mutations. We analyzed the effect of FLT3-ITD/FLT3wild-type (FLT3wt) ratio depending on NPM1 mutation (NPM1mut) in 303 patients with intermediate-risk cytogenetics AML treated with intensive chemotherapy. Among NPM1mut patients, FLT3wt and low ratio (<0.5) subgroups showed similar overall survival, relapse risk, and leukemia-free survival, whereas high ratio (≥0.5) patients had a worse outcome. In NPM1wt AML, FLT3-ITD subgroups showed a comparable outcome, with higher risk of relapse and shortened overall survival than FLT3wt patients. Allogeneic stem cell transplantation in CR1 was associated with a reduced relapse risk in all molecular subgroups with the exception of NPM1mut AML with absent or low ratio FLT3-ITD. In conclusion, effect of FLT3burden is modulated by NPM1mutation, especially in patients with a low ratio.

Published
2013
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10. Favorable outcome of patients with acute myeloid leukemia harboring a low-allelic burden FLT3-ITD mutation and concomitant NPM1 mutation: relevance to post-remission therapy

Author

Pratcorona, Marta, Brunet, Salut, Nomdedéu, Josep, Ribera, Josep Maria, Tormo, Mar, Duarte, Rafael, Escoda, Lourdes, Guàrdia, Ramon, Queipo de Llano, M. Paz, Salamero, Olga, Bargay, Joan, Pedro, Carmen, Martí, Josep Maria, Torrebadell, Montserrat, Díaz-Beyá, Marina, Camós, Mireia, Colomer, Dolors, Hoyos, Montserrat, Sierra, Jorge, and Esteve, Jordi

Abstract

Risk associated to FLT3 internal tandem duplication (FLT3-ITD) in patients with acute myeloid leukemia (AML) may depend on mutational burden and its interaction with other mutations. We analyzed the effect of FLT3-ITD/FLT3 wild-type (FLT3wt) ratio depending on NPM1 mutation (NPM1mut) in 303 patients with intermediate-risk cytogenetics AML treated with intensive chemotherapy. Among NPM1mut patients, FLT3wt and low ratio (<0.5) subgroups showed similar overall survival, relapse risk, and leukemia-free survival, whereas high ratio (≥0.5) patients had a worse outcome. In NPM1wt AML, FLT3-ITD subgroups showed a comparable outcome, with higher risk of relapse and shortened overall survival than FLT3wt patients. Allogeneic stem cell transplantation in CR1 was associated with a reduced relapse risk in all molecular subgroups with the exception of NPM1mut AML with absent or low ratio FLT3-ITD. In conclusion, effect of FLT3 burden is modulated by NPM1 mutation, especially in patients with a low ratio.

Published
2013
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11. Prognostic Impact of MLL Partial Tandem Duplication in Acute Myeloid Leukemia of Intermediate Cytogenetic Risk: A Subgroup Analysis of Cetlam Protocol 2003 & 2012

Author

Pratcorona, Marta, Garrido, Ana, Brunet, Salut, Esteve, Jordi, Estivill, María Camino, Queipo De Llano, M. Paz, Vives, Susana, Arnan, Montserrat, Gallardo, David, Tormo, Mar, Garcia-Guiñon, Antoni, Sampol, Antonia, Salamero, Olga, Martí, Josep Ma, Bargay, Joan, Pedro, M Carmen, Hoyos, Montserrat, Diaz-Beya, Marina, Escoda, Lourdes, Guàrdia, Ramon, Ribera, Josep, Sierra, Jorge, and Nomdedeu, Josep F.

Abstract

No relevant conflicts of interest to declare.

Published
2015
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12. The Impact Of European Leukemia Net (ELN) Genetic Classification On The Outcome Of Allogeneic Stem Cell Transplantation (ALLOHCT) For Acute Myeloid Leukemia (AML) In First Complete Remission

Author

Sierra, Jorge, Garrido, Ana, Tormo, Mar, Guardia, Ramon, Nomdedeu, Josep F, Esteve, Jordi, Ribera, Josep-Maria, Duarte, Rafael F., Paz Queipo De Llano, M., Salamero, Olga, Pedro, Carmen, Bargay, Joan, Besalduch, Juan, Llorente, Andreu, Hoyos, Montserrat, Arnan, Montserrat, Pratcorona, Marta, Vives, Susana, Calabuig, Marisa, Gallardo, David, and Brunet, Salut

Abstract

The improvements in genetic characterization of AML allowed the ELN to propose a prognostic classification into 4 categories: Favorable, Intermediate I, Intermediate II and Adverse. Several groups have tested the outcome of AML patients based on these genetic subgroups in registries and databases from prospective trials. Since ALLOSCT recommendations are being established based on the ELN risk categories, we considered of interest to investigate whether these also have an impact on the results of allogeneic transplants. This could be helpful to identify the patients that may benefit the most from ALLOHCT in the first complete remission (CR1).To investigate whether the ELN genetic groups of AML have any impact on the results of ALLOHCT performed in CR1. To identify the patients who are best candidates for transplantation, based on the ELN categories as well as in other characteristics.Patients were transplanted between 1990 and 2012. In all cases, treatment prior to transplant had consisted of anthracycline based induction and intermediate-dose cytarabine consolidation according to the CETLAM AML-88, AML-94, AML-99 and AML-03 trials. Upper age limit for transplantation was 60 years until 2002 and 70 years thereafter. Most patients above 50 years received either CD34 selected grafts or reduced intensity conditioning. GVHD prophylaxis after transplant was usually based on cyclosporine and prednisone or methotrexate. The main characteristics of patients and transplants were included in the exploratory analysis of variables influencing survival; those with a p- value up to 0.1 were incorporated as covariates to the multivariable model.One hundred ninety two patients in CR1 received an ALLOHCT from HLA-identical siblings (n=140), adult unrelated donors (n=26) or umbilical cord blood (n= 26). Age distribution of the patients was as follows: 16-35 years-old (y-o) n=65 (34%), 36-50 y-o n= 55 (29%), 51-60 y-o n= 54 (28%), >60 y-o n=18 (9%). Twenty-three patients (12%) were classified as in the favorable ELN category, 54 (28%) in the intermediate I, 41 (21%) in the intermediate II and 74 (39%) in the adverse. One-hundred fifty-seven patients (82%) had achieved CR1 after a single course of chemotherapy. Conditioning was myeloablative (MA) in 139 (72%) patients and reduced-intensity (RIC) in 53 (28%). In 76 cases of the MA regimens total body irradiation was included.Thirty-eight patients (20%) died due to transplant complications other than relapse and 47 (24%) experienced a leukemia recurrence. Overall survival (OS) and leukemia-free survivals at 8-years were 55±4% and 53±4%, respectively. Multivariate analysis of factors influencing OS included as covariates age at diagnosis of AML, ELN categories, courses to CR1 and conditioning regimen (MA versus RIC), since they had a p-value <0.1 in the univariate comparisons. The variables with independent on OS impact were age (p=0.01), courses to CR (p=001) and ELN classification (p=0.01). OS at 8 years in the favorable, intermediate I, intermediate II and adverse categories were 69±10%, 53±8%, 69±7% and 42±6%, respectively. In patients from the adverse ELN category, independent factors influencing OS in the multivariate analysis of this subgroup were age (16-60 y-o vs>60, p=0.01) and courses to CR (1 vs more, p=0.03).The ELN genetic categories have impact on OS of AML patients who receive an ALLOHCT in CR1. The results were very good in the favorable category and, most important, in intermediate II patients. Even patients in the adverse category had a substantial probability of long-term survival. This is remarkable, since the outcome of patients with adverse genetic features when treated with CT only is very poor.No relevant conflicts of interest to declare.

Published
2013
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13. Micafungin as antifungal prophylaxis in non-transplanted haemotological patients.

Author

Villaescusa T, Vázquez L, Bergua JM, García J, Romero A, Olave MT, García Belmonte D, and Queipo de Llano MP

Subjects
Adult, Aged, Aged, 80 and over, Anemia, Aplastic complications, Female, Humans, Leukemia, Myeloid, Acute complications, Lymphoma complications, Male, Middle Aged, Precursor Cell Lymphoblastic Leukemia-Lymphoma complications, Retrospective Studies, Young Adult, Antifungal Agents therapeutic use, Aspergillosis prevention & control, Candidiasis prevention & control, Hematologic Diseases complications, Micafungin therapeutic use
Abstract

Objective: Fungal infections are a major cause of morbidity and mortality in the haematological patients. These infections are mainly due to Candida spp. and Aspergillus spp. Mortality by these infections is high, but rates have descended in the latest series due to better antifungal agents. Echinocan-dins are, in vitro, very active against Candida and Aspergillus spp. The objective of the study is to analyse the efficacy and safety of micafungin in the antifungal prophylaxis of haema-tological patients on chemotherapy., Methods: A multicentre, observational retrospective study was performed in 7 Haematology Depart-ments in Spain. Patients admitted to these departments with chemotherapy or immunosuppressive treatment, and who had received antifungal prophylaxis with micafungin between 1 January 2009 and 31 December 2014 were included., Results: There were 5 cases of probable or proven fun-gal infection (4.8%) according to the 2008 EORTC criteria: 2 proven, 3 probable. The types of fungal infection were 3 as-pergillosis and 2 candidiasis. There were no drop-outs from the prophylaxis with micafungin due to toxicity., Conclusions: Micafungin is an antifungal agent which, used in prophylaxis, has demonstrated good efficacy and an excellent toxicity profile, making it an apparently interesting option in patients requiring antifungal prophylaxis during their hospitalisation episode., (©The Author 2020. Published by Sociedad Española de Quimioterapia. This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)(https://creativecommons.org/licenses/by-nc/4.0/).)

Published
2020
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15. Adverse prognostic impact of CD36 and CD2 expression in adult de novo acute myeloid leukemia patients.

Author

Perea G, Domingo A, Villamor N, Palacios C, Juncà J, Torres P, Llorente A, Fernández C, Tormo M, Queipo de Llano MP, Bargay J, Gallart M, Florensa L, Vivancos P, Martí JM, Font L, Berlanga J, Esteve J, Bueno J, Ribera JM, Brunet S, Sierra J, and Nomdedéu JF

Subjects
Acute Disease, Adolescent, Adult, Antibodies, Monoclonal, Bone Marrow metabolism, Bone Marrow pathology, Chromosome Aberrations, Chromosome Inversion, Female, Flow Cytometry, Humans, Immunophenotyping, Karyotyping, Leukemia, Myeloid genetics, Leukemia, Myeloid pathology, Male, Middle Aged, Prognosis, Survival Rate, CD2 Antigens metabolism, CD36 Antigens metabolism, Leukemia, Myeloid metabolism
Abstract

Background and Objectives: A consecutive series of acute myeloid leukemias (AML) patients was analyzed in conditions which reduce the inter-assay variations (the same flow cytometer, the same observers and the same panel of monoclonal antibodies) in order to investigate the prognostic information provided by flow cytometry., Design and Methods: Two hundred and sixty-six bone marrow (BM) samples from 326 patients enrolled in the LMA-99 protocol from the CETLAM group were studied by multiparametric flow cytometry. Immunophenotyping studies were performed on erythrocyte-lysed BM samples. Antigen expression of leukemic cells was analyzed using triple stainings with fluorochrome-conjugated combinations of monoclonal antibodies., Results: CD2 was positive in 21 cases (8%); an associated inv(16) was detected in eight CD2+ cases (38%). Two-year overall survival (OS) rate for CD2+/inv(16)+ patients was 75%, whereas it was 0% for CD2+/inv(16)- patients and 47% for CD2- patients (p=0.0001). CD36 was expressed in 37% of patients (n=98). Two-year leukemia-free survival (LFS) rate was 34% for CD36+ patients and 55% for CD36- patients (p=0.001). In the multivariate analysis, CD2+ (RR=8.4; p=0.0001) and adverse karyotype (RR=10.2; p=0.0001) were associated with a lower CR rate, CD36+ (RR=1.5; p=0.03), CD2+ (RR=2; p=0.04) and adverse karyotype (RR=4; p=0.0001) were associated with a lower OS and CD36+ (RR=2; p=0.002) and adverse karyotype (RR=3.5; p=0.005) predicted a lower LFS., Conclusions: CD2+ patients had a very poor OS when CD2/inv(16)+ cases were excluded. CD36 and CD2 expression at diagnosis can provide prognostically important information in adult de novo AML.

Published
2005
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16. MLL tandem duplication in two cases of acute myelocytic leukemia with unbalanced translocations: der(16)t(11;16)(q23;p13) and der(18)t(11;18)(q22;p11.2).

Author

Aventín A, La Starza R, Casas S, Nomdedéu J, Queipo de Llano MP, Cimino G, Lo Coco F, Sierra J, and Mecucci C

Subjects
Adult, Blotting, Southern, Cytogenetic Analysis, Female, Histone-Lysine N-Methyltransferase, Humans, In Situ Hybridization, Fluorescence, Leukemia, Myeloid, Acute etiology, Leukemia, Myeloid, Acute therapy, Male, Middle Aged, Myeloid-Lymphoid Leukemia Protein, Reverse Transcriptase Polymerase Chain Reaction, Chromosomes, Human, DNA-Binding Proteins genetics, Gene Duplication, Leukemia, Myeloid, Acute genetics, Proto-Oncogenes, Transcription Factors, Translocation, Genetic
Abstract

We describe two cases of acute myelocytic leukemia (AML), classified as M4 and M1 in the French-American-British classification, with unbalanced translocations der(16)t(11;16)(q23;p13) and der(18)t(11;18) (q22;p11.2), respectively. Molecular studies using Southern blot and reverse transcriptase-polymerase chain reaction showed an MLL rearrangement due to an internal duplication of the gene in both cases. Fluorescence in situ hybridization disclosed the presence of an extra copy of the MLL gene on 16p13 and 18p11.2, respectively, as a result of the partial trisomy of chromosome 11q. Our two cases clearly show that tandem duplication of the MLL gene may occur in AML with a partial 11q trisomy. Thus, systematic screening of this molecular defect should be performed in patients with unbalanced translocations involving 11q22 approximately q23-->qter.

Published
2003
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18. [System mastocytosis: presentation of a case evolving into myelofibrosis and no response to interferon alfa 2b].

Author

de las Nieves M, Poveda F, Queipo de Llano MP, and González-Hermoso C

Subjects
Bone Marrow pathology, Cerebral Hemorrhage etiology, Combined Modality Therapy, Fatal Outcome, Female, Histamine Antagonists therapeutic use, Humans, Interferon alpha-2, Ketotifen therapeutic use, Mastocytosis drug therapy, Mastocytosis pathology, Mastocytosis surgery, Mastocytosis therapy, Middle Aged, Prednisone therapeutic use, Primary Myelofibrosis pathology, Prognosis, Recombinant Proteins, Splenectomy, Immunologic Factors therapeutic use, Interferon-alpha therapeutic use, Mastocytosis complications, Primary Myelofibrosis etiology
Published
1997

20. [Thalassemia minor with iron overload: genetic and clinical study of a family].

Author

Queipo de Llano MP, Yebra M, Moreno M, Lacoma F, Gea JC, and Berrocal E

Subjects
Adult, Aged, Child, Child, Preschool, Female, Hemochromatosis blood, Humans, Male, Pedigree, Thalassemia blood, Thalassemia complications, Family Health, Hemochromatosis etiology, Thalassemia genetics
Abstract

A patient with thalassemia minor (TM) is reported who ingested 80 g of alcohol/day and presented an important overload of iron with deposits and a hepatic iron ratio compatible with primary hemochromatosis. The results obtained from the study of histocompatibility antigens, clinical manifestations and family analysis discarded the possibility of two genetic diseases, beta-thalassemia and primary hemochromatosis, being concomitantly present in the same progeny. Thalassemia minor and alcoholic hepatopathy are considered as having acted together and being responsible for the iron overload. The relation between alcohol ingested, TM and iron deposits is discussed.

Published
1991

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