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1.
Clin Lymphoma Myeloma Leuk ; 22(12): 883-893, 2022 12.
Artigo em Inglês | MEDLINE | ID: mdl-36057522

RESUMO

BACKGROUND: B-cell acute lymphoblastic leukemia is frequent in Hispanic adolescents and young adults. Outcomes of implementation of pediatric-inspired regimens in low-and middle-income countries are not well known. METHODS: In this study we treated 94 adolescents and young adults with a local BFM regimen designed to be affordable with the use of native L-asparaginase and mitoxantrone administered in an outpatient fashion, and the of BCR/ABL and measurable residual disease (MRD) determined by high sensitivity flow cytometry for risk stratification. RESULTS: Induction mortality was 11%; 25% of patients had to abandon treatment or be transferred to another health system. Two-year overall (OS) and event free survival (EFS) were 61.5% and 49.8%, MRD-negative patients had a 24-month OS of 85.6% vs. 69.6% (p = .024) and EFS of 76% vs. 45.5% (p = .004). Patients older than 40 years and those who abandoned treatment had worse EFS. Overall drug costs in our regimen were 52% lower than those of CALGB10403. CONCLUSION: The treatment of AYAs with ALL with an outpatient focus was implemented successfully at a reduced cost. Genetic risk assessment, treatment abandonment and lack of access to novel therapies remain major barriers for improving outcomes.


Assuntos
Pacientes Ambulatoriais , Leucemia-Linfoma Linfoblástico de Células Precursoras , Adolescente , Humanos , Adulto Jovem , Intervalo Livre de Doença , Asparaginase/uso terapêutico , Neoplasia Residual/tratamento farmacológico , Protocolos de Quimioterapia Combinada Antineoplásica/uso terapêutico , Prognóstico , Resultado do Tratamento
2.
J Oncol Pharm Pract ; 28(5): 1264-1268, 2022 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-35060420

RESUMO

INTRODUCTION: Brentuximab vedotin (BV) is a monoclonal antibody that targets CD30 antigen. It is indicated for the treatment of CD30 + lymphomas and classical Hodgkin lymphoma (HL), including advanced (stage III-IV) untreated disease, relapsed/refractory disease, and consolidation after autologous hematopoietic stem cell transplantation. In clinical trials the incidence of a hypersensitivity reaction is 1.2%. CASES REPORT: We present 3 cases of patients with refractory HL and anaphylaxis to the administration of BV ( Table 1). Symptoms are analyzed using a grading system described by Brown (2004) and a desensitization protocol was performed with a total dose of 100 mg of BV in 4 solution bags with an initial concentration of 1:1000 of total dose for cases of severe anaphylaxis, and desensitization of 3 solution bags with baseline concentration of 1: 100 for cases of moderate anaphylaxis. MANAGEMENT & OUTCOME: Intradermal skin tests were positive. Before desensitization, premedication with methylprednisolone and chlorphenamine was administered, as well as fluid therapy with 0.9% physiological solution at 100 cc/hour at induction stage, 250 cc/hour at maintenance stage, and increased to 500 cc/hour in case of hypersensitivity reaction. DISCUSSION: Drug desensitization in 12 or 16 steps allows tolerable administration of brentuximab vedotin after moderate to severe anaphylaxis. The favorable response to treatment of these patients may indicate that desensitization is a viable strategy for patients with relapsed or refractory HL.


Assuntos
Anafilaxia , Doença de Hodgkin , Imunoconjugados , Humanos , Brentuximab Vedotin/uso terapêutico , Doença de Hodgkin/tratamento farmacológico , Anafilaxia/induzido quimicamente , Anafilaxia/tratamento farmacológico , Imunoconjugados/efeitos adversos , Recidiva Local de Neoplasia/tratamento farmacológico
3.
López-Arroyo, José L.; Pérez-Zúñiga, Juan M.; Merino-Pasaye, Laura E.; Saavedra-González, Azucena; Alcivar-Cedeño, Luisa María; Álvarez-Vera, José Luis; Anaya-Cuellar, Irene; Arana-Luna, Luara L.; Ávila-Castro, David; Bates-Martín, Ramón A.; Cesarman-Maus, Gabriela; Chávez-Aguilar, Lénica A.; Peña-Celaya, José A. de la; Espitia-Ríos, María E.; Estrada-Domínguez, Patricia; Fermín-Caminero, Denisse; Flores-Patricio, Willy; García Chávez, Jaime; García-Lee, María T.; González-Pérez, María del Carmen; González-Rubio, María del Carmen; González-Villareal, María Guadalupe; Ramírez-Moreno, Fabiola; Hernández-Colin, Ana K.; Hernández-Ruiz, Eleazar; Herrera-Olivares, Wilfrido; Leyto-Cruz, Faustino; Loera-Fragoso, Sergio; Martínez-Ríos, Annel; Miranda-Madrazo, María R.; Morales-Hernández, Alba; Nava-Villegas, Lorena; Orellana-Garibay, Juan J.; Palma-Moreno, Orlando G.; Paredes-Lozano, Eugenia P.; Peña-Alcántara, Paula; Pérez-Lozano, Uendy; Pichardo-Cepín, Yayra M.; Reynoso-Pérez, Ana Carolina; Rodríguez-Serna, Mishel; Rojas-Castillejos, Flavio; Romero-Rodelo, Hilda; Ruíz-Contreras, Josué I.; Segura-García, Adela; Silva-Vera, Karina; Soto-Cisneros, Paulina M.; Tapia-Enríquez, Ana L.; Tavera-Rodríguez, Martha G.; Teomitzi-Sánchez, Óscar; Tepepa-Flores, Fredy; Valencia-Rivas, María D.; Valle-Cárdenas, Teresa; Varela-Constantino, Ana; Javier-Morales, Adrián; Martínez-Ramírez, Mario A.; Tena-Cano, Sergio; Terrazas-Marín, Ricardo; Vilchis-González, Shendel P.; Villela-Peña, Atenas; Mena-Zepeda, Verónica; Alvarado Ibarra, Martha.
Gac. méd. Méx ; 157(supl.1): S1-S37, feb. 2021. tab, graf
Artigo em Espanhol | LILACS-Express | LILACS | ID: biblio-1375490

RESUMO

resumen está disponible en el texto completo


Abstract Hemophilia is a hemorrhagic disorder with a sex-linked inherited pattern, characterized by an inability to amplify coagulation due to a deficiency in coagulation factor VIII (hemophilia A or classic) or factor IX (hemophilia B). Sequencing of the genes involved in hemophilia has provided a description and record of the main mutations, as well as a correlation with the various degrees of severity. Hemorrhagic manifestations are related to levels of circulating factor, mainly affecting the musculoskeletal system and specifically the large joints (knees, ankles and elbows). This document is a review and consensus of the main genetic aspects of hemophilia, from the inheritance pattern to the concept of women carriers, physiopathology and classification of the disorder, the basic and confirmation studies when hemophilia is suspected, the various treatment regimens based on infusion of the deficient coagulation factor as well as innovative factor-free therapies and recommendations for the management of complications associated with treatment (development of inhibitors and/or transfusion transmitted infections) or secondary to articular hemorrhagic events (hemophilic arthropathy). Finally, relevant reviews of clinical and treatment aspects of hemorrhagic pathology charachterized by acquired deficiency of FVIII secondary to neutralized antibodies named acquired hemophilia.

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