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13 results on '"Cid-Haro, Ana Rosa"'

1. Determinants of bleeding before and during immune tolerance in 222 boys with severe hemophilia A and inhibitors >5 BU

Author

Alvarèz Román, MT, Benitez Hidalgo, O, Blatny, J, Bührlen, M, Carvalho, M, Castaman, G, Chambost, H, Rosa Cid, A, Escuriola-Ettingshausen, C, Fischer, K, Van Geet, C, Gretenkort Andersson, N, Kartal-Kaess, M, Knudsen, H, Königs, C, Koskenvuo, M, Male, C, Stamm Mikkelsen, T, Molinari, A, Motwani, J, Nolan, B, d’Oiron, R, Oldenburg, J, Olivieri, M, Oudot, C, Pergantou, H, Pinto, F, Ranta, S, Zápotocká, E, Kenet, G, Carcao, M, Rivard, G, Fischer, Kathelijn, Kenet, Gili, Kurnik, Karin, Carcao, Manuel, Oldenburg, Johannes, Stamm-Mikkelsen, Torben, Cid Haro, Ana Rosa, Koskenvuo, Minna, Blatny, Jan, and Königs, Christoph

Published
2024
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2. Determinants of bleeding before and during immune tolerance in 222 boys with severe hemophilia A and inhibitors >5 BU

Author

Fischer, Kathelijn, Kenet, Gili, Kurnik, Karin, Carcao, Manuel, Oldenburg, Johannes, Stamm-Mikkelsen, Torben, Cid Haro, Ana Rosa, Koskenvuo, Minna, Blatny, Jan, Königs, Christoph, Alvarèz Román, MT, Benitez Hidalgo, O, Blatny, J, Bührlen, M, Carvalho, M, Castaman, G, Chambost, H, Rosa Cid, A, Escuriola-Ettingshausen, C, Fischer, K, Van Geet, C, Gretenkort Andersson, N, Kartal-Kaess, M, Knudsen, H, Königs, C, Koskenvuo, M, Male, C, Stamm Mikkelsen, T, Molinari, A, Motwani, J, Nolan, B, d’Oiron, R, Oldenburg, J, Olivieri, M, Oudot, C, Pergantou, H, Pinto, F, Ranta, S, Zápotocká, E, Kenet, G, Carcao, M, and Rivard, G

Abstract

•In 222 boys with severe hemophilia A and inhibitors of >5 BU, bleeding was reduced from 6.1 to 4.4 per year during ITI.•Before ITI, bleeding was independent of inhibitor titer; during ITI, bleeding increased with higher inhibitor titer and nondaily ITI.

Published
2024
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3. Emicizumab-induced photosensitivity

Author

Asensi Cantó, Pedro, additional, Rodríguez Serna, Mercedes, additional, Lloret Madrid, Pilar, additional, Solís Ruiz, Jürgen, additional, Cid Haro, Ana Rosa, additional, Bonanad Boix, Santiago, additional, and Haya Guaita, Saturnino, additional

Published
2022
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5. A genome-wide association study of resistance to HIV infection in highly exposed uninfected individuals with hemophilia A

Author

Lane, Jérôme, McLaren, Paul J., Dorrell, Lucy, Shianna, Kevin V., Stemke, Amanda, Pelak, Kimberly, Moore, Stephen, Oldenburg, Johannes, Alvarez-Roman, Maria Teresa, Angelillo-Scherrer, Anne, Boehlen, Francoise, Bolton-Maggs, Paula H.B., Brand, Brigit, Brown, Deborah, Chiang, Elaine, Cid-Haro, Ana Rosa, Clotet, Bonaventura, Collins, Peter, Colombo, Sara, Dalmau, Judith, Fogarty, Patrick, Giangrande, Paul, Gringeri, Alessandro, Iyer, Rathi, Katsarou, Olga, Kempton, Christine, Kuriakose, Philip, Lin, Judith, Makris, Mike, Manco-Johnson, Marilyn, Tsakiris, Dimitrios A., Martinez-Picado, Javier, Mauser-Bunschoten, Evelien, Neff, Anne, Oka, Shinichi, Oyesiku, Lara, Parra, Rafael, Peter-Salonen, Kristiina, Powell, Jerry, Recht, Michael, Shapiro, Amy, Stine, Kimo, Talks, Katherine, Telenti, Amalio, Wilde, Jonathan, Yee, Thynn Thynn, Wolinsky, Steven M., Martinson, Jeremy, Hussain, Shehnaz K., Bream, Jay H., Jacobson, Lisa P., Carrington, Mary, Goedert, James J., Haynes, Barton F., McMichael, Andrew J., Goldstein, David B., and Fellay, Jacques

Published
2013
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6. Risk Factors for the Progression from Low to High Titres in 260 Children with Severe Haemophilia A and Newly Developed Inhibitors

Author

Mancuso, Maria Elisa, Fischer, Kathelijn, Santagostino, Elena, Oldenburg, Johannes, Platokouki, Helen, Königs, Cristoph, Escuriola-Ettingshausen, Carmen, Rivard, George E, Cid-Haro, Ana Rosa, Carcao, Manuel, Ljung, Rolf, Petrini, Pia, Altisent, Carmen, Kenet, Gili, Liesner, Raina, Kurnik, Karin, Auerswald, Günther, Chambost, Hérvè, Mäkipernaa, Anne, Molinari, Angelo Claudio, Williams, Mike, van den Berg, H Marijke, and European Pediatric Network for Haemophilia Management (PedNet) the REMAIN (REal life MAnagement of children with INhibitors) Study Group

Subjects
immune tolerance induction, congenital, hereditary, and neonatal diseases and abnormalities, children, hemic and lymphatic diseases, inhibitors, haemophilia A, high titre
Abstract

In children with severe haemophilia A, inhibitors to factor VIII (FVIII) usually develop during the first 50 treatment exposure days and are classified as low or high titre depending on the peak inhibitor titre being greater or less than 5 Bethesda units/mL (BU/mL). Classification of the inhibitor may change with time, as some low-titre inhibitors progress to high titre following re-exposure to FVIII concentrate. The aim of this study was to investigate potential risk factors for such a progression in children with severe haemophilia A and newly diagnosed inhibitors. This study was a follow-up study of the PedNet Registry and included 260 children with severe haemophilia A and inhibitors born between 1990 and 2009 and recruited consecutively from 31 haemophilia centres. Clinical and laboratory data were collected from the date of each child's first positive inhibitor test for at least 3 years. At the time of first positive inhibitor test, 49% (n = 127) had low-titre inhibitors, with 50% of them progressing to high titre and only 25% maintaining low titres. The FVIII gene (F8) mutation type was known in 247 patients (95%), and included 202 (82%) null mutations. The progression to high-titre inhibitors was associated with null F8 mutations (odds ratio [OR]: 2.6; 95% confidence interval [CI]: 1.0-6.5), family history of inhibitors (OR: 7.2; 95% CI: 1.8-28.4) and the use of high-dose immune tolerance induction, defined as >= 100 IU FVIII concentrate/kg/d (OR: 3.9; 95% CI: 1.5-10.0). These results suggest that high-dose immune tolerance induction should be avoided as the initial strategy in patients who develop low-titre FVIII inhibitors.

Published
2017

7. Risk Factors for the Progression from Low to High Titres in 260 Children with Severe Haemophilia A and Newly Developed Inhibitors

Author

Cardiovasculaire Epi Team 1, Circulatory Health, JC onderzoeksprogramma Cardiovasculaire Epidemiologie, Poli Van Creveldkliniek Medisch, Child Health, Datamanagement 1, Mancuso, Maria Elisa, Fischer, Kathelijn, Santagostino, Elena, Oldenburg, Johannes, Platokouki, Helen, Königs, Cristoph, Escuriola-Ettingshausen, Carmen, Rivard, George E, Cid-Haro, Ana Rosa, Carcao, Manuel, Ljung, Rolf, Petrini, Pia, Altisent, Carmen, Kenet, Gili, Liesner, Raina, Kurnik, Karin, Auerswald, Günther, Chambost, Hérvè, Mäkipernaa, Anne, Molinari, Angelo Claudio, Williams, Mike, van den Berg, H Marijke, European Pediatric Network for Haemophilia Management (PedNet) the REMAIN (REal life MAnagement of children with INhibitors) Study Group, Cardiovasculaire Epi Team 1, Circulatory Health, JC onderzoeksprogramma Cardiovasculaire Epidemiologie, Poli Van Creveldkliniek Medisch, Child Health, Datamanagement 1, Mancuso, Maria Elisa, Fischer, Kathelijn, Santagostino, Elena, Oldenburg, Johannes, Platokouki, Helen, Königs, Cristoph, Escuriola-Ettingshausen, Carmen, Rivard, George E, Cid-Haro, Ana Rosa, Carcao, Manuel, Ljung, Rolf, Petrini, Pia, Altisent, Carmen, Kenet, Gili, Liesner, Raina, Kurnik, Karin, Auerswald, Günther, Chambost, Hérvè, Mäkipernaa, Anne, Molinari, Angelo Claudio, Williams, Mike, van den Berg, H Marijke, and European Pediatric Network for Haemophilia Management (PedNet) the REMAIN (REal life MAnagement of children with INhibitors) Study Group

Published
2017

8. Intercambio guiado por farmacocinética de factores VIII de vida media estándar a factores VIII de vida media extendida pegilados en la terapia de la hemofilia A en práctica clínica

Author

Choví-Trull, Maria, Megías-Vericat, Juan Eduardo, Bonanad Boix, Santiago, Haya Guaita, Saturnino, Cid Haro, Ana Rosa, Aguilar Rodriguez, Marta, and Poveda Andrés, Jose Luis

Abstract

analizar las diferencias en los parámetros farmacocinéticos y clínicos (tasas de sangrado y salud articular) antes y después del intercambio de factores VIII (FVIII) de vida media estándar a FVIII de vida media extendida pegilados en pacientes con hemofilia A grave/moderada en profilaxis, un año antes y después del intercambio en vida real.

Published
2024
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11. A genome-wide association study of resistance to HIV infection in highly exposed uninfected individuals with hemophilia A

Author

Lane, Jérôme, McLaren, Paul J., Dorrell, Lucy, Shianna, Kevin V., Stemke, Amanda, Pelak, Kimberly, Moore, Stephen, Oldenburg, Johannes, Boehlen, Francoise, Alvarez-Roman, Maria Teresa, Angelillo-Scherrer, Anne, Bolton-Maggs, Paula H. B., Brand, Brigit, Brown, Deborah, Chiang, Elaine, Cid-Haro, Ana Rosa, Clotet, Bonaventura, Collins, Peter, Colombo, Sara, Dalmau, Judith, Fogarty, Patrick, Giangrande, Paul, Gringeri, Alessandro, Iyer, Rathi, Katsarou, Olga, Kempton, Christine, Kuriakose, Philip, Lin, Judith, Makris, Mike, Manco-Johnson, Marilyn, Tsakiris, Dimitrios A., Martinez-Picado, Javier, Mauser-Bunschoten, Evelien, Neff, Anne, Oka, Shinichi, Oyesiku, Lara, Parra, Rafael, Peter-Salonen, Kristiina, Powell, Jerry, Recht, Michael, Shapiro, Amy, Stine, Kimo, Talks, Katherine, Telenti, Amalio, Wilde, Jonathan, Yee, Thynn Thynn, Wolinsky, Steven M., Martinson, Jeremy, Hussain, Shehnaz K., Bream, Jay H., Jacobson, Lisa P., Carrington, Mary, Goedert, James J., Haynes, Barton F., McMichael, Andrew J., Goldstein, David B., and Fellay, Jacques

Subjects
610 Medicine & health, 3. Good health
Abstract

Human genetic variation contributes to differences in susceptibility to HIV-1 infection. To search for novel host resistance factors, we performed a genome-wide association study (GWAS) in hemophilia patients highly exposed to potentially contaminated factor VIII infusions. Individuals with hemophilia A and a documented history of factor VIII infusions before the introduction of viral inactivation procedures (1979-1984) were recruited from 36 hemophilia treatment centers (HTCs), and their genome-wide genetic variants were compared with those from matched HIV-infected individuals. Homozygous carriers of known CCR5 resistance mutations were excluded. Single nucleotide polymorphisms (SNPs) and inferred copy number variants (CNVs) were tested using logistic regression. In addition, we performed a pathway enrichment analysis, a heritability analysis, and a search for epistatic interactions with CCR5 Δ32 heterozygosity. A total of 560 HIV-uninfected cases were recruited: 36 (6.4%) were homozygous for CCR5 Δ32 or m303. After quality control and SNP imputation, we tested 1 081 435 SNPs and 3686 CNVs for association with HIV-1 serostatus in 431 cases and 765 HIV-infected controls. No SNP or CNV reached genome-wide significance. The additional analyses did not reveal any strong genetic effect. Highly exposed, yet uninfected hemophiliacs form an ideal study group to investigate host resistance factors. Using a genome-wide approach, we did not detect any significant associations between SNPs and HIV-1 susceptibility, indicating that common genetic variants of major effect are unlikely to explain the observed resistance phenotype in this population.

12. A genome-wide association study of resistance to HIV infection in highly exposed uninfected individuals with hemophilia A

Author

Lane, Jérôme, McLaren, Paul J., Dorrell, Lucy, Shianna, Kevin V., Stemke, Amanda, Pelak, Kimberly, Moore, Stephen, Oldenburg, Johannes, Alvarez-Roman, Maria Teresa, Angelillo-Scherrer, Anne, Boehlen, Francoise, Bolton-Maggs, Paula H.B., Brand, Brigit, Brown, Deborah, Chiang, Elaine, Cid-Haro, Ana Rosa, Clotet, Bonaventura, Collins, Peter, Colombo, Sara, Dalmau, Judith, Fogarty, Patrick, Giangrande, Paul, Gringeri, Alessandro, Iyer, Rathi, Katsarou, Olga, Kempton, Christine, Kuriakose, Philip, Lin, Judith, Makris, Mike, Manco-Johnson, Marilyn, Tsakiris, Dimitrios A., Martinez-Picado, Javier, Mauser-Bunschoten, Evelien, Neff, Anne, Oka, Shinichi, Oyesiku, Lara, Parra, Rafael, Peter-Salonen, Kristiina, Powell, Jerry, Recht, Michael, Shapiro, Amy, Stine, Kimo, Talks, Katherine, Telenti, Amalio, Wilde, Jonathan, Yee, Thynn Thynn, Wolinsky, Steven M., Martinson, Jeremy, Hussain, Shehnaz K., Bream, Jay H., Jacobson, Lisa P., Carrington, Mary, Goedert, James J., Haynes, Barton F., McMichael, Andrew J., Goldstein, David B., Fellay, Jacques, Lane, Jérôme, McLaren, Paul J., Dorrell, Lucy, Shianna, Kevin V., Stemke, Amanda, Pelak, Kimberly, Moore, Stephen, Oldenburg, Johannes, Alvarez-Roman, Maria Teresa, Angelillo-Scherrer, Anne, Boehlen, Francoise, Bolton-Maggs, Paula H.B., Brand, Brigit, Brown, Deborah, Chiang, Elaine, Cid-Haro, Ana Rosa, Clotet, Bonaventura, Collins, Peter, Colombo, Sara, Dalmau, Judith, Fogarty, Patrick, Giangrande, Paul, Gringeri, Alessandro, Iyer, Rathi, Katsarou, Olga, Kempton, Christine, Kuriakose, Philip, Lin, Judith, Makris, Mike, Manco-Johnson, Marilyn, Tsakiris, Dimitrios A., Martinez-Picado, Javier, Mauser-Bunschoten, Evelien, Neff, Anne, Oka, Shinichi, Oyesiku, Lara, Parra, Rafael, Peter-Salonen, Kristiina, Powell, Jerry, Recht, Michael, Shapiro, Amy, Stine, Kimo, Talks, Katherine, Telenti, Amalio, Wilde, Jonathan, Yee, Thynn Thynn, Wolinsky, Steven M., Martinson, Jeremy, Hussain, Shehnaz K., Bream, Jay H., Jacobson, Lisa P., Carrington, Mary, Goedert, James J., Haynes, Barton F., McMichael, Andrew J., Goldstein, David B., and Fellay, Jacques

Abstract

Human genetic variation contributes to differences in susceptibility to HIV-1 infection. To search for novel host resistance factors, we performed a genome-wide association study (GWAS) in hemophilia patients highly exposed to potentially contaminated factor VIII infusions. Individuals with hemophilia A and a documented history of factor VIII infusions before the introduction of viral inactivation procedures (1979-1984) were recruited from 36 hemophilia treatment centers (HTCs), and their genome-wide genetic variants were compared with those from matched HIV-infected individuals. Homozygous carriers of known CCR5 resistance mutations were excluded. Single nucleotide polymorphisms (SNPs) and inferred copy number variants (CNVs) were tested using logistic regression. In addition, we performed a pathway enrichment analysis, a heritability analysis, and a search for epistatic interactions with CCR5 Δ32 heterozygosity. A total of 560 HIV-uninfected cases were recruited: 36 (6.4%) were homozygous for CCR5 Δ32 or m303. After quality control and SNP imputation, we tested 1 081 435 SNPs and 3686 CNVs for association with HIV-1 serostatus in 431 cases and 765 HIV-infected controls. No SNP or CNV reached genome-wide significance. The additional analyses did not reveal any strong genetic effect. Highly exposed, yet uninfected hemophiliacs form an ideal study group to investigate host resistance factors. Using a genome-wide approach, we did not detect any significant associations between SNPs and HIV-1 susceptibility, indicating that common genetic variants of major effect are unlikely to explain the observed resistance phenotype in this population

13. Pharmacokinetic-guided switching from standard half-life factor VIII to extended half-life pegylated factor VIII in the therapy of hemophilia A in clinical practice.

Author

Choví-Trull M, Megías-Vericat JE, Bonanad Boix S, Haya Guaita S, Cid Haro AR, Aguilar Rodriguez M, and Poveda Andrés JL

Abstract

Objective: To analyze the differences in pharmacokinetic and clinical parameters (bleeding rates and joint health) before and after switching from standard half-life factor VIII (FVIII) to extended half-life pegylated FVIII in patients with severe/moderate hemophilia A on prophylaxis, one year before and after the switch in real-life., Method: This is a single-center, comparative, observational, sequential, retrospective, and multidisciplinary study. Population pharmacokinetic models from the WAPPS-Hemo® application were used to calculate pharmacokinetic parameters and individualize prophylaxis. The annual rate of total and joint bleeds, joint health (Hemophilia Joint Health Score), plasma half-life and area under the curve ratios, FVIII consumption, administration frequency, and cost were analyzed., Results: Thirty-eight adult patients with hemophilia A who switched from standard half-life FVIII to extended half-life pegylated FVIII were analyzed. Significant improvements (p < 0.05) were observed in all pharmacokinetic parameters, with plasma half-life and area under the curve improvement ratios of 1.5 and 1.9, respectively, as well as reductions in annual total and joint bleeding rates were registered. A higher number of patients with zero total (16.0 vs. 29.0) and joint bleeds (23.0 vs. 33.0) was also observed. The median reductions in administration frequency and dose/kg/week were 30.0% and 19.7%, respectively, avoiding 44.3 infusions/patient/year, resulting in savings of 20,843 €/patient/year. Furthermore, joint health improved (23.0 vs. 21.0; p = 0.017), and target joints resolved after the switch., Conclusions: The pharmacokinetically guided switch from standard half-life FVIII to pegylated FVIII demonstrated significant clinical benefits with reduced bleeding rates and improvements in joint health. Additionally, improvements in pharmacokinetic parameters were observed, allowing for reduced treatment burden by decreasing administration frequency, as well as lower consumption and costs., (Copyright © 2024. Publicado por Elsevier España, S.L.U.)

Published
2024
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