¿Cómo diseñar, aplicar y evaluar un programa de Mentoring en enfermedad renal crónica? evaluación narrativa del impacto en 6 centros asistenciales

Antecedentes y objetivo La enfermedad renal crónica (ERC) requiere de un proceso de adaptación en el paciente, que se puede facilitar con el apoyo de los profesionales sanitarios, así como por iguales capacitados. El objetivo de este estudio es presentar la puesta en marcha de un programa piloto de paciente mentor para promover la adaptación de los pacientes con ERC. Materiales y método Diseño mixto (cuantitativo y cualitativo) pre-post. El estudio se llevó a cabo en 6 hospitales de España. Los instrumentos utilizados para medir el impacto fueron escalas elaboradas ad-hoc (formato de respuesta escala de Likert de 10 puntos) de satisfacción y adquisición de competencias, así como la creación de grupos focales con 8 pacientes mentores y 10 profesionales sanitarios. Se dividió el programa en 4 fases: 1) Diseño y validación de contenidos del programa manualizado y selección de pacientes mentores; 2) Formación a mentores, satisfacción con la formación y competencias adquiridas por los mentores; 3) Implementación de los grupos de apoyo mutuo y perfil de los asistentes a los grupos de apoyo mutuo, y 4) Evaluación y resultados del programa de Mentoring. Resultados Se han formado a un total de 39 mentores en habilidades para conducción de grupos, así como para facilitar apoyo emocional. Se han conducido 22 grupos de apoyo con 121 participantes (22% cuidadores). El 65% de los pacientes estaban en consulta de ERC. Un 65% de los pacientes participantes consideraron hacer algún cambio en su estilo de vida tras la asistencia al programa. Todos los ítems que evalúan satisfacción y utilidad han mostrado una puntuación muy elevada, por encima del valor 8, 5 sobre 10. Conclusiones Este es el primer programa manualizado de Mentoring en ERC llevado a cabo de manera simultánea en 6 hospitales españoles. La naturaleza del programa, manualizado y altamente estructurado, permite su replicabilidad minimizando el riesgo de error. Background and objective Chronic kidney disease (CKD) requires patients to participate in an adaptation process, which may be facilitated with the support of healthcare professionals and trained peers. The objective of this study is to present the implementation of a pilot patient mentoring programme to promote adaptation in patients with CKD. Materials and method Pre-test-post-test design (quantitative and qualitative). The study was carried out in six hospitals in Spain. The instruments used to measure impact were ad-hoc scales (10-point Likert scale response format) on satisfaction and skill acquisition, as well as the creation of focus groups with eight patient mentors and 10 healthcare professionals. The programme was split into four phases: 1. Design and validation of the manualised programme''s content, and selection of patient mentors; 2. Mentor training, satisfaction with training and skills acquired by the mentors; 3. Implementation of mutual support groups and profile of those attending these mutual support groups; 4. Assessment and results of the Mentoring programme. Results In total, 39 mentors were trained on group management skills, as well as how to provide emotional support. 22 support groups were held, with 121 participants (22% carers). The 65% of the patients were attending the CKD clinic. 65% of the participating patients considered making some form of lifestyle change after taking part in the programme. All the items assessing satisfaction and usefulness scored very highly, achieving 8.5 out of 10 or above. Conclusions This is the first manualised mentoring programme in CKD to be undertaken simultaneously in six Spanish hospitals. The manualised and highly structured nature of the programme make it easy to replicate, minimising the risk of error

Expression of MALT1 oncogene in hematopoietic stem/progenitor cells recapitulates the pathogenesis of human lymphoma in mice

Chromosomal translocations involving the MALT1 gene are hallmarks of mucosa-associated lymphoid tissue (MALT) lymphoma. To date, targeting these translocations to mouse B cells has failed to reproduce human disease. Here, we induced MALT1 expression in mouse Sca1(+)Lin(-) hematopoietic stem/progenitor cells, which showed NF-κB activation and early lymphoid priming, being selectively skewed toward B-cell differentiation. These cells accumulated in extranodal tissues and gave rise to clonal tumors recapitulating the principal clinical, biological, and molecular genetic features of MALT lymphoma. Deletion of p53 gene accelerated tumor onset and induced transformation of MALT lymphoma to activated B-cell diffuse large-cell lymphoma (ABC-DLBCL). Treatment of MALT1-induced lymphomas with a specific inhibitor of MALT1 proteolytic activity decreased cell viability, indicating that endogenous Malt1 signaling was required for tumor cell survival. Our study shows that human-like lymphomas can be modeled in mice by targeting MALT1 expression to hematopoietic stem/progenitor cells, demonstrating the oncogenic role of MALT1 in lymphomagenesis. Furthermore, this work establishes a molecular link between MALT lymphoma and ABC-DLBCL, and provides mouse models to test MALT1 inhibitors. Finally, our results suggest that hematopoietic stem/progenitor cells may be involved in the pathogenesis of human mature B-cell lymphomas

Analysis of renal impairment in MM-003, a phase III study of pomalidomide + low‐dose dexamethasone versus high‐dose dexamethasone in refractory or relapsed and refractory multiple myeloma

Pomalidomide + low-dose dexamethasone is effective and well tolerated for refractory or relapsed and refractory multiple myeloma after bortezomib and lenalidomide failure. The phase III trial MM-003 compared pomalidomide + low-dose dexamethasone with high-dose dexamethasone. This subanalysis grouped patients by baseline creatinine clearance ≥ 30 - < 60 mL/min (n=93, pomalidomide + low-dose dexamethasone; n=56, high-dose dexamethasone) or ≥ 60 mL/min (n=205, pomalidomide + low-dose dexamethasone; n=93, high-dose dexamethasone). Median progression-free survival was similar for both subgroups and favored pomalidomide + low-dose dexamethasone versus high-dose dexamethasone: 4.0 versus 1.9 months in the group with baseline creatinine clearance ≥ 30 - < 60 mL/min (P<0.001) and 4.0 versus 2.0 months in the group with baseline creatinine clearance ≥ 60 mL/min (P<0.001). Median overall survival for pomalidomide + low-dose dexamethasone versus high-dose dexamethasone was 10.4 versus 4.9 months (P=0.030) and 15.5 versus 9.2 months (P=0.133), respectively. Improved renal function, defined as an increase in creatinine clearance from < 60 to ≥ 60 mL/min, was similar in pomalidomide + low-dose dexamethasone and high-dose dexamethasone patients (42% and 47%, respectively). Improvement in progression-free and overall survival in these patients was comparable with that in patients without renal impairment. There was no increase in discontinuations of therapy, dose modifications, and adverse events in patients with moderate renal impairment. Pomalidomide at a starting dose of 4 mg + low-dose dexamethasone is well tolerated in patients with refractory or relapsed and refractory multiple myeloma, and of comparable efficacy if moderate renal impairment is present. © 2016 Ferrata Storti Foundation